The Acutely Ill Patient: Key Investigations

Hannah Cooke, 2016/17
The Acutely Ill Patient
Key Investigations
Arterial Blood Gas
ABGs are indicated in many circumstances
- Respiratory failure
- Any severe illness that could potentially lead to metabolic acidosis (sepsis, cardiac failure,
liver failure, renal failure, DKA)
- Where quick blood results are needed
Contraindications and cautions to ABG sampling include
- Sampling from an arm with an IV infusion in progress

- Abnormal or infectious skin processes at the puncture site
- Arterial graft, surgical shunt, or AV fistula in the arm
- History of arterial spasm following previous ABG
- History of clotting disorders or anticoagulant use
- Known, or suspected, aneurysm at the puncture site
Complications of ABG include
- Vascular thrombosis or spasm

- Distal and proximal embolus
- Bleeding or haematoma formation
- Pain, infection, and local damage
Procedure
First, clarify the following with the patient
- Identity check and informed consent. Inform the patient that it will be more painful than
venous blood sampling
- Known allergies, previous difficulties, or complications
- Ask the patient if they have a preferred site
The radial artery is used where possible as this is more superficial (0.5 – 1cm below the skin) and
therefore pressure is easily applied to stop bleeding
- The radial artery cannot be used where there is absent ulnar circulation, impaired circulation
to the hand, underlying skeletal trauma, or an AV fistula
Ulnar circulation is assessed using the modified Allen’s test

1. Raise the patient’s hand and occlude the radial and ulnar circulations
2. Ask the patient to make a fist for 20 seconds
3. Ask the patient to open their hand, observe for blanching
4. Release pressure on the ulnar artery, and ensure that colour returns to the hand within 7
seconds
The femoral artery is used as an alternative, this lies 2 – 4 cm below the skin, and therefore pressure
cannot be as easily applied to arrest bleeding
- The femoral artery cannot be used where there is extensive vascular disease (due to risk of
plaque embolus), arterial grafts, or in children
Collect and prepare equipment
- Identify where the blood gas machine is and record the patient’s FiO2
- Gloves, apron, sharps bin
- ABG dry heparin self-venting syringe with stopper and needle safety device
o Radial needles are 23g (blue)
o Femoral needles are 21g (green)
- Gauze and tape
- Chlorhexidine skin prep
The steps in performing an ABG are listed below
1. Wash hands and don gloves, ensure the patient’s wrist is supported comfortably, loosen the
needle sheath and expel air from the syringe
2. Palpate the radial artery for the point at which the pulse is maximal
3. Keeping your finger at the point of maximal pulse, clean the skin in front
4. Holding the syringe like a pen, steadily insert the needle at a 45 angle, allow to fill with 1 –
2ml of blood
5. Remove needle and apply pressure to the site for a minimum of 5 minutes
6. While applying pressure: activate needle safety device, invert syringe for 30 seconds to mix
heparin
7. Ensure sample is analysed within 15 minutes
Interpretation
Many values are given on an ABG; these are summarised below – alongside normal ranges
Factor Reference Range
pH 7.35 – 7.45
Base Excess +/- 2
Bicarbonate 22 – 26
PaO2 11.0 – 13.0

PaCO2 4.7 – 6.0
Lactate <2.0
Other factors that can be measured include
- SaO2
- Hb
- Glucose
- Electrolytes
The stepwise approach to their interpretation is as follows
1. Is the patient adequately oxygenated?

- Oxygenation should be around 10 less than inspired concentration i.e. 10-13kPa on
air (21%), but if on 100% oxygen it should be >70kPa
2. Is there type 1 or type 2 respiratory failure
- Type 1 = PaO2 <8kPa
- Type 2 = PaO2 <8kPa and PaCO2 >6kPa
3. What is the pH
4. Is there a metabolic/respiratory alkalosis/acidosis
- Look at PaCO2 if this is high in acidosis = respiratory, if this is low in alkalosis =
respiratory. Vice versa/ normal = metabolic
- Bicarbonate and base excess. Base excess is negative where bicarbonate is low, and
positive where bicarbonate is raised
- Lactate, this will be raised in metabolic acidosis (including sepsis)
5. Is there are mixed picture or any compensation occurring
6. Are there any other abnormalities e.g. Hb, glucose, electrolytes
There are two further factors that can be assessed where relevant
- Alveolar-arterial oxygen gradient

- If this is normal in T2RF it indicates the cause is not related to lung disease
- If this is raised it indicates intrinsic lung disease
- Anion gap (10 – 18mmol/L) is useful in distinguishing causes of metabolic acidosis
Acidosis Alkalosis
Respiratory Hypoventilation (T2RF) Hyperventilation
- Lung disease - Anxiety

- Neuromuscular dysfunction - Hypoxia
- Mechanical lung dysfunction - Acute pulmonary insult (T1RF)
Metabolic High anion gap (new acid added to Loss of H+
body or retaining H+)
- Vomiting
- Lactic acidosis* - Hyperaldosteronism
- DKA
- Drugs/toxins**
- Renal failure
Low/normal anion gap (losing HCO3-)
- RTA
- Hypoaldosteronism e.g.
medications, Addison’s
- GI tract losses (diarrhoea,
fistula)
*Lactate can be raised in sepsis, poor tissue perfusion, seizure, liver failure, or as a side effect of
salbutamol or metformin
** Drugs and toxins causing metabolic acidosis include salicylate, ethylene glycol, and methanol
Following CPR, there is generally a mixed respiratory and metabolic acidosis
Venous Blood Gas
Venous blood gas can be used as an alternative to ABG, particularly where respiratory causes are not
thought to be the patient’s primary issue
- VBGs can only give accurate information about metabolic derangement

VBGs are best taken from a vein without a tourniquet, however in reality this is difficult
When analysing VBG results, it is important to remember the following
- pH is 0.02 – 0.04 lower

- HCO3- is comparable
- Lactate is comparable
- PaO2 and PaCO2 cannot be reliably interpreted
NEWS Chart
NEWS is the national early warning score, this is a chart used to record the patient’s vital signs and
indicate derangement in the following fields
- Heart rate: 51 – 90
- Respiratory rate: 12 – 20
- Temperature: 36.1 – 38.0
- Systolic Blood pressure (diastolic is also recorded): 111 – 219
- SpO2: >96%
- Level of consciousness (AVPU): A
The NEWS chart also contains space to record pain severity and urine output, although these do not
form part of the score itself
NEWS allows risk stratification of the patient, adjustment of monitoring frequency, and clinical
response
NEW score Clinical Risk Monitoring Frequency Clinical Response

0 Low 12 hourly Continue routine NEWS
1–4 Low 4 – 6 hourly Assessment needed by registered

nurse
5–6 Medium 1 hourly Medical team urgently informed
3 in one parameter Urgent assessment by doctor
>7 High Continuous Medical team immediately
informed
Emergency assessment by doctor
?Transfer to HDU/ITU
PEWS
Paediatric early warning scores are also routinely used, these are age specific
- <1
- 1 – 5 years
- 5 – 12 years
- 12 – 18 years
The following features are assessed and scored
- Respiratory rate
- SpO2
- Respiratory distress
- Heart rate
- Systolic blood pressure
- CRT
The maximum score on a PEWS chart is 26, and risk stratification is based upon this
PEW Score Clinical Response

1 – 4, or GCS decrease by 1 point Discuss with nurse in charge
Increase frequency of observations
5 – 8, or GCS decrease by 2 points Inform nurse in charge
Medical team informed for urgent assessment
>9, or GCS <11 Medical team informed immediately
Transfer to PICU/HDU
ECG Interpretation
With any ECG, it is first important to check the time that it was taken, and the patient details. Then
look at the calibration – paper speed should be 25mm/s and height 10mm
A 12 lead ECG should be reported in a set method, covering the following
- Rate and rhythm

- Conduction intervals and abnormalities
- Cardiac axis
- QRS complex
- ST segments and T wave
First, the rhythm strip should be assessed
1. What is the rate, 300/ the number of large squares in the R-R interval. If irregular, rate is the
total number of R waves x10
2. Is the rhythm regular or irregular
3. Are there any p waves (NB: look for p-mitrale (left atrial hypertrophy) and p-pulmonale
(right atrial hypertrophy)) i.e. sinus rhythm
4. Is the PR interval normal (>0.12s, <0.2s (3 - 5 small squares) – constant length)
5. Do all P waves conduct to form QRS complexes
6. Is the QRS complex normal (widened if >0.12s (3 small squares))
Arrhythmias can be detected on the rhythm strip
- Supraventricular arrhythmias, in which the QRS complex will be narrow (including SAN
arrhythmias such as AF and atrial flutter)
- Ventricular arrhythmias, in which the QRS complex will be broad
- Bradyarrhythmias, where the cause is heart block
If the rate is >100bpm, but all other aspects are normal – this is simply sinus tachycardia. If the rate
is <60bpm, but all other aspects are normal – this is sinus bradycardia.
Atrial Fibrillation
1. Rate will usually be normal to fast

2. Irregular rhythm
3. No p waves
4. Normal QRS
In atrial fibrillation, there will be an absence of p waves on the ECG trace
- This is because all p waves are fragmented, due to deregulated SAN activity
This p wave fragmentation manifests as a wondering baseline on the trace. As there is no

coordinated p wave firing, QRS complexes occur at random irregular intervals
Atrial Flutter
Atrial flutter is not as serious as, but can progress to, atrial fibrillation. In atrial flutter there is a ‘saw-
tooth’ appearance to the ECG, with p waves occurring frequently
- QRS complexes are regular, and will follow a certain number of p waves
Paroxysmal Atrial Tachycardia
In paroxysmal atrial tachycardia, there is an occasional run of ECG trace in which the t waves will
fuse with the p waves following them
This is often an adverse effect of digoxin
- Other adverse effect is ‘reverse tick’ T waves on ECG
Wolff-Parkinson-White
WPW syndrome is a congenital supraventricular tachycardia due to an accessory pathway between

the atria and ventricles, bypassing the AV node delay
1. Normal rate
2. Regular rhythm
3. P waves present
4. Short PR interval
5. Broad QRS showing a delta wave pattern – slurred upstroke into QRS
6. There can be right or left bundle branch block
Ventricular Tachycardia
1. Fast rate >200bpm

2. Regular rhythm
3. No p waves
4. Broad QRS
Ventricular tachycardia leads to a broad-complex tachycardia (as opposed to the narrow complex
tachycardia seen above). The p waves will be obscured on the trace. The QRS complexes may vary in
amplitude (Toursades-du-Pointe) where the cardiac axis twists around the iso-electric line
Ventricular Fibrillation
1. Very fast rate

2. Irregular rhythm
3. No p waves
4. Broad QRS with abnormal morphology
Conduction Blocks
Conduction blocks result in bradyarrhythmias; there are three main forms of these
First degree heart block is where there is a prolongation of the PR interval (delay in conduction), this
should usually be no more than 5 small squares
1. Rate will be bradycardic ~50bpm

2. Regular rhythm
3. Present p waves
4. Prolonged PR interval
5. All p waves conduct to a QRS complex
6. QRS normal
This does not typically require any treatment
Second degree heart block is in two types; Mobitz 1 and 2 (intermittent failure of conduction)
Mobitz type 1 (Wenckebach) heart block occurs where the PR interval elongates each time until
there is a dropped beat
1. Rate will be bradycardic, but not drastically

2. Irregular rhythm
3. Present p waves
4. PR interval will elongate each time
5. Not all p waves will be conducting
6. QRS will be normal, but some will be absent
Mobitz type 2 heart block occurs where there is a fixed PR interval with a fixed heart block e.g. 3 p
waves to 1 QRS complex
1. Rate will be bradycardic, around 30bpm

2. Rhythm will be regular
3. Present p waves
4. Prolonged PR interval
5. There will be a fixed ratio of p waves to QRS complexes (example below is 2:1)
6. QRS normal when it occurs
Third degree heart block occurs where there is no conduction at the AVN, therefore the ventricles
and atria contract independently
1. Rate will be bradycardic, around 30bpm

2. Rhythm will be regular
3. Present p waves
4. No regular PR interval
5. P waves will not be followed by QRS complexes, the two are completely divorced
6. QRS broad, as the contraction stems from ventricular conduction alone
With any of these arrhythmias, if the patient is not in sinus rhythm and is symptomatic – a
pacemaker should be considered (nb. A pacing spike will replace the p wave on ECG and the QRS will
be broad)
Once the rhythm strip has been assessed, all 12 leads should be analysed for the following
1. Cardiac axis
2. Is there ST elevation or depression in any of the leads
3. Which leads are affected
4. Are there any pathological Q waves. A pathological Q wave is one that appears in a lead axis
where there are normally no Q waves e.g. the chest leads – this also indicates an old MI.
Pathological Q waves prevent normal R wave progression
5. Are there any T wave abnormalities. T wave inversion can occur in the days following MI,
tall/tented T waves can occur in hyperkalaemia
• T waves are normally inverted in aVR and V1, occasionally in V2
6. Is there prolongation of the QTc interval (0.32 – 0.42s)? This can occur in some adverse drug
reactions, electrolyte imbalances, or in congenital abnormalities
• Antipsychotics, TCAs, sotalol
• Hypokalaemia, hypocalcaemia, hypomagnesaemia
7. Is there any bundle branch block?
8. Is there any left or right ventricular hypertrophy
Cardiac Axis
Normal cardiac axis is -30 to +90. Normally, all limb leads are positive, with the extremes tending
towards being isoelectric
- If Lead I and II are positive, there is no axis deviation

- A positive limb lead is where r>s and negative is where s>r
To understand axis deviation, it is fist important to understand the position of the heart relative to
Einthoven’s triangle
In left axis deviation, the heart axis becomes more negative < -30, therefore as the heart is pointing
towards AVL and I and away from II, AVF and III the leads will change
- II, III and AVF will be negative

- I and AVL will be positive
In right axis deviation, the heart axis becomes more positive > 90, therefore the heart points
towards AVF and III and away from I and AVL
- III and AVF will be positive

- I and AVL will be negative
Left Axis Deviation Right Axis Deviation

Left anterior hemiblock Left posterior hemiblock
Inferior MI Anterolateral MI
VT from LV focus PE
WPW WPW
LVH RVH
ST Segment Changes
ST elevation indicates STEMI, if it is present in two continuous leads. The lead location of the ST
elevation indicates the region of the heart that is infarcted; this is seen mainly on chest leads but can
be verified on limb leads
- ST elevation is defined as anything >2 small squares

Leads Infarcted Region Artery
II, III, aVF Inferior surface Right coronary
V1, V2, V3, V4 Anterior surface LAD
I, aVL, V5, V6 Lateral surface Circumflex
ST depression in V1, V2, V3 Posterior surface Right coronary
Dominant V2 R wave
ST depression indicates ischaemia, the same territories as above apply.
Widespread ST elevation with a saddle shaped ST segment indicates pericarditis
Bundle Branch Block
Bundle branch block only exists in the presence of a prolonged QRS complex, as the ventricular
contraction will be prolonged
- The changes of bundle branch block are best seen in V1
In right bundle branch block there is an RSR pattern in V1, V2 and V3
- Normally there is no R wave visible in V1 (r wave progression means that r waves become
gradually more prominent and the leads become more positive (V4/V5/V6 should be
positive))
- In RBB there is a peaked T wave in V1
Right bundle branch block can be due to cor pulmonale and PE
In left bundle branch block there will be broad and deep QRS complexes
- There will be ST elevation in LBBB, therefore where patients have known LBBB myocardial
infarction should only be suspected where there are symptoms and troponin rise as the ECG
is not informative
LBBB can be caused by impaired left ventricular function, ischaemic heart disease, and acute MI
Ventricular Hypertrophy
Left ventricular hypertrophy is >35mm where the two deepest chest QRS complexes are added
together (usually S wave in V1 + R wave in V5)
Right ventricular hypertrophy should be suspected where there is a dominant R wave in V1 and a
deep S wave in V6
Performing an ECG
4 ECG electrodes are applied when recording from the limbs, each is internationally colour coded
- The red electrode is placed on the right arm, RA

- The yellow electrode is placed on the left arm, LA
- The green electrode is placed on the left leg, LL
- The black electrode is a neutral electrode, this serves to stop interference by grounding the
lead being measured and is placed on the right leg, N
The ECG electrodes are placed on the chest as shown below
- V1 is placed on the right sternal edge, 4th intercostal space

- V2 is placed on the left sternal edge, 4th intercostal space

- V3 is placed halfway between V1 and V2
- V4 is placed on the left 5th intercostal space at the mid clavicular line
- V5 is placed on the left 5th intercostal space at the anterior axillary line
- V6 is placed on the left 5th intercostal space at the mid-axillary line
Orthopaedic X-Rays
X-rays are the commonest investigation in orthopaedics, they should be assessed in the following
method
- Check ID and date

- Site
- View e.g. AP, lateral, oblique (nb: spine is always PA view)
- Technical adequacy
- The film should show all the joints in question from at least two views
- Exposure must be sufficient to differentiate bone from soft tissue
- Soft tissue
- Describe as for a lump
- Size, shape, density, borders, relation to underlying structures
- Density indicates the substance air > fat/ soft tissue > fluid > bone > metal
- Look in particular for lipohaemarthrosis, as this is a sign of intra-articular
fracture
- Bone
- Lytic or sclerotic lesions
- Fracture*
- Joint
- Alignment
- Dislocations
- Subluxations
- Osteoarthritic changes
*Fractures can be seen as an area of sclerosis or increased lucency, dependent on the overlap
between the bone segments; there is a discontinuity of the bony cortex and there may be
irregularity in shape. Fractures should be described by noting the following features
- The bone involved

- Position of the fracture
- Intrarticular
- Epiphysis
- Metaphysis
- Diaphysis (proximal, middle, or distal third)
- Type of fracture
- Simple (oblique or transverse): single fracture line with two bone fragments
- Spiral: twisting injury with two bone fragments
- Comminuted: complex fracture with >2 fragments
- Crush: loss of bone volume due to compression
- Avulsion: bony attachment of ligament/muscle is pulled off
- Hairline: barely visible with no displacement
- Greenstick: incomplete fracture of immature bone
- Displacement
- Relationship of the distal to the proximal fracture e.g. anterior, posterior, medial or
lateral displacement
- Angulation
- Movement of the distal fragment in relation to the proximal bone in degrees
- Rotation
- Internal or external rotation along the longitudinal axis of the bone
Healing fractures are seen as areas of callus, with an ill-defined region of bone alongside fusiform
swelling.
Cervical Spine
Ideally there should be three views: AP, lateral, and open mouth
- Lateral view
- Check vertebral alignment looking for a smooth anterior spinal line, posterior spinal
line, and spinolaminar line
- Check that the vertebral bodies are regular, with no wedging
- Anterior view
- Check that the spinous processes are aligned and equally spaced
- Peg view
- Alignment of the lateral aspects of C1 and C2
- The peg should be equidistant from the lateral masses of C2
Thoracic/Lumbar Spine
AP and lateral films should be used
- Assess alignment in three columns

- Anterior, middle (posterior aspect of the vertebral boby), posterior (bone arch)
- Spinous processes in a straight line
- Check the vertebral bodies for wedge fracture
- Comment on any lordosis, kyphosis, or scoliosis
Chest X-ray Interpretation
Initial assessment of the x-ray should be the patient’s demographics, when the film was taken,
laterilsation of the image (indicated by a left or right side marker) and the direction of the
radiograph (AP or PA)
- PA radiographs are preferred, however the patient must stand erect as the x-rays are passed
through their back
- AP radiographs are taken when the patient is unable to stand; they are lying supine as the x-
rays pass through their front. The main issue with AP views is that the heart, hila, aorta, and
lung markings will be magnified due to diverging of the x-rays. As well as this, pleural
effusions and pneumothoraces are more difficult to detect. Inspiration is also poorer
- AP can be identified as the scapulae will be present
There should then be assessment of the adequacy of the film
- Rotation: the spinous process should be midway between the medial ends of the clavicles
- The clavicle closer to the midline is rotated forward

- Rotation causes altered transradiancy of the lungs, an abnormal mediastinum (one
hilum and side of the mediastinum will appear enlarged), and tracheal position
cannot be assessed
- Inspiration: 5 – 7 anterior ribs should lie at the mid-clavicular line above the diaphragm
- If <5 ribs are visible this could indicate small volume lungs or fibrosis. If there is
simply under-inspiration there will be apparent congestion on the film and lesions at
the lung bases may be missed
- Large lung volumes can indicate emphysema
- Penetration: the vertebrae up to T6 and left hemidiaphragm should be visible behind the
heart
CXR should be assessed in an ABCDE format
- A is airway, is it open and not deviated. The trachea is pulled towards collapse, and pushed
away from pneumothorax and large pleural effusions
- B is bones, are the ribs all intact. B is also breathing space, are the lung fields normal
- Checking the lung fields should look at the zones (comparing side to side),
costophrenic angles, hila, and silhouette sign
- C is circulation are all the heart borders visible (1/3 to the right and 2/3 to the left), is it a
normal size, is the mediastinum deviated or widened. Are the hila enlarged or deviated
- D is diaphragm, is it unduly flattened or raised (there should be <1.5cm between the right
and left diaphragm), or is there air surrounding it
- E is extras
- Check the soft tissues, particularly the breast shadows
- Note any artefacts such as NGT, ETT, chest drains, prosthetic heart valves,
pacemakers, and surgical clips
Abnormalities
Patchy lung opacifications have many different terms to describe them
- Nodular lesions are roughly circular; they can be discrete or confluent. This suggests
consolidation (air space opacity) or discrete lesions such as malignancy
- Reticular opacification is used to describe an apparent mesh of lines on the image, this
suggests fibrosis
- Annular opacification is used to describe ring shaped lesions, this suggests abscess or
bronchiolar abnormality
The silhouette sign is used for localising abnormalities on CXR, where normal interfaces between
structures are not visible it indicates that there is an abnormality present at that interface obscuring
the definition
- Right and left lower lobe pathology shows loss of the right/left hemidiaphragm
- Right middle lobe or left lingula shows loss of the heart border
It is common to detect cardiomegaly on CXR, however heart size can only be assessed PA. The
cardiothoracic ratio is used to determine abnormality, this is the width of the heart compared to
chest diameter; anything over 50% is abnormal
Pulmonary oedema due to left ventricular failure has several key signs
- Bat-wing appearance, in which the oedema (shadowing) extends out from the hilum
- Kerley B lines, which indicate fluid trapped in the space between lobules
- Fluid in the horizontal fissure
- Upper lobe diversion, where there is shadowing at the apices due to increased blood flow
- Bilateral pleural effusion
- Cardiomegaly
Enlargement of the hila bilaterally is known as bilateral hilar lymphadenopathy
- This can be due to malignancy, sarcoidosis, lymphoma, or infection
Free gas in the abdomen, pneumoperitoneum (due to bowel perforation), can be seen as black areas
below the diaphragm; the patient should sit upright for 10 minutes so the free air can rise. There
may also be Riggler’s sign around the bowel, where both sides of the bowel wall are visible
- This shouldn’t be mistaken for the Chileditti sign however, where there is bowel below the
diaphragm (above the liver/stomach) – this can be distinguished by the presence of haustra
in the air.
CXR can be performed following NG and ET tube placement
- NG tubes can be misplaced into the lung rather than the stomach. The tube should follow a
straight course along the midline to below the diaphragm at the stomach
- ET tubes should sit 5cm above the carina to ensure both lungs are ventilated, however they
may be out of place. If they are placed down one bronchus, the other lung will collapse as it
is not inflated
Both consolidation and collapse will cause a loss of the normal silhouette (see above). They can be
differentiated by several signs
- Consolidation is patchier (heterogenous), and collapse more solid (homogenous)

- In collapse the hemidiaphragm will be raised, ribs will be crowded, horizontal fissure
displaced, and mediastinal shift may be evident. This is all due to volume loss
Consolidation is most commonly due to pneumonia, but can also be due to malignant cells or blood
in the small airways
- There may also be air bronchograms, which is air trapped in the large airways within the
consolidation
Collapse occurs where air doesn’t enter a part of the lung, and the air already in the alveoli is
reabsorbed. This is commonly due to obstruction from e.g. a tumour, foreign body, or mucus plug
- Left lower lobe collapse is often hard to spot, but will show the sail sign – a triangle shaped
opacity within the heart shadow – often appearing as two left heart borders. There will also
be a loss of the left hemidiaphragm silhouette
- Left upper lobe collapse shows the veil sign, where the upper lung is white getting
progressively darker inferiorly (this is because the left lower lobe is posterior to the left
upper lobe, and more prominent inferiorly)
Pleural effusion will show a fluid meniscus at the costophrenic angle, or above in significant
effusions Loculated effusion appears as a localised heterogenous opacity extending from the lateral
aspect of the lung. There may also be tracheal deviation away from the affected side.
COPD will show increased lung spaces, flattening of the diaphragm, and a tubular heart.
Fibrosis will show interstitial shadowing, which appears as many white lines over the chest x-ray
Pneumothorax will show increased radiolucency on the affected side with a loss of lung markings,
the visceral pleural border may be visible
- Check for any signs of tension, tracheal deviation is later than diaphragmatic flattening and
increased rib spacing
Complete white-out of a hemithorax has several key causes
- Trachea pulled towards opacification: pneumonectomy, total lung collapse (ET tube
misplacement)
- Trachea central: consolidation, ARDS
- Trachea pushed away from opacification: pleural effusion
Abdominal X-ray Interpretation
A methodical approach to assessment is key
1. Patient demographics, and the time and date of the x-ray

2. Details of the x-ray should be analysed. Usually AXR are supine AP radiographs
o In suspected pneumoperitoneum, where erect CXR is not possible, patients may
have a decubitus AXR where they lie on their side
3. Adequacy of the film should be assessed next with exposure to both hemi-diaphragms and
both hip joints. Penetration should be enough to see the lumbar vertebrae
4. Gases (bowels)
5. Masses (soft tissues)
6. Bones
7. Stones (calcifications)
8. Artefacts
Gases (Bowels)
In terms of gases, abnormal luminal gas patterns within the small and large bowel should be checked
- There should not be any gas in the small bowel, it should have a 3cm diameter and is
centrally positioned and traversed completely by plicae circularis/ valvulae conneventes
- The large bowel will have some gas in it, as well as mottling from faeces. The caecum will be
around 9cm across but the rest of the colon should be 6cm. Normally it will be positioned
peripherally, and not be completely traversed by haustra
Large bowel obstruction will present as dilated (>6cm) loops of gas filled bowel, which will be
peripherally located and have visible haustra. There may also be air-fluid levels
- This can be decompressed into the small bowel where the ileocaecal valve is incompetent,
decreasing chance of perforation
- If there is any gas in the rectum, this should be noted as it indicates that the obstruction is
not complete
- Causes include colon cancer, diverticular strictures, volvulus, and (less commonly) hernias
Small bowel obstruction will present as multiple dilated (>3cm) loops of gas filled bowel, which will
be centrally located and have visible valvulae conneventes. There may also be air-fluid levels
- Causes include adhesions, hernias, foreign bodies, tumours, and gallstone ileus
Ileus will present similarly to obstruction on AXR, but can be differentiated with a history of very
recent surgery or peritonitis as well as absent bowel sounds on auscultation
- Other causes of ileus include hypokalaemia and medications, it can also be idiopathic
Pneumoperitoneum can show as ‘football sign’ on supine AXR, as well as Rigler’s sign where there is
air both inside and outside of the bowel wall
Ulcerative colitis and other inflammatory bowel diseases can have several signs on AXR
- Thumbprinting occurs due to oedema of the haustra

- Mucosal islands are the radiological appearance of pseudopolyps
- Lead pipe colon occurs in chronic inflammation, where there is a featureless segment of
bowel due to loss of bowel markings
Toxic megacolon appears on AXR as dilated bowel with signs of inflammation
- This can be caused by ulcerative colitis, pseudomembranous colitis (C.diff), or ischaemic

colitis
Volvulus occurs when either the caecum or sigmoid colon rotates on its mesentery
- Sigmoid volvulus presents with a ‘coffee bean sign’ where there are two loops of closely
opposed dilated (>6cm) bowel
- Caecal volvulus presents with an empty RIF due to displacement of the caecum to the LUQ,
the displaced caecum will be highly distended (>9cm)
Masses (Soft Tissues)
Masses should be distinguished from normal anatomy. The size and position of the normal organ
shadows (liver, spleen, kidneys, and bladder) should be assessed, and the psoas muscle shadow
identified
- If there is a bulging of the lateral aspect of the psoas shadow, this could indicate psoas
abscess
Any organomegaly should be noted
Bones
Abnormalities of the visible bones should be checked. This includes the lower ribs, lumbar and sacral
spine, and pelvis
- Any bone fractures

- Osteoarthritic changes
- Tumours of bone, or metastatic deposits may be seen
o Lytic metastasis will be blacker e.g. myeloma, lung, breast, renal, thyroid
o Sclerotic metastasis will be whiter e.g. prostate, osteosarcoma
Stones (Calcification)
Stones may be gallbladder, renal, ureteric, or bladder; they can also indicate calcification of organs,
lymph nodes, and vessels
- Ureteric stones can be identified as they follow a path down the transverse processes of the
spine, and following this the sacroiliac joint, before joining the bladder at the ischial spine
o Staghorn calculus may be visible in the renal pelvis, this forms due to struvite (triple
phosphate/ magnesium-ammonium-phosphate) formation in response to certain
UTIs
- In elderly patients there may be visible phleboliths of veins (particularly in the bladder)
- Mesenteric lymph nodes may be calcified
- The transpyloric plane (L1) can show gallstones on the right (<10% of gallstones are visible
on AXR), and pancreatic calcification (due to chronic pancreatitis) on the left
- There may be calcification of AAA visible
- Costochondral calcification of the ribs is common and benign
Artefact
Surgical clips, nephrostomies, foreign bodies, catheters, and stents (bile duct/ ureteric) can all be
visible
- Ureteric stents are typically double J stents, and are looped on either end
- Bile duct stents are patent if there is air in the biliary tree
Intensive Care
Airway Maintenance, Ventilation, Pulse Oximetry and Oxygen
Therapy
Airway Obstruction
In trauma patients, airway obstruction can result from many different factors
- Coma results in airway obstruction due to loss of protective airway reflexes

- Blood or vomit may block the airway
- The airway may be disrupted by direct trauma, haematoma, or oedema following burns
Choking
Choking can cause mild or severe airway obstruction
- In severe airway obstruction the patient cannot speak or breathe, and attempts at coughing
are silent
- In mild airway obstruction the patient can speak, cough, and breathe
When a patient shows signs of mild airway obstruction they should be encouraged to cough. In
severe airway obstruction there should be a cycle of 5 back blows and 5 abdominal thrusts
- Back blows should be delivered with the heel of the hand between the scapulae. Stand to
the side of the patient, and lean them over your forearm
- Abdominal thrusts should be delivered standing behind the patient, placing a clenched hand
under the xiphisternum and pulling upwards and inwards
Where a choking patient loses consciousness, commence ALS protocol and try to retrieve the object
with forceps/suction where possible
Airway Maintenance
There are many techniques that can be used to open the airway
First, look in the mouth and pharynx for foreign bodies, blood and vomit
- Remove any obstruction with Magill’s forceps or Yankauer sucker
Basic Manoeuvres
Head tilt and chin lift is the standard technique used to open the airway where there is no risk of c-
spine injury.
Jaw thrust is used as alternative to this, and should be first-line in any trauma patient (or chin lift
without head-tilt)
- Jaw thrust is performed by the following technique:

o Place fingers behind the angle of the mandible and apply anterior pressure
o Use thumbs to open the mouth slightly by downward displacement of the chin
Airway adjuncts can be used to help secure an airway, and maintain it in an opened state.
- Guedel airways are used for oropharyngeal airway maintenance

oThe size of the guedel used should be from the incisors to the angle of the mandible
(most adults require size 3)
o Insert upside-down and rotate into place to avoid pushing the tongue backwards
- Nasopharyngeal airways can be used where there is no risk of skull base fracture
o The size of the device should be from the incisors to the tragus (most men are 7.0
and women 6.0)
o Insert (lubricated) by twisting slightly along the floor of the nose
Laryngeal Mask Airways (LMA)
LMA are used in around 50% of elective surgery in the UK as they avoid the need for a laryngoscope
and therefore prevent damage to the teeth or cords. LMAs are also used during ALS to temporarily
establish an airway before an ET tube is inserted
- Lubricate the cuff and slide over the palate so the device sits over the larynx
- Inflate the cuff when the LMA is in situ and tie the device in place
An i-gel is similar to an LMA, but the cuff does not require inflation
Intubation
Intubation involves passing an ET tube through the cords and into the trachea to establish an airway.
This is commonly needed in
- Surgical procedures where

o There is a risk of vomiting and aspiration
o The patient has a difficult airway
- The patient is in an ICU setting, and will likely need airway protection for a prolonged period
of time
- In an acute setting as a superior alternative to an LMA/i-gel where an appropriately trained
individual is present
Muscle relaxation increases the ease of intubation, and usually suxamethonium is used as a short
acting agent in surgical patients. In cardiac arrest patients, muscle relaxation is not used. Following
this these steps are taken
- Position the patient with neck and head extended

- Slide the laryngoscope blade down with the right side of the tongue into the vallecular
(between tongue and epiglottis) while protecting the teeth
- Lift the laryngoscope blades and visualise the cords, pass the lubricated ET tube through
them
- Remove the laryngoscope and inflate the cuff
Intubation can be difficult in the following patients
- Obese
- Short neck/ impaired neck flexion and extension
- Receding chin
- Protruding teeth
- TMJ disorder/ fractured mandible
Cricothyroidotomy
A cricothyroidotomy is used as an emergency surgical airway
- Needle cricothyroidotomy is performed by passing a large IV cannula into the cricothyroid

membrane (between the cricoid and thyroid cartilages). This should only be used in children
- Surgical cricothyroidotomy is similar to a PCT (below) but specifically at the cricothyroid

cartilage
Percutaneous Tracheostomy (PCT)
A tracheostomy is an airway that is inserted subglotically through the neck tissues directly into the
trachea
- Percutaneous tracheostomy involves Seldinger technique and dilation of the trachea

between cartilage rings before passing the tracheostomy tube
This is indicated in the following situations
- Bypassing upper airway obstruction

- Prolonged mechanical ventilation, as it is easier to wean patients from tracheostomy than it
is from intubation
- Requirement for airway protection, and a need for frequent suctioning (airway toilet)
- Other advantages include
o Patients can communicate by phonation (if a fenestrated tube is used)
o Sedation can be reduced as it is more comfortable than an ET tube
o Nursing care in terms of mouth care and mobility is easier
Complications include
- At the time of insertion: bleeding, hypoxaemia, loss of the airway, injury to the posterior
tracheal wall, pneumothorax
- Later complications include: dislodgement and obstruction of the tube, tracheoesophageal
fistula, stenosis of the trachea, and swallow dysfunction
Aspiration
Aspiration of foreign material is common in anaesthesia, but is unlikely if a tracheal tube is in situ. If
aspiration is suspected there should be the following steps
1. Apply cricoid pressure and use suction to remove debris from the mouth
2. Intubate with an ET tube and refrain from ventilating (if oxygen saturation is adequate)
3. Empty the stomach with an NG tube
Ventilation
Mouth-to-Mask Ventilation
Ensure the airway is patent using head tilt and chin lift, maintaining the neck in an extended position
- Apply the mask to the patient’s face, ensuring a tight seal by using two hands. Thumbs and
forefingers making a c-shape on the mask, and other fingers lifting the angle and ramus of
the mandible
- Blow a normal breath through the inspiratory valve and watch for chest rise and fall
Bag-Valve-Mask Ventilation
A bag-valve-mask is used in the pre-operative and emergency setting to ventilate a patient that is no
longer breathing on their own, prior to establishing a secure airway ± mechanical ventilation
- Apply the mask to the patient’s face, ensuring a tight seal by using two hands. Thumbs and
forefingers making a c-shape on the mask, and other fingers lifting the angle and ramus of
the mandible
- Gently squeeze the bag by 2/3rd at a rate of 10 – 12 breaths per minute
Non-Invasive Ventilation
NIV is the application of ventilatory support without using an invasive artificial airway. It is delivered
via a sealed face-mask, nasal mask or helmet
- This is therefore indicated in patients that require HDU level support, but are not yet
candidates for intubation
Positive pressure is applied to drive oxygen into the lungs in two main forms
- CPAP is continuous positive airway pressure

- BiPAP is bi-livel positive airway pressure, the air pressure increases during inspiration
o ePAP = pressure during expiration
o iPAP = pressure during inspiration
o Pressure support = difference between ePAP and iPAP
Hypoxia is determined by FiO2 and PEEP
- PEEP is positive end expiratory pressure, and is increased by CPAP (or ePAP)
- Therefore, for T1RF, CPAP is sufficient
- Start at 4 cmH2O and increase as needed to a maximum of 12 cmH2O
Hypercapnia is determined by minute volume (respiratory rate x tidal volume)
- Tidal volume is determined by pressure support

- Therefore, for T2RF, BiPAP is required
- Start at 12/4 cmH2O and increase to a maximum of 20/12 cmH2O
o Increase iPAP to reduce hypercapnia, and ePAP to reduce hypoxia
For NIV, the patient must be conscious and able to maintain their airway
Invasive Mechanical Ventilation
Invasive mechanical ventilation requires intubation. Indications for this include
- Respiratory or cardiorespiratory arrest (or impending arrest)

- NIV is failing to reduce PaCO2 or maintain SpO2
- Surgical procedures requiring paralysis
- A sedated patient in an ITU setting that is not self-ventilating
Mechanical ventilation is titrated to give appropriate inspiratory and expiratory airway pressures
- Where the patient is paralysed and intubated IPPV is used, with tidal volume and pressure
used are altered as necessary
- PEEP is often used as an adjunct to this, helping to splint open alveoli and increase the
surface area for gas exchange
Principles of Pulse Oximetry and Capnography
Pulse Oximetry
Over 90% of oxygen in the bloodstream is carried bound to haemoglobin, with each molecule of
haemoglobin 100% saturated when carrying four molecules of oxygen
- Oxygen saturation (SO2) = saturated haemoglobin/ total haemoglobin x100

Saturated haemoglobin appears redder in colour as it absorbs more high frequency blue light,
whereas reduced haemoglobin absorbs more low frequency red visible light (and some near infrared
light) and hence appears bluer in colour
- Overall reduced and oxyhaemoglobin absorb different wavelengths of light, but there are
some areas of the visible light spectrum where they are very similar in terms of absorption
and one point (the isosbestic point) the absorption is identical
o This gives the baseline of the total absorption of all haemoglobin
- The wavelength of the visible spectrum is predominantly absorbed by oxyhaemoglobin and
the isosbestic point gives the total haemoglobin. The ratio between the two is therefore
closely related to SO2
A pulse oximeter uses two wavelengths of light, one high frequency in the visible spectrum (660nm)
and one close to the isosbestic point (910nm).
SO2 can only be calculated from the ~2% of the total signal where there is variable absorption of
light, this is from the pulsatile (arterial) ends of the capillaries
Limitations of pulse oximetry include
- Falsely low readings can occur in methaemoglobinaemia, injection of methylene blue or

indocyanine green, fluourescent lighting, shivering, nail varnish, use of surgical diathermy,
and venous congestion (e.g. tricuspid regurg, high airway pressure) will decrease pulsitility
- Falsely high readings can occur in carboxyhaemoglobin
- Other false readings can occur in poor perfusion and anaemia
Additionally, older pulse oximeters can give inaccurate readings and pulse oximetry does not give
any information about carbon dioxide
- The impact of carbon dioxide is right-shifting the dissociation curve (low pH and high 2,3-
DPG also do this), therefore a patient can desaturate even at high PO2
Capnography
Capnography is used to measure the level of CO2 in expired air, this is widely used in general
anaesthesia and critical care
- The mostly widely used method of measuring the carbon dioxide is with infra-red
spectrometry, but different systems exist
Specific wavelengths of infrared are selectively absorbed by carbon dioxide, and the amount of light
absorbed is proportional to the concentration of CO 2
- Therefore, the concentration of CO2 in expired air can be calculated by comparing

absorption to that of a known standard concentration
A typical capnogram is shown below
- Inspiration ends at A and expiration begins at B. Inspiration starts again at D (the end
expiratory point)
The capnograph can enable calculation of respiratory rate and estimation of PaCO 2. It can also alert
to disconnection or displacement of equipment, rebreathing and circuit failures, and reduced
pulmonary blood flow
Errors can be generated in capnography
- Calibration errors
- Wrong sample site in the breathing equipment
- Blockages or water in the sampling hose
Oxygen Therapy
Oxygen therapy is the administration of oxygen at concentrations greater than that in ambient air
(21%), with the intent of treating or preventing hypoxia.
Oxygen saturation is also referred to as SpO2 (peripheral) and SaO2 (arterial)
- When the partial pressure of oxygen in the blood is reduced, this is hypoxaemia. This can
cause hypoxia (insufficient oxygen reaching the body tissues)
There are many possible causes of low saturations, which may or may not be related to the
respiratory tract
- Respiratory disease e.g. pneumonia, ARDS, oedema, asthma, COPD

- Cardiac disease e.g. arrhythmias, ischaemia, oedema
- Other conditions particularly where there is raised respiratory rate, metabolic acidosis, or
hypotension e.g. trauma, neurological impairment, renal failure, liver failure
Oxygen is a drug, and therefore must be prescribed as inappropriate dosage and poor monitoring
can have serious consequences
The prescribing guidelines are summarised below
- It is important to document the litres per min the patient is receiving, as well as the
percentage FiO2
- Healthy patients have oxygen saturations >94%, and inspiratory flow rate of 25 - 30 L/min
Oxygen Delivery
Nasal cannulae are widely used as they are comfortable and well tolerated. Every extra L/min should
give 3-4% more oxygen above air concentration, however as they are variable performance the
inspired oxygen concentration is dependent on rate, pattern (mouth v nose) and depth of breathing
- Slower, deeper breathing will achieve a higher FiO2

- The flow rate of the nasal specs is < peak inspiratory flow rate
- Patients will be breathing air through their mouth as well as their nose
- Oxygen through nasal specs should only be given up to 6 L/min, anything above 4 L/min can
cause irritation
Simple face masks (Hudson masks) provide 35-50% oxygen at flow rates of 5-10 L/min. The mask is
attached to a supply of 100% oxygen, but there is extensive air entrainment through holes in the
mask
- Simple face masks are variable performance masks, meaning that they do not give a fixed
inspired oxygen concentration and are dependent on the rate and depth of breathing
o Peak inspiratory flow rate > Hudson mask flow rate, hence at peak inspiration the
patient will largely be entraining air through the holes as opposed to the 100%
oxygen flowing through the mask
- Long term use of these devices can lead to skin irritation and pressure sores
Non-rebreathe masks are simple face masks with a reservoir bag attached. These masks can give a
fixed oxygen concentration: during expiration oxygen flows into the reservoir bag (a one way valve
prevents expired air from entering the bag) and therefore during inspiration there is little dilution of
inspired oxygen with room air
- This is able to achieve high oxygen concentrations, with 60-80% oxygen at a 10 - 15 L/min
flow rate
- These are not suitable for long term use as the gas cannot be humidified
Venturi masks will also achieve fixed oxygen concentrations as they use high air flow oxygen
entrainment. These masks work by generating a 30 L/min flow rate at different ratios of entrained
air and oxygen
- Venturi valves are colour coded according to the percentage of oxygen (FiO2) they deliver
These are used in very specific situations e.g. COPD, where the inhaled oxygen concentration needs
to be carefully calculated
Device Type of Patient

Nasal Cannulae Normal vital signs but lowered SaO2, post operatively, LTOT
Venturi Masks Chronic respiratory failure, CO2 retention, COPD
Non-rebreathe Masks Emergency situations e.g. severe asthma, LVF, pneumonia, trauma,
sepsis
Humidification of air normally takes place in the upper airways, therefore long term oxygen therapy
can dry out the nasal mucosa leading to nosebleeds and poor tracheobronchial clearance
- Oxygen given through certain modalities can be humidified before administration to prevent
this
Cylinders
Oxygen cylinders can be ambulatory or non-ambulatory. The colour of the cuff indicates the gas
within
- Medical oxygen is white

- Medical N2O is dark blue
- Medical air is black and white
- Entonox is dark blue and white
Fluids and Blood Products

Physiological Requirements
Total body water is around 42L, making up 60% of body weight. The highest proportion of body
water is in neonates, and is higher in male adults than female adults
- 14L of this is extracellular, of which 4L is intravascular fluid

Fluid losses occur in many different forms
- Normal urine output is 1500ml/day, but should be 0.5ml/kg/hour minimum

- Good output from a catheter is around 35 – 70ml/hr
- Insensible losses are around 500ml/day. This includes sweating and breathing
- These losses increase considerably in burns and tachypnoea
- Third space losses (fluid sequestration)
- These are losses due to inflammation and injury causing increased capillary
permeability
To cover for losses, normal people will require around 2500ml of fluid per day
- 1500ml of this is usually ingested through drinking

Other requirement in 24 hours for nil-by-mouth individuals include electrolytes and glucose
- For Na+, K+, and Cl- it is easiest to consider a need of 1mmol/kg/hr (60 – 80mmol/day)
- More specifically, there is a physiological requirement for 100mmol of Na+ and
70mmol of K+
- 50 – 100g glucose
- 5% dextrose contains 5g/100ml
The maximum safe rate for potassium administration outside of ITU is 10mmol/hr
Fluid Assessment and Fluid Balance
Before prescribing fluids, it is important to assess the patient’s fluid balance. There are several
clinical markers that can be used for this purpose
Underfilled Overfilled
Tachycardia Raised JVP
Postural hypotension Pitting oedema
Decreased capillary refill Tachypnoea
Decreased urine output Basal crepitations
Cool peripheries Pulmonary oedema on CXR
Dry mucous membranes
Decreased skin turgor
Sunken eyes
Urine output <0.5ml/kg/hr
Raised urea and haematocrit
Where a patient is catheterised, looking at the colour of the urine is key in fluid assessment,
measurement of specific gravity will give a more accurate assessment of urine concentration
Formal assessment of fluid balance is achieved by catheterising the patient and closely recording
their output and input
- It is also important to consider alongside ongoing losses from

vomit/diarrhoea/drains/stomas/fever
Fluid Prescribing
There are many different crystalloid fluids that can be prescribed, dependent on need. These are
sterile, cheap and safe solutions that have a short intravascular half-life. 5% glucose, 0.9% saline and
Hartmann’s are isotonic
- 5% or 10% dextrose is given for rehydration, but is not normally used in resuscitation
- There can be add on 20 or 40mmol KCl
- 0.9% saline contains 150mmol of Na, this is used for fluid resuscitation or rehydration
- There can be add on 20 or 40mmol KCl
- Hartmann’s solution is given for fluid resuscitation or rehydration, and is often preferred to
normal saline as it is more physiological
- It contains Na, Cl, lactate, K, bicarbonate, and Ca
Colloid solutions are large molecular weight compounds e.g. albumin, gelatin, dextrin, and starch.
These have a longer intravascular half-life and can be used for fluid resuscitation
- Issues with synthetic colloids include anaphylaxis, anti-thrombotic effects, pruritis, and
impaired renal function
Fluid Prescribing
Fluids are very commonly prescribed in patients, and there are many aspects to consider when
describing rate and type of infusion
- Typical maintenance requirements for adults are 30ml/kg/day, equating to 2 – 2.5L/day

- As much of this as possible should come from PO intake, and the remainder can be
IV where necessary
- Compensation fluids; these are additional volumes on top of maintenance fluid, dependent
on the clinical status of the patient
- This additional fluid covers increased insensible losses (pyrexia, burns, wounds),
third space losses (sepsis, post-op), and GI/GU tract losses (polyuria, vomiting,
diarrhoea)
- Usually, this is around an extra 0.5 – 1.5L/day
- Replacement fluid, correcting the fluid deficit that the patient already has
Ideally fluids should be prescribed on the basis of a fluid balance chart, estimating requirements
over 24 hours
In a NBM patient who is otherwise well, 2.5L of fluid is appropriate. A normal schedule to meet all
physiological requirements is detailed below (2 sweet, 1 salty)
- 1L 5% glucose over 10 hours with 20mmol added KCl x2

- 500ml 0.9% saline over 4 hours with 20mmol added KCl
Fluid deficit and compensation is usually covered with additional 0.9% saline or Hartmann’s solution,
the volume and rate should be titrated to maintain neutral fluid balance
For patients with fluid overload use a sodium restricted diet with a fluid restriction of 1.5L/day
(including both PO and IV fluid)
Resuscitation Fluids
Fluid resuscitation is different, and is given rapidly through a wide-bore cannula
- 500ml crystalloid (250ml if frail or heart problems, 10ml/kg in children) should be given stat
i.e. over <15 minutes
- Re-assess and repeat as necessary, seeking senior help where patients are transient or non-
responders
Raising the patient’s legs can also help to increase blood pressure in shocked patients
Blood Products and Transfusion
Blood and blood products should be given in certain situations
Formulation Dose Use

Red Cells Red cell concentrate in 250ml over 2 – 4hr Anaemia, haemorrhage.
(SAG-M RBC) optimal additive solution (unless haemorrhagic Target is usually Hb 90
of saline, glucose, adenine shock)
+ mannitol (Hb >40g) No more than 4 units
without FFP/platelets
Platelets Unit containing 2.4x1011 1 unit (300ml) Active bleeding (or
platelets (from apheresis prevention). Aim to increase
or 4 units) platelet count by 20 – 40, or
STORE AT ROOM TEMP stop bleeding
FFP Fresh frozen plasma with Each pack is 250ml, Increase clotting
clotting factors and with a dose of 15ml/kg Target PT and APTT <1.5x
fibrinogen normal
HUS Human albumin at 4.5% or Hypoalbuminaemia
20%
Cryoprecipitate Concentrated plasma 500ml (2 units) Significant bleeding in
trauma to keep fibrinogen
>1.5g/L
Taking Group & Save/ Crossmatch
1. Check patient’s name and DOB, comparing to their identity bracelet to ensure they match
2. Take blood
3. Copy the patient details by hand onto the bottles at the bedside
4. Complete blood transfusion request form
- Patient details
- Transfusion required (blood product, number of units, CMV negative/irradiated)
Administering Transfusion
1. Ensure the blood has been out of the refrigerator for <30 minutes and that the patients has
had baseline observations
2. Request another doctor/ nurse to go through the checking process

3. Ensure patient details match exactly on
- Patient’s bracelet and patient when directly asked
- Blood unit to be transfused
- Blood compatibility report
4. Check the unit of blood and bag
- Expiry date and time
- Discolouration, leaks/ evidence of tampering, clots
- The blood group on the bag matches that of the patient’s notes
- The donation number on the bag matches the number on the notes
Monitoring the Patient
Take the patient’s baseline observations (HR, RR, BP, SpO2, temperature) at 0, 15, 30, and 60
minutes from onset of transfusion then hourly until transfusion has finished
- If there is any evidence of transfusion reaction (near immediate SIRS), it is essential to

disconnect the blood before any further investigation/ management takes place
- Fever alone is common during transfusion, if they are feverish but systemically well
the transfusion can continue
Complications
Complication Presentation Action

Acute Haemolysis (ABO Within minutes Stop the transfusion
incompatability) - Spike in temperature Resuscitate using ABC
(>40) approach
- Hypotensive and Check the blood against the
tachycardic patient ID and documentation
- Agitated, flushed Give IV saline
- Pain
- Bleeding from cannula
site
Anaphylaxis Within minutes Stop transfusion
- Bronchospasm Resuscitate using ABC
- Cyanosis approach
- Hypotension and Adrenaline 0.5ml,
tachycardia chlorphenamine 10mg,
- Swelling and rash hydrocortisone 200mg
IV saline
Non-haemolytic febrile Slow rising temperature 60 Slow or stop transfusion
reaction mins after onset of infusion Resuscitate using ABC
approach
Check the correct blood has
been given
1g paracetamol
IV fluids
Fluid overload After 30 – 60 mins Slow or stop transfusion
- SOB Oxygen
- Hypoxia with bibasal IV furosemide
crepitations
- Tachycardia
- Raised JVP
Urticarial reaction Rash Stop transfusion

Re-check blood
Flush cannula with saline
Chlorphenamine 10mg
Haemodynamic Monitoring
Mean arterial pressure (MAP) = (Cardiac output x systemic vascular resistance) + central venous
pressure
- This can be calculated by DBP + 1/3(SBP – DBP)
Blood pressure is determined by many different parameters
- BP = CO x SVR
o CO = HR x SV
o SVR ~ myocardial contractility and venous return
- Therefore, BP ~ CV, MC, HR, SVR
Stroke volume is the volume of blood ejected by the left ventricle in one contraction
- SV = end diastolic volume – end systolic volume

Systemic vascular resistance is the resistance the left ventricle must overcome to pump blood
through the systemic circulation i.e. the resistance to blood flow offered by the vasculature
(excluding the pulmonary vasculature)
- Vasoconstriction of vessels will increase the SVR

Parameter Normal Range
MAP 65 – 105 mmHg
Systolic Blood Pressure 90 – 140 mmHg
Central Venous Pressure 3 – 8 mmHg (0 – 6)
Urine Output 0.5 – 1 ml/kg/hr
~ 30 – 50 ml/hr
Heart Rate 60 – 100 bpm
Circulating Volume ~5 L
Stroke Volume 50 – 100 ml
Hypotension can be defined in two main ways
1. MAP <65
2. SBP <90 (or >40mmHg lower than normal)
Non-Invasive BP Monitoring
With automated blood pressure machines, the measurement of blood pressure is determined by
oscillometry
- The cuff inflates rapidly to the point where oscillations against it start to become significant,
this is systolic blood pressure
- The cuff then deflates in a step-wise fashion

o Where oscillations reach their maximum, this is the mean arterial pressure
o Diastolic pressure is calculated by looking at the shape of overall change (envelope)
in oscillations, therefore diastolic pressure is an estimate through automated
machines
Where the envelope of oscillations is not uniform, for example in AF or where there is external
pressure on the arm, the diastolic pressure cannot be estimated accurately by the machine
There are several other potential errors in BP measurement
- The cuff must be the right size and in the right position, for example if the cuff is too small it
will over-read
- The machine must be accurately calibrated
Arterial Lines
Arterial line insertion is indicated in two circumstances
1. Continuous beat-to-beat blood pressure measurement

2. Frequent ABG analysis
Usually, the arterial cannula (usually pink 20G) is inserted in the radial artery, as this is associated
with the lowest complication rates. Other sites of insertion can include the femoral, posterior tibial,
dorsalis pedis, and brachial arteries
- Where the radial artery is used, Allen’s test should be undertaken prior to insertion to
ensure that there is adequate collateral flow to the hand
Arterial cannulas are connected to pressurized bags of normal saline. The pressure in the bag must
be higher than arterial SBP to prevent backflow from the cannula into the giving set, and to enable a
continuous 3 – 4ml/hr slow flush to prevent clotting in the line
Complications of arterial line insertion include
- Haemorrhage can occur if there are leaks in the system

- Thrombosis, particularly where the line has been in situ for a long period of time. The risk of
total occlusion of the vessel increases in pre-existing arterial disease, hypotension, and use
of vasopressors
- Infection
- Emboli
- Accidental drug injection. No drugs should ever be injected via an arterial line, and the line
should be labelled in red to prevent this
Invasive blood pressure monitoring occurs as the column of saline in the arterial giving set transmits
the pressure changes within the vessel to an electric signal transducer, this is displayed as an arterial
waveform
- Waveforms give three forms of information

o Blood pressure
o Myocardial contractility (indicated by the rate of change of pressure i.e. the gradient
of the arterial wave upstroke)
o Circulating volume (hypovolaemia is suggested by a narrow wave form, low dicrotic
notch, and pressure varying with inspiration)
- Peripheral artery waveforms differ from aortic waveforms: higher peak systolic pressure,
wider pulse pressure, more prominent dicrotic notch
Limitations of invasive blood pressure monitoring include dampening and resonance, these result in
inaccurate recording of systolic and diastolic pressures (MAP is usually still recorded accurately)
- Dampening occurs due to a reduction in transmission of the arterial pressure to the

transducer e.g. blood clots, kinking in the line, compression of the line
- Resonance occurs when oscillations in the line are caused by something other than the
arterial pressure
Advantages and disadvantages of invasive v non-invasive blood pressure monitoring are summarised
below
Advantages Disadvantages
Continuous blood pressure recording Expensive
Accurate BP even when patients are profoundly Potential complications (above)
hypotensive
Other information can be gathered from the Skilled technique for insertion
arterial trace
Central Venous Lines
Central lines (central venous catheters) are cannulas placed in a central vein. Typically this is the
subclavian, internal jugular, or femoral vein
There are many indications for central line insertion
- IV access where peripheral access is not possible

- CVP monitoring
- ScvO2 monitoring
- Infusions of irritant substances e.g. chemotherapy, TPN, vasoactive agents
- Renal replacement therapy
- Transvenous pacing
There are many potential complications from central line insertion
- Immediate/early complications include: pneumothorax, haemothorax, haematoma,

haemopericardium, tamponade, surgical emphysema, and air embolus
- Late complications include: infection, catheter fracture, vascular erosion, thrombosis, and
vessel stenosis
Four main types of central venous access device are commonly used
1. Direct access central catheters are for short term use as they have a high infection risk
2. PICC lines are for longer term use, and are inserted via an arm vein
3. Hickman lines are for longer term used, and are inserted surgically
4. Implanted ports are for long term use, and are inserted surgically
Central venous pressure (CVP) is the pressure recorded from the right atrium or SVC, and represents
the filling pressure of the right side of the heart
- CVP = venous blood volume/ venous compliance, there are many factors that determine this
o Right atrial pressure
o Intravascular volume
o Venous tone
o Pulmonary vascular resistance and intrathoracic pressure
CVP, like invasive arterial pressure monitoring, is measured from a pressure trace generated by the
backpressure into the vein (recorded at the end of expiration)
a = atrial contraction
c = closing of the tricuspid valve
x = atrial relaxation
v = passive atrial filling
y = opening of the tricuspid valve
There are therefore many factors that can cause CVP to be raised
- Right ventricular failure

- Tricuspid valve disease
- SVC obstruction
- Fluid overload
- High PEEP settings in intubated/NIV patients
- Pulmonary hypertension
Measurement of Cardiac Output
Cardiac output is the heart rate multiplied by the stroke volume. Non-invasive blood pressure,
arterial line monitoring, and central venous monitoring will all give an indication into the adequacy
of cardiac output.
Non-invasive methods of measuring cardiac output include
- Transoesophageal echocardiography (or TTE)

- Doppler ultrasound probes at the suprasternal notch can give the same information as
echocardiography, but are more inaccurate
Invasive methods of measuring cardiac output include
- Cardiac catheterisation and angiograpy

- Dilution techniques (radioisotope dye or thermodilution)

o Inject a known quantity of tracer substance proximally to the right ventricle, and
measure the concentration distally e.g. pulmonary/peripheral artery
o Concentration vs time is plotted, and area under the curve calculated to give cardiac
output
Vasoactive and Anti-Arrhythmic Medications
Vasoactive medications include the following
- Inotropes are agents that increase myocardial contractility

- Vasopressors are agents that cause vasoconstriction, leading to increased SVR
- Inodilators are agents with positive inotropic effect that also lead to vasodilation and
decreased SVR
Catecholamines
The most commonly used inotropes and vasopressors are catecholamines
- Catecholamines act on  and  adrenergic receptors (g-protein coupled receptors). Their

effects are described in the table below
Drug Receptor Affinity Action

Noradrenaline 1 agonist Vasoconstriction
(1 agonist)
Adrenaline 1 agonist (at high doses) Vasoconstriction
1 agonist (at low doses) Increased HR, SV, and CO
Dobutamine 1 agonist Increased HR and CO
2 agonist Vasodilation
Dopamine 1 (at high doses) Vasoconstriction
1 (at low doses) Increased contractility, SV and CO
Catecholamines are given as continuous infusions through a central line due to their short half-life
- Patients should be adequately fluid resuscitated before using catecholamines
Non-Catecholamine Vasoactive Drugs
Drug Mechanism Action

Enoxamine, PDE III inhibitor Increases cardiac contractility
milrinone and SV
Levosimendon, Increases the sensitivity of myocardial troponin Increases cardiac contractility
glucagon to calcium
Vasopressin, Vasopressors Vasoconstriction and
phenylephrine increased circulating volume
Anti-Arrhythmic Drugs
Class I drugs, such as lidocaine and flecainide, target voltage gated Na+ channels
- The particular group of voltage gated Na+ channels they influence are those used in the fast
depolarisation phase of the ventricular cell action potential
- When they are blocked, depolarisation is slowed, and the ventricular contraction rate is
slowed
Class II drugs are the β-blockers, such as propranolol, these target the β-1 receptors in the heart
- By blocking the binding of noradrenaline to the β-1 receptors, sympathetic stimulation of

the heart falls
- This slows the pacemaker potential of the conducting cells, meaning it takes longer for
conducting cells to reach threshold and depolarise, dampening cardiac activity
Class III drugs, such as amiodarone and sotalol, are drugs that prolong cardiac action potentials
- Their exact mechanism of action is unknown, but they are thought to block K+ channels
therefore slowing repolarisation
- This leads to a longer refractory period between action potentials, slowing heart rate
Class IV drugs include verapamil and diltiazem, these target Ca2+ channels
- Specifically, class IV drugs target the voltage gated L-type Ca2+ channels
- Class IV drugs are therefore relatively cardioselective, as L-type Ca2+ channels are only found
in the heart and these drugs only have a strong effect on the AV node
Adenosine and digoxin are non-classified anti-arrhythmic
Nutrition in the Critically Ill Patient
The nutrition, electrolyte and fluid requirements of a critically ill patient in 24 hours are summarised
in the table below
Calories 25 kcal/kg ~ 2000 kcal

Energy 100 kJ/kg ~ 7000 kJ
Water 30 mL/kg ~2L
Sodium 2 mmol/kg ~ 140 mml
Potassium 1 mmol/kg ~ 70 mmol
Carbohydrate 4 g/kg ~ 300 g
Protein 1.5 g/kg ~ 100g
Fat 1 g/kg ~ 70g
In critically ill patients, there are many issues surrounding achieving adequate nutrition
- Comatose or sedated patients

- Patients that cannot swallow
- Post-operative patients with limited oral intake due to e.g. pain
Enteral Nutrition
Access for enteral feeding is usually achieved with a nasogastric (NG), percutaneous endoscopic
gastrostomy (PEG) or nasojejunal (NJ) tube
- Usually a continuous feeding rate of 30ml/hr is used
Two main types of enteral feed are used
- Standard enteral feeds

- ‘Pre-digested’ feeds; these contain nitrogen are short peptides or free amino acids
Reflux occurs frequently in patients with enteral feeding, particularly in those with impaired
consciousness/ poor gag reflex. PPIs and feeding the patient at a 30 angle can improve this
Parenteral Nutrition
Parenteral feeding may be supplementary to enteral nutrition or may be TPN
- It is used in patients who are malnourished or are at risk of malnutrition and have a non-
functioning GI tract
o In ITU, the lack of absorption of an enteral feed (high PR output, or feed remaining
in the stomach) indicates that a patient may require TPN
Central venous access devices should be used to administer parenteral nutrition, and a line should
be specifically dedicated to feeding (not used for drugs or blood sampling)
- Peripheral venous access cannot be used as the feed is irritant to the vein
TPN usually consists of a balanced mix of amino acids, glucose, fat, and electrolytes suspended in a
lipid emulsion
There are many potential complications of TPN
- Re-feeding syndrome
- Catheter related complications e.g. infection, stenosis, kinking etc.
- Cholestasis and gallstones
- Hyperglycaemia. Oral hypoglycaemics or insulin should be given if this occurs
Re-Feeding Syndrome
Re-feeding syndrome occurs in malnourished patients who are fed with high carbohydrate loads.
This is because of a rapid increase in insulin
- Insulin results in a rapid fall in phosphate, potassium, and magnesium alongside an

increased extracellular fluid volume
- Alongside the electrolyte disturbance, there is an increase in oxygen consumption, and
increased respiratory and cardiac effort. This demand for nutrients and oxygen may
outweigh supply
Features of re-feeding syndrome usually become apparent after around 4 days of re-feeding. Later
manifestations can include
- Rhabdomyolysis, cardiac failure, respiratory failure, seizure, and coma

To avoid this, feeds should be started slowly and electrolytes closely monitored and replaced as
needed
Coma
A coma is a state of profound unconsciousness caused by disease, injury or toxins. The patient is
unresponsive and cannot be roused
- GCS in coma is <8, <3 indicates deep coma or death
Coma results from damage to the ascending reticular activating system (responsible for arousal)
and/or extensive bilateral damage to the cerebral cortex (responsible for awareness)
Initial Assessment
Initial assessment, investigation, and management should follow an A to E approach to resuscitate

and stabilise the patient
- Ensure the airway is patent; where GCS <8 use adjuncts to maintain airway until a definitive
airway can be established
- Assess breathing, use a bag-valve-mask to ventilate where necessary
- Assess circulation
o Blood tests should include
▪ ABG
▪ FBC, U&Es, LFTs, clotting, ESR/CRP, CK, TFTs, cardiac enzymes, glucose
▪ Drug and toxin screen (including paracetamol, ethanol and salicylate levels)
▪ Blood cultures
▪ Autoantibody screen
o Perform a 12 lead ECG
- Assess disability, formally calculating GCS
- Expose the patient and undertake a more thorough assessment (below)
Formal Assessment
Formal assessment of patients in coma is with GCS
Score Eye Opening Motor Response Verbal Response

1 None None None
2 To pain Extension (Decerebrate) Sounds
3 To speech Abnormal flexion (Decorticate) Inappropriate words
4 Spontaneously Withdrawal Confused speech
5 Localises Orientated
6 Obeys commands
Perform a full general examination of the systems, and assess for any skin changes. Focussed
examination should include the following
- Observe for seizure activity

- Check for meningism
- Perform fundoscopy to assess for papilloedma, subhyaloid haemorrhage (SAH), and
retinopathy (infection)
- Assess tone, posture, and reflexes in all limbs
Examination of brainstem function should also take place
- Pupillary responses
o Unilateral fixed dilated pupil indicates CN III palsy
o Bilateral fixed dilated pupils indicate severe brainstem damage/ drugs
o Mid-point fixed pupils indicate midbrain lesion
o Small pinpoint pupils indicate pontine lesion/ opiates
o Small reactive pupils indicate thalamic lesion
- Corneal reflex to assess afferent (CN V) and efferent (CN VII) function
- Resting eye position
o Dysconjugate gaze indicates disorder of III, IV or VI
- Spontaneous eye movements
o Repetitive horizontal deviations indicate a brainstem lesion
o Nystagmus indicates a midbrain lesion
o Downward ocular bobbing indicates a pontine lesion
- Reflex eye movements
o Oculocephalic manoeuvre (head moved side to side, eyes deviate to the opposite
side). If eyes are fixed there is a brainstem lesion affecting the III, VI and/or VIII
nerve nuclei
o Oculovestibular test (20ml ice cold water into external acoustic meatus: eyes deviate
to side tested with nystagmus and then move away). If there is no response, there is
a brainstem lesion
- Swallowing reflex to assess the reticular formation centre of the medulla
- Respiratory pattern
o Central neurogenic hyperventilation is rapid, regular, deep breathing
o Apneustic breathing is prolonged inspiration followed by apnoea. This indicates
pontine damage
o Ataxic breathing is chaotic in pattern. This indicates medullary damage
Further investigations can include
- Urine drug screen and urinalysis

- CXR
- Head CT/ MRI
- EEG
- Lumbar puncture
Differential Causes
Trauma Haemorrhage, depressed cranial fracture

Toxic Ethanol, drug overdose, sedatives, poisons
Metabolic Hypo/hyperglycaemia, hypo/hypernatraemia, hypercalcaemia,
hypopituitarism, hypercapnia, hypoxia, hypothyroidism, liver failure, renal
failure
Neurological Status epilepticus, raised ICP, hydrocephalus
Ischaemic CVA, cerebral hypoperfusion (e.g. impaired cardiac output)
Infective Meningitis, encephalitis, septicaemia, cerebral abscess, cerebral malaria
Autoimmune Vasculitis
Structural Space occupying lesions with raised ICP
Secondary Transport of the Critically Ill
Patients that are critically ill, particularly in an ICU setting, may require transfer for investigation
- This can include CT or MRI scanning
There are many risks to transferring patients, as during transfer the equipment and support of staff
at hand decreases
- While patients are in a CT scanner, they are on their own without any immediate support by
staff. Therefore, it is essential that they are stable enough to be left alone
The healthcare professionals involved in transfer must have the knowledge and skills required to
deal with any event that may occur during transfer
- It is best that a senior doctor (registrar or above) leads the transfer, and is always
accompanied by an experienced nurse or another doctor
Pre-Transfer Assessment
Prior to transfer it is essential to ensure the following
ABCDE should be stable and acceptable
- Consider intubation and mechanical ventilation to secure the airway

- Ensure adequate vascular access is established
Check that the patient is attached to appropriate monitoring
- Ensure that all lines and tubes are secured, and their correct position has been confirmed
- Monitoring during transfer can include non-invasive/invasive BP, end-tidal CO2, SpO2, and
ECG
Equipment at hand should include
- Transport ventilator
- Monitor
- Bag-valve-mask and reintubation equipment
- Oxygen cylinders
- Defibrillator
- Insulin pumps as needed
- IV fluids
- Medications including sedative drugs, muscle relaxants, and resuscitation drugs
Comfort and Recovery in ICU
Pain Management
Pain should be routinely monitored in the ICU. In patients that are unable to self-report pain but
have intact motor function and observable behaviours, there are several tools that can be used to
assess pain
- The Behavioural pain scale and Critical-care pain observation tool can both be used
o Facial expression, body movements, muscle tension, and compliance with the
ventilator all give clues as to pain
Vital signs can also be used as a cue to pain, which should then be further assessed
- Increasing heart rate and blood pressure indicate that the patient may be in pain
It is important to give ICU patients pre-emptive analgesia prior to any form of invasive or potentially
painful procedure
- IV opioids alongside non-opioid analgesics are typically used
In some post-operative ICU patients, epidural anaesthesia may be appropriate as a method of pain
control for the first few days following surgery
Rehabilitation
Prolonged stays in critical care are associated with several physical and psychological consequences
- Weakness, loss of energy, pain, contractures, and respiratory and swallowing difficulties are
all common
- Critical illness polyneuropathy, motor neuropathy, and myopathy
- Anxiety, depression, PTSD, and cognitive dysfunction
Rehabilitation goals should be set from the beginning of the patient’s admission. Physiotherapy and
occupational therapy referral is essential in this, developing a structured rehabilitation programme
lasting at least 6 weeks
- Short-term goals are to be achieved before discharge

- Medium-term goals are set to get the patient back to their normal level of functioning, and
are typically achieved post-discharge
Patients should be assessed early to determine their risk of developing psychical and/or non-physical
problems, and on the basis of this, a plan consisting of short and medium-term goals initiated
There are many rehabilitation factors that can be established while the patient is still in ICU, for
example sitting patients upright and mobilising where possible
- This increases ventilation, lung compliance, and mobilisation of secretions and helps to
decrease the work of breathing and risk of pneumonia
- Mobilisation can include passive exercises, transfer to a chair, and ambulation where
possible
When patients are discharged from ICU onto a general ward, they should be visited by a member of
ICU staff to see how they are managing
Rehabilitation is on-going in the community, and the patient’s goals should be removed 2 – 3
months’ post-discharge from hospital
- Review the physical and non-physical problems listed above, and refer to specialists where
necessary
ICU Acquired Weakness
ICUAW includes critical illness myopathy, critical illness polyneuropathy, or a mixture of both. This is
a very common consequence of long-term mechanical ventilation
- It is thought that this develops due to immobility and catabolism leading to mitochondrial
dysfunction, sodium channelopathy, and microvascular ischaemia
Risk factors include sepsis, poor glycaemic control, steroids, neuromuscular blocking agents,
immobility, and malnutrition.
ICUAW typically occurs about 1 week into critical illness
- There is symmetrical proximal muscle weakness, atrophy and diminished reflexes

- Sensation is normal in myopathy, but will be lost peripherally (touch and pain) in
polyneuropathy
- Cranial nerve and autonomic function is usually normal
Investigations are not normally necessary, but can include
- Mild elevation in CK
- Normal CSF findings
- Nerve conduction studies showing normal conduction velocity, but decreased muscle action
potentials
- Muscle biopsy can show a loss of thick filaments
Management of ICUAW can include
- Intensive glycaemic control

- Minimising use of corticosteroids and neuromuscular blockade, ideally minimising sedation
- Physiotherapy and early mobilisation
- Electrical muscular stimulation
- Electrolyte replacement
- Optimise nutrition
Ethical and Legal Factors in Intensive Care

DNACPR
Any patient at the end of life and/or at risk of cardiorespiratory arrest should ideally have
anticipatory decisions made as to whether or not CPR should be attempted
- This should take place in the wider context of advanced care planning, before there is a
necessity to make the decision in an emergency setting
All decisions made about CPR should be reviewed frequently enough to allow a change of decision in
response to the patient’s clinical progress/ deterioration
Where possible, there should be involvement of the patient in the decision-making process, and if
the patient lacks capacity there should be discussion with their next of kin. Effective communication
is essential to ensure that decisions about CPR are made well and understood by all involved
- Where a patient with capacity refuses CPR, or there is an advanced directive detailing this,
then their wishes must be respected.
DNACPR should be considered in the following circumstances
- Attempting CPR is medically futile

- There is no benefit in quality or length of life in restarting the patient’s heart
- The expected benefit is outweighed by the burdens of CPR
Where it is determined that a DNACPR is appropriate this should be communicated to the patient/
their family, and the reasoning behind it explained
- Making a decision not to attempt CPR does not require the consent of the patient or their
family
- It is important to note that the patient/their family cannot demand CPR, and the decision as
to whether or not to place a DNACPR rests with healthcare professionals
It is important that clear and full documentation of the decisions made, the reasons for them, and
the discussions that informed those decisions takes place
- This requires further documentation in the notes than just filling in a DNACPR decision form
A DNACPR does not override clinical judgement, and if the patient has a cardiopulmonary arrest that
does not match the circumstances envisaged there can be intervention at the discretion of the
healthcare professionals involved
If a cardiorespiratory arrest occurs in the absence of a recorded decision, there should be an initial
presumption in favour of attempting CPR
Capacity
Mental Capacity Act (2005)
There are five key principles to the mental capacity act
1. Capacity is assumed for adults unless proven otherwise

2. Anything done or any decision made on behalf of a person who lacks capacity must be in
their best interests
3. Unwise decisions do not necessarily indicate lack of capacity
4. Where capacity cannot be determined, act in the least restrictive way
5. A person must be given all practicable help to facilitate decision making e.g. provide glasses
or hearing aids
Independent mental capacity advocates (IMCAs) are a requirement of the mental capacity act.
IMCAs are individuals with authority to contribute to the decision by representing the patient’s best
interests
- They are appointed where the patient lacks capacity and there is no other person (relative
or friend) willing or able to support/represent the patient
IMCAs are involved in major decisions e.g. change of habitation or serious medical treatment
Assessment of Capacity
A patient with capacity is intellectually able to make a decision for themselves. There are several key
aspects to assessment of capacity
- Capacity is assumed for adults unless proven otherwise

- Capacity is decision specific, questions that are more complex demand a higher level of
capacity
- Capacity levels may fluctuate
Assessment of capacity is in four steps
1. Does the patient understand the information

2. Can the patient retain information related to the decision
3. Can the patient weigh up the pros and cons associated with the decision
4. Can the patient communicate their decision
It is important to document the results of the assessment using observations and patient quotes. If
the patient lacks capacity state how the substituted decision will be made (e.g. medical decision in
best interests)
Deprivation of Liberty Safeguards
Deprivation of liberty safeguards (DoLS) are put into place to protect people in care homes and
hospitals, they apply to vulnerable adults who lack capacity but not those who are detained under
the mental health act
Care homes and hospitals must ask a local authority if they can deprive a person of their liberty, this
is called a standard authorisation. Standard authorisation is granted after assessment of the
following factors
1. The person is >18

2. The person is suffering from a mental disorder and lacks capacity
3. The proposed restrictions are in the person’s best interests
4. The person should not be considered for detention under the mental health act
The assessment is made by a best interests assessor (independent advisor) and mental health
assessor (psychiatrist)
The mental capacity act and DoLS allow restrictions and restraint to be applied, this can include the
use of physical restraint and sedation if there is no alternative option
Consent in the Acutely Ill

Any medical intervention should have the consent of the patient; this need not be written but must
be informed.
If consent cannot be obtained, as the patient lacks capacity, there are several options
Advanced Directives
An advanced directive is made when the patient has capacity and designed to come into force if the
patient becomes loses capacity. They may be verbal or written statements, but must clearly relate to
the condition of procedure in question
- Refusal of life-sustaining treatments must be written
Lasting Power of Attorney
Lasting power of attorney (LPA) is in two main forms: property and finance, and health and welfare
(the two are often combined). LPAs are put into place when the patient still has capacity as a
contingency for if they are to lose capacity in the future, LPA is granted by the Office of the Public
Guardian (OPG)
- A welfare and health LPA can be used when the form is registered at the OPG and the
patient has become mentally incapable of making decisions about their own welfare
- A property and finance LPA is used as above. Decisions relating to paying bills, collecting
income and benefits, and selling property are referred to the donor
In the context of LPA the patient is termed the donor, and the person given LPA is their attorney
- The donor can place any restrictions or conditions on the attorney that they deem necessary
while they have the capacity to do so
- A registered LPA can be revoked by the donor if they have capacity
Emergency Treatment
In an emergency, a patient can be treated without their consent
- The treatment must be immediately necessary to save their life or prevent a serious
deterioration in their condition
- The treatment provided must be the least restrictive option of their future choices
When the patient regains capacity they should be informed of what has been done and why
Other Circumstances
When making decisions about the treatment of patients who lack capacity, and do not have an LPA
or advanced directive, there are several factors to consider
- Treat patients with respect and do not discriminate against them

- Which treatment options would provide overall clinical benefit?
- Which option, including the option not to treat, would be least restrictive of the patient’s
future choices?
- What are the views of the people close to the patient on the patient’s feelings, beliefs and
values? Do the people close to the patient consider the proposed treatment to be in their
best interest?
- What do the healthcare team believe to be the patient’s wishes, beliefs, and values?
It is important to recognise that patients/ their families do not have the right to demand treatment
when healthcare professionals determine that it is not in their best interests.
Organ Donation
There are three ways of donating an organ
- Deceased organ donation has two forms

- Donation after brainstem death (patient on a ventilator)
- Donation after circulatory death (patient not on a ventilator – organs must be
removed within a few minutes to avoid hypoxic damage)
- Living organ donation
Potential deceased donors should be identified as early as possible, based on the following criteria
- The patient is receiving end of life care, has had a catastrophic brain injury, there is absence
of >1 cranial nerve reflexes, and GCS <4 that is not explained by sedation
- It is expected that withdrawal of life-sustaining treatment would result in circulatory death
Consent for Donation
It is important to determine what is known about the patient’s views
- Registration on the NHS organ donor register

- Advance statements
- Views that have been expressed to family/ friends (check in advance if there is an LPA)
If the relatives objet to organ donation when the patient made their decision clear before they died,
they have no legal right to override the patient’s decision.
Management of an Organ Donation Patient
It is important to identify potential organ donors early, and discuss them with a transplant co-
ordinator. Alongside this, there should be early establishment of rapport with the family, and non-
coercive discussion regarding potential donation.
When a patient is a potential organ donor, there should be tissue typing, viral screening, and organ
functioning testing
- Echocardiography, renal tract USS, bronchoscopy, CT TAP, and biopsies may all be required
- Relevant blood tests should be performed early
It is essential to maintain extra-cerebral physiological stability to keep the organs viable
- Ventilatory support ensuring adequate oxygenation and normocapnia

- Circulatory support involves fluid, vasopressors, and anti-arrhythmic agents to stabilise the
initial sympathetic surge and subsequent hypotension following brainstem death
- Neurological support involves keeping patients normothermic
- Endocrine/ metabolic support can involve giving steroids and T3
- Usual supportive care e.g. VTE prophylaxis, glucose control, correction of electrolytes
Brain Stem Death
Brain death is defined as the irreversible loss of the capacity for consciousness alongside irreversible
loss of the capacity to breathe
- These patients may survive for several weeks provided they are mechanically ventilated and
have a normal circulation. Eventually, despite this, cardiorespiratory arrest will develop
Preconditions for diagnosing brain stem death include
- No doubt that the patient has irreversible structural brain damage (head injury,
haemorrhage, anoxia)
- Apnoeic coma with no spontaneous respiratory effort
- No possibility of drug intoxication, and no recent administration of anaesthetic or paralysing
drugs
- Core temperature >35
- No significant metabolic, endocrine, or electrolyte disturbance
When these preconditions are confirmed, there can be tests to determine brain stem death
- Pupils fixed and unresponsive to bright light

- Absent corneal reflexes
- Absent vestibulo-ocular reflexes (irrigation of the ear with ice-cold water)
- No motor response within the cranial nerve distribution elicited by stimulation of any
somatic area
- An example of this would be no facial grimace to nail bed pressure
- No gag or cough reflex
- Apnoea
- No respiratory movements when the ventilator is disconnected and PaCO2 reaches
6.65kPa
The above tests must be performed by two experienced clinicians and repeated at least once.
Emergency Medicine
Resuscitation from Cardiac Arrest
When initially assessing an unwell patient if there is no response/ immediate signs of life it is first
essential to call for help from a colleague
- Open the airway using head-tilt chin-lift and spend 10 seconds assessing if the patient is in
cardiorespiratory arrest
o Look for chest movement
o Listen for breath sounds
o Feel for air on your cheek, feel the carotid pulse
Where there are no signs of life, call 2222 (or ask a colleague to do so) and follow the ALS protocol
Ensure high quality chest compressions
- Heel of one hand in the centre of the chest in the middle lower half of the sternum, other
hand on top, inter-lock fingers
- Depth of 5 – 6cm
- Rate of 100 – 120bpm
- Allow the chest to completely recoil between compressions
Give 30 chest compressions followed by two ventilations using a pocket mask. If a pocket mask is not
available, continuous chest compressions are best.
When support from colleagues arrives, ventilation should commence
- If ventilation is occurring with a bag-valve-mask, continue a rate of 30:2

o Airway adjuncts should be used where required
- Ventilation can be continuous with an LMA, i-gel, or endotracheal intubation. This should
occur during one of the 2 minute blocks of CPR between rhythm analyses, when suggested
by the team leader
o When airway is secured through one of these methods, chest compressions should
be continuous
o Ventilate at a rate of 10 breaths per minute, giving enough volume to produce a
visible rise of the chest
- Waveform capnography should be used alongside this
One member of the resuscitation team should focus on gaining IV access, or IO access where this is
not possible
- IO access is usually achieved using an EZ-IO kit. It is best to use the humeral head where
possible, and ensure to use pressure bags to deliver the fluids/ medications
When the defibrillator arrives, attach pads to the patient’s chest to check the heart rhythm
- Attach the pads below the right clavicle and in the V6 mid-axillary position
- Ensure that interruption to chest compressions for rhythm assessment/ shocking is minimal
o Always plan and communicate all interruptions before stopping chest compressions
o The pause between chest compressions for assessment of rhythm should be <5
seconds
Shockable Rhythms
VF and pulseless VT are shockable rhythms, when this is identified on the defibrillator there should
be DC cardioversion
- The person operating the manual defibrillator should tell all staff other than the person
performing chest compressions to stand clear (for AED all must stand clear as soon as pads
are attached until after the shock has been delivered)
o Ensure all oxygen is removed, unless the patient has a definitive airway (LMA, i-gel,
ET intubation as these are closed circuits)
- An appropriate energy setting should be charged e.g. >150J for the first shock increasing for
subsequent shocks (if in doubt, start at the highest available charge)
- When the defibrillator is charged, the person operating the defibrillator should tell the
person performing chest compressions to stand clear
- Perform one final check that all are clear and deliver shock. The time between stopping
chest compressions and shock delivery should be <5 seconds
- After the shock is delivered, immediately resume CPR for 2 minutes before re-assessing
rhythm
Repeat these steps for up to a total of 3 shocks before resuming chest compressions and giving 1mg
adrenaline (10ml I:10,000 strength) followed by 300mg amiodarone IV, ensuring to flush between
boluses
- Re-assess rhythm every 2 minutes, and continue with shocks where the patient remains in
VT/VF
- Additional 150mg amiodarone IV can be given after the 5 th shock
- Give 1mg adrenaline every 5 minutes (usually after alternate shocks)
Do not stop this sequence to check the patients pulse unless there are signs of life suggesting return
of spontaneous circulation, or if the AED analysing rhythm states that the rhythm is no longer
shockable
- Do not give adrenaline where there are signs of ROSC
Non-Shockable Rhythms
PEA and asystole are non-shockable rhythms. Continuous chest compressions and ventilation should
carry on
- Give 1mg adrenaline as soon as IV/IO access is secured, and repeat this every 3 – 5 minutes
(after alternate rhythm analyses)
- Re-check the rhythm every 2 minutes
Do not stop this sequence to check the patients pulse unless there are signs of life suggesting return
of spontaneous circulation. Do not give adrenaline where there are signs of ROSC
NB: it is generally recognised that >20 minutes of asystole with a non-reversible cause constitutes a
reasonable ground for stopping resuscitation
Treating Reversible Causes
While the 2 minute sequences of CPR between rhythm analyses are occurring, it is the responsibility
of the team leader to consider and check for reversible causes of cardiac arrest
Hypoxia
- Ensure the patient is adequately ventilated with maximal inspired oxygen

- Check for adequate chest rise and bilateral breath sounds
Hypovolaemia
- Look for haemorrhage and restore adequate volume with fluid and blood produces
- Activate the major haemorrhage protocol where required
Hyperkalaemia, hypokalaemia, hypocalcaemia, hypoglycaemia and other metabolic disorders
- Perform an ABG to look for derangement and treat
Hypothermia is suggested by the history
- Check temperature
- Actively re-warm quickly
Tension pneumothorax
- Check for tracheal deviation

- Decompress rapidly using needle thoracocentesis, insert a chest drain
Thromboembolism
- 12 lead ECG is not possible during chest compressions. If MI is suspected, refer for urgent
angiography ± PCI
o Where PCI is not available, thrombolyse and continue CPR
- If PE is thought to be the cause, thrombolyse immediately
Tamponade
- Cardiac tamponade usually only occurs where there has been blunt/ penetrating chest
trauma
- Use USS to check and treat
Post-Resuscitation Care
Return of spontaneous circulation (ROSC) can occur at any point, but is usually recognised during
rhythm analysis where pulse check is suggested. Other signs include
- Increased end-tidal CO2 on capnography

- Respiratory effort and chest movement
- Movement
- Eye opening
In the immediate post-resuscitation phase where ROSC occurs the patient should be treated using
the ABCDE approach and transferred to an ITU setting
Most patients will be unable to maintain their airway following cardiac arrest, and there should
therefore be consideration of intubation and controlled ventilation
- Monitoring of carbon dioxide and oxygen concentration with ABG is important

- Exclude post-CPR pneumothorax from rib fracture with CXR
Monitor with ECG and exclude signs of cardiac failure, it may be required to insert an arterial blood
pressure monitoring line
- Record 12 lead ECG as soon as possible, as STEMI is a common cause of cardiac arrest and
will require urgent treatment
- Take bloods for FBC, U&Es (including magnesium and calcium), serial troponins, and glucose
Consider inserting an NG tube to decompress the stomach following bag-valve-mask or mouth-to-

mouth ventilation
Where the cause for cardiac arrest has not been identified, consider CT head and/or CTPA
ICU management should include
- Temperature control to maintain 32 – 36 for >24 hours, ensuring to prevent fever for >72
hours
- Optimisation of haemodynamic state e.g. MAP, lactate, urine output
- Maintain normoglycaemia
- Diagnose and treat seizures if they occur, these are usually myoclonic seizures
Prognostication is not usually available until >72 hours post cardiac arrest. This involves
categorisation of the following tests
- Clinical examination: GCS, pupillary responses, corneal reflex, seizures

- EEG and SSEPs
- Biochemical markers e.g. neuron-specific enolase (NSE)
- CT and MRI findings
Assessment and Management of the Acutely Ill
Assessment of the acutely ill patient in any situation should follow an ABCDE approach to clinical
examination and bedside investigation
With any stage of the assessment, issues should be managed as they are detected
- Treat and reassess at each stage of ABCDE and do not move on to the next stage until all
important abnormalities have been optimised
Prior to assessment it is important to quickly wash hands and put on gloves ± apron, and shout for
help from colleagues
When assessing the patient initially, if there are no signs of life initiate the ALS protocol and call the
resuscitation team. If there are signs of life, proceed with ABCDE
Airway
The best way of initially assessing whether the airway is to see if the patient can talk, if the patient is
talking the airway is patent
If the patient is not talking then follow a look, listen, feel approach
- Look for any obstructions to the airway, paradoxical chest and abdominal movement,
excessive drooling, and cyanosis
- Feel for breath on your cheek
- Listen for breath sounds and added sounds e.g. stridor (inspiratory), wheeze (expiratory),
gargling
o A snoring/rasping airway indicates positioning and soft tissue obstruction
o A bubbling/gargling airway indicates fluid
If there is no patent airway after assessment, call for help (2222). Then begin initial airway
management and reassessment
- Remove any solid obstructions with Magill forceps, and liquid obstructions with a Yankauer
sucker
- Establish a clear airway with simple manoeuvres such as head-tilt/chin-lift or jaw thrust,
ensuring to protect the cervical spine
- To further protect the airway, adjuncts can be used
o GCS >8 use nasopharyngeal
o GCS <8 use Guedel
- Intubation or surgical airway e.g. cricothyroidotomy, emergency tracheostomy may be
required in some
Breathing
Breathing should be assessed using a look, measure, listen, feel, measure approach
- Look for signs of respiratory distress

o Use of accessory muscles
o Sweating
o Cyanosis
o Gasping
o Pursed lips
o Nasal flaring
o Thoracic wounds or flail segments
- Measure pulse oximetry and respiratory rate
- Feel for tracheal deviation, asymmetry in chest expansion, or change in percussion note
- Listen for asymmetry of breath sounds, added sounds, crepitations, and wheeze
- Consider ordering CXR or performing ABG
If following examination there are lesions acutely impairing ventilation, act immediately
- Tension pneumothorax: needle thoracostomy 2nd ICS MCL

- Pneumothorax/pleural effusion: contact on-call registrar for chest drain

- Anaphylaxis: IM adrenaline
Where patients have respiratory distress or oxygen saturations <94% (if long-standing type 2
respiratory failure <88%), it is important to intervene
- Give oxygen 15L/min via a high flow (non-rebreathe) mask to achieve a delivery of ~85%
oxygen, aim for saturations >94%
- If the patient has COPD, but has acutely low oxygen saturations give oxygen as above, but
keep a close eye on saturations
o Aim for 88 – 92%
o Perform regular ABGs to ensure that acidosis is not developing and refer the patient
to respiratory clinicians early
- Where patients with COPD have saturations <88% but not extremely low give oxygen at
4L/min via a white venturi mask to achieve a delivery of 28% oxygen
o If there is no improvement, increase the size of the venturi valve (yellow, red, green
then black), use a non-rebreathe mask as above, or progress to NIV
o Use clinical judgement, hypoxia will kill the patient much faster than hypercapnia
and acidosis
If the patient’s rate or depth of breathing is inadequate, consider using a bag-valve-mask to improve
ventilation, NIV can also be considered here. Contact ITU or 2222 for ventilatory support; the patient
may require RSI and intubation for mechanical ventilation
As with airway, any identified concerns should be immediately escalated to senior colleagues
Further treatment depends on the cause of respiratory distress
- In infection, consider antibiotics

- If there is wheeze, consider salbutamol
Circulation
Circulation should again be assessed using a look, measure, listen, feel, approach
- Look for pallor, cyanosis, sweating, JVP, and signs of blood loss (4 and the floor)
o Intrathoracic (respiratory distress, clinical signs of haemothorax)
o Intra-abdominal (tenderness, peritonism)
o Long bones (swelling, tenderness, or deformity)
o Pelvis (signs of pelvic fracture)
o Blood on the floor
- Measure heart rate, blood pressure, peripheral and central capillary refill
o Consider catheterisation to closely monitor urine output
o Consider ECG
- Listen for heart sounds e.g. gallop rhythm, significant murmur
- Feel for peripheral temperature, peripheral and central pulse rate and character, and
peripheral oedema
In patients with evidence of haemodynamic instability (detected after measure), initial management
should include the following
- Direct manual pressure should be used to stem visible bleeding

- Insert 2 wide bore IV cannulae (grey 16G or green 18G)
o From initial venous access take bloods as necessary, including cross match and
group & save where appropriate
o Give IV fluids. If there are signs of shock give 250 – 500mls stat fluid challenge over
15 minutes, if 1000 ml of bolus does not improve BP contact ITU
▪ Inadequate fluid replacement, active bleeding, vasodilation, heart failure,
and tamponade are all reasons why patients may not respond to fluid
challenge
- Where peripheral IV access cannot be established, there are several alternatives
o IO access using an EZ-IO kit (drill) gives temporary access for delivery of resuscitation
▪ It is best to use the humeral head where possible, and ensure to use
pressure bags to deliver the fluids/ medications
o Central venous access may be required
- Where necessary, activate the major haemorrhage protocol for urgent O- blood until cross-
matched blood arrives
o The major haemorrhage protocol involves the provision of O- blood, urgent cross-
matching of several units of blood, and provision of blood in packs containing
appropriate clotting factors alongside packed red cells
Disability (Neurological Status)
Assess conscious level
- Initially use AVPU

o Alert, responds to voice, responds to pain, unresponsive
- Formal assessment of GCS is required in any patient not alert
o Patients with GCS <8 (or <P) cannot protect their own airway and should have
immediate re-assessment of airway and nursing in the recovery position
Score Eye Opening Motor Response Verbal Response

1 None None None
2 To pain Extension (Decerebrate)* Sounds
3 To speech Abnormal flexion (Decorticate)* Inappropriate words
4 Spontaneously Withdrawal Confused speech
5 Localises Orientated
6 Obeys commands
*Decorticate posturing occurs in patients with cerebral hemisphere damage; the arms flex towards
the spine, and the legs scissor to the midline. Decerebrate posturing occurs in patients with
brainstem damage; the arms and wrists extend
Where pain is applied to check posture, this should not be with sternal rub as it is hard to distinguish
localisation and decorticate posture. Alternatives include
- Supraorbital pressure
- Finger nail pressure
- Clavicle rub
Brief neurological examination should include

- Examine for pupillary response

o Pupils should be 2 – 3mm, equal, and reactive
- Papilloedema
- Evidence of gross neurological deficit, including lateralising signs
There should be measurement of the following
- Blood glucose, intervene if hypoglycaemic

- Temperature
- Check the patient’s drug chart for reversible drug-induced causes of reduced consciousness
Other interventions relevant to disability include the administration of any antidotes or antagonists
to medications or toxins
Exposure
Exposure involves a top-to-toe examination of the patient
- Undress the patient, maintaining dignity, to check for the following

o Haemorrhage
o Rash
o Bruising
o Infection
o Injury
- Focussed examination then follows, with full assessment of the relevant system
Ensure that hypothermia after exposure is prevented using warming devices etc.
Secondary Assessment
Continue to regularly reassess the patient and ensure discussion with senior colleagues. Where vital
signs have normalised, secondary survey should begin
- History should follow the brief AMPLE format

o Allergies
o Medication currently used
o Past illnesses
o Last oral intake
o Events leading up to deterioration
Ensure to look through the patient’s notes and charts. Review the results of any investigations
ordered
SBAR
When dealing with an acutely ill patient, it is very important to ask for senior help. Referrals should
follow the SBAR format
Situation
- Who and where you are, and clarify you are speaking to the person you intended
- State what the problem is and what you need e.g. I am here with a patient in DKA and was
hoping to ask for your advice on management etc.
Background
- Brief summary of the patient

- Presenting complaint and reason for admission
- Brief summary of relevant past medical history and relevant medications
Assessment
- Positive and relevant negative findings on ABCDE

- Current vital signs
- NEWS score
Recommendations
- What you have done so far

- What you would like the person to do for you
Shock
Shock can be defined as global tissue hypoperfusion resulting in inadequate oxygen delivery to meet
metabolic demands and metabolic acidosis
Inadequate systemic oxygen delivery activates an autonomic response to maintain oxygen delivery
and cardiac output. This includes activation of the systemic nervous system and renin-angiotensin
axis
- Vasoconstriction to cutaneous, muscle and visceral circulation protects the heart, kidneys
and brain
- Pre-load is increased by venous vasoconstriction, this utilises Starlings law to increase stroke
volume
- There is also increased heart rate, water and sodium retention, and increases in blood
volume and pressure
Pulse pressure will initially decrease due to this autonomic activation increasing peripheral vascular
resistance. Hypotension will follow when these compensatory mechanisms begin to fail.
At the cellular level, when oxygen supply is removed there will be ATP depletion; this leads to a loss
of ion pump activity and resultant cellular oedema that can lead to hydrolysis.
- The endothelial inflammation and disruption from hypoxia results in lactic acidosis,
cardiovascular insufficiency and increased metabolic demands
A common physiological progression in shock is cardiac depression, respiratory distress, renal
failure, DIC, and organ failure
Types of Shock
Inadequate cardiac output

- Hypovolaemia: through either blood or fluid loss

- Cardiogenic shock (pump failure or obstruction)
Peripheral circulatory failure, leading to loss of systemic vascular resistance
- Sepsis
- Anaphylaxis
- Neurogenic
Multiple causes may co-exist in the same patient
Assessment
If possible, the patient’s history should be taken, this should cover
- Recent illness or fever

- Chest pain, abdominal pain, and shortness of breath
- Comorbidities and medications
- Ingestion of any toxins
- Recent hospitalisation or surgery
In shock there is hypotension, generally <90 systolic or <65 MAP in severe cases, urine output will
also be decreased to <0.5ml/kg/hr
- The posterior tibial pulse tends to disappear at 90mmHg, the radial at 80mmHg, the femoral
at 70mmHg, and the carotid at 60mmHg
- Low diastolic pressure suggests arterial vasodilation e.g. septic or anaphylactic shock
- Narrowed pulse pressure suggests arterial vasoconstriction e.g. cardiogenic or hypovolaemic
Management
ABCDE assessment and management is essential.
Ensure the airway is patent.
Shocked patients will usually be tachypnoeic. It is important to optimise breathing by reducing the
oxygen demands of the tissue and increasing the oxygen content of the blood
- Give supplemental oxygen in all cases, usually through a non-rebreathe

- Monitor SpO2
- Perform breathing assessment as normal, correcting as required e.g. tension pneumothorax
causing cardiogenic shock
- Perform ABG to monitor lactate
o Lactate will usually be >2 in shock
Circulatory interventions include
- Assess heart rate, CRT, and blood pressure

- Lie the patient flat and elevate their legs
- Gain IV access using two large bore (grey or green) cannulae
o Take routine bloods: FBC, U&Es, LFTs and coagulation studies, group and save, cross
match, and cultures
o Give IV fluid in initial 250 - 500ml boluses
▪ Where BP improves, switch from boluses to high rate infusion. Rate of

infusion should be titrated to keep HR<100, SBP>90, and UO>0.5ml/kg/hr
▪ If two fluid boluses fail to improve BP, refer to ITU
- Perform an ECG
- Catheter placement to monitor urine output
Ensure in disability that the patient is sufficiently able to maintain their airway, and consider spinal
shock
Exposure should be focussed at looking further for signs of infection and haemorrhage, and
assessment of fluid balance
- In septic shock the patient may feel warm and well perfused, with a bounding pulse
- In cardiogenic shock the patient may have a raised JVP, pulmonary and peripheral oedema
- In anaphylactic shock the patient may be flushed and warm, with additional signs including
urticaria, stridor, wheeze, and swelling
- In hypovolaemic shock the patient is usually pale and cool to touch
In further assessment there are other important factors to consider
- Mechanical ventilation may be required to reduce the work of breathing

o As propofol will further decrease blood pressure, volume resuscitation may be
required prior to ventilation
- Further interventions that can help with oxygen consumption can include
o Analgesia and anxiolytics to relax muscles and avoid shivering
- Central venous pressure monitoring may be required using a central line. CVP should be 5 –
10mmHg
o CVP >10 can indicate cardiogenic shock and fluid overload
o CVP <5 can indicate hypovolaemic shock or loss of systemic vascular resistance
Hypovolaemic Shock
Several factors can affect how patients present with hypovolaemic shock
- Younger, fitter patients have better compensatory mechanisms

- CNS injury can lead to disruption of cardiovascular reflexes and auto-regulatory systems
- Medications e.g. beta-blockers, antihypertensives
- Pregnancy tends to lead to later presentation with shock, due to higher circulating volumes
Haemorrhage
Haemorrhage may be due to external or internal bleeding
- Internal bleeding can include ruptured AAA and GI bleed

Classification of haemorrhagic shock is summarised below
I II III IV
Blood Loss <750ml 750 – 1500ml 1500 – 2000ml >2000ml
% Blood Volume <15% 15 – 30% 30 – 40% >40%
HR <100 100 – 120 120 – 140 >140
BP Normal Normal Decreased Un-recordable
Pulse Pressure Normal Narrow Narrow Narrow
RR <20 20 – 30 30 – 40 >35
Cap Refill Normal >2 >2 Absent
Urine Output >30 ml/hr 20 – 30 ml/hr 5 – 15 ml/hr ~0 ml/hr

Mental Status Anxious Anxious Confused Lethargic
Management should follow the above A to E approach
In haemorrhagic shock it is essential to gain definitive control of the haemorrhage, as fluid

replacement cannot correct shock where haemorrhage is ongoing. There are many interventions
that may be used
- Direct pressure (± elevation where possible)

- Indirect pressure is used where a wound is too large for direct pressure. This involves
applying pressure over the supplying artery against underlying bone, cutting off blood supply
to the wound
- Tourniquets are used where pressure is ineffective. Apply the tourniquet to a single bone
above the wound, as close to the wound as possible
For internal bleeding, consider the following options
- Traction and re-alignment of any fractures

- Application of a pelvic binder
- Emergency surgery or interventional radiology
Consider giving 1g bolus of tranexamic acid
The patient’s vital signs may differ dependent on how adequate their physiological response to
shock is, this can help to predict what interventions they may need. They can be broadly divided into
three groups
- Rapid responders have normal vital signs, and a low need for fluids and blood products
o For these patients it is best to order a group & save and cross-match, so that units of
appropriate blood are available if later required
- Transient responders will initially have normal vital signs, but these will begin to fall. The
need for fluids is high, and there may be a need for blood products
o For these patients both group & save and cross-match should be ordered, so that
cross-matched blood is ordered and ready to use
o Full cross-match takes around 45 minutes, so if the patient needs blood faster,
group-specific blood can be ordered (15 minutes)
- Non responders have abnormal vital signs, and a very high need for fluids and blood
products.
o For these patients there should be activation of major haemorrhage protocol
Where patients have had a massive haemorrhage, there may be a need for urgent O– blood. This is
achieved by activating the major haemorrhage protocol
- Massive haemorrhage is >150ml/min of blood loss, loss of >50% of blood volume in 3 hours,
or haemorrhage causing a >25% reduction in SBP
- Tranexamic acid should be used alongside packed red cells
- Due to the risk of consumption coagulopathy, no more than 4 units of blood should be
transfused without FFP or platelets
Consider transfusing patients with a Hb of <8, aiming to keep Hb >10
- 1 unit of packed red cells should increase Hb by 1g, if this does not occur, consider that the
patient is continuing to bleed
- For cross-match of blood, at least 2 samples are required. Therefore, in any new patient,
send both G&S and X-match
Fluid Loss
Shock due to fluid loss is in three main forms
- Inadequate fluid intake

- Salt and fluid loss: vomiting, diarrhoea, burns, polyuria
- Third space losses: bowel obstruction, post-operative ileus, pancreatitis, ascites
Management should be follow the above A to E approach, and then directed at the underlying cause
and correcting the fluid deficit
Anaphylactic Shock
Anaphylaxis is a type-1 IgE mediated hypersensitivity reaction
- Food triggers include peanuts, eggs, shellfish, and milk

- Drug triggers include antibiotics, opioids, NSAIDs, IV contrast agents, anaesthetic agents, and
blood transfusions
The release of histamine leads to widespread vasodilation and shock, alongside other clinical
features
- Bronchospasm and wheeze, urticaria, angioedema (particularly of the eyes, lips, tongue, and
larynx), diarrhoea, vomiting, abdominal pain
Management of anaphylaxis is urgent due to the immediate risk of airway obstruction; this follows
an A to E approach (and should be identified by stridor in A)
- Secure the airway and give 100% oxygen. Remove the offending cause immediately
- Give adrenaline 0.5mg IM (0.5ml of 1:1000), repeating every 5 minutes as needed
o <6 years old give 0.15mg (0.15ml of 1:1000)
o 6 – 12 years old give 0.3mg (0.3ml of 1:1000)
- Ensure that the resuscitation team have been contacted on 2222
- Assess breathing and attach SpO2 monitoring
o Consider ABG
o Where there is wheeze, give nebulised salbutamol
- Secure IV access
o IV 0.9% saline at a rate of 2L/hr
o 10mg Chlorphenamine
o 200mg Hydrocortisone
Continue to reassess and monitor the patient’s observations, perform continuous ECG recording.
Serum mast-cell tryptase should be measured as soon as possible to confirm anaphylaxis
Cardiogenic Shock
The causes of cardiogenic shock can be broadly divided into two groups
- Pump failure: MI, arrhythmia, myocarditis, acute valve failure, aortic dissection
- Obstruction: PE, tamponade, tension pneumothorax
Management of cardiogenic shock should again follow an A to E approach, attempting to identify the
underlying cause
- Perform careful assessment of fluid balance, but if the patient is hypotensive it is best to
give fluid and correct later unless pulmonary oedema is present
Treat any reversible causes
Spinal Shock
Spinal (neurogenic) shock has two main causes
- Cervical and upper thoracic spine (<T6) injury leading to loss of sympathetic tone
- Iatrogenesis from spinal anaesthesia
Signs include hypotension, no narrowing of pulse pressure, no tachycardia (bradycardia may be
present), and no cutaneous vasoconstriction
- Focal neurological deficit may be present

Management should follow the A to E approach above. If iatrogenic, stop the epidural infusion and
contact an anaesthetist urgently
Maxillofacial Injuries
Injuries to the face and jaw are common, and can cause significant morbidity and mortality
- It is important to remember at any injury above the clavicle could be associated with c-spine
injury, therefore immobilisation should always be considered
Assessment
Approach the patient using a <C>AcBCDE assessment
- Establishing an airway in a patient with significant facial injury is usually difficult. Using jaw
thrust, chin lift, and suction will generally establish a temporary airway; but a surgical airway
may be required as ET tube placement can be difficult
If patients have active bleeding, it is important to establish wide-bore IV access and give fluids
titrated to SBP
After assessment and stabilisation, take a history where possible
- Causative events
- LOC
- Visual or hearing disturbance
- Past medical and drug history e.g. anticoagulants, bleeding tendency
Focussed examination should involve the following
- Inspect the face from the front, side, and above. Look for asymmetry, cheek flattening, nasal
deviation, CSF leak, subconjunctival haemorrhage
- Palpate the facial bones checking for pain, deformity, crepitus, and movement
- Examine cranial nerve function, look at the eyes and eye movements carefully
- Examine inside the mouth to check for dental malocclusion, and loose/missing teeth
Investigations
In patients with multiple injuries, other investigation will usually take priority over imaging of the
face
- Multiple facial views are usually taken including

o Occipitomental (OM) and OM30. This is to visualise the orbit, maxillary sinus, and
zygomatic arch
o PA and OPG for the mandible
- CT scanning is often required prior to any maxfax surgery
Nasal Fractures
Nasal injuries are the most common facial traumas, and the nasal bones are the most commonly
fractured of the face
Presentation and Assessment
ABC assessment and stabilisation should precede any of the following.
Assessment of nasal injury should include careful search for other facial injuries, this includes
palpation of the facial skeleton while feeling for crepitus. The risk of head trauma increases
significantly with multiple facial fractures
- Significant head injury and/or cervical spine injury needs to be excluded before proceeding
with any other aspect of management
Important features to note in the history include
- The mechanism of injury, as high-impact accidents are more likely to be associated with
multiple facial and head injuries
- Timing of the injury, as after several hours facial swelling may obscure obvious deformities
- Patient age
- Previous nasal procedures, trauma, ENT problems, or use of intranasal
decongestants/steroids
Examination of the nose is best from above and behind, looking along the nose from bridge to tip.
There should also be intranasal examination using a speculum and cranial nerve examination.
Features to note in the examination include
- Significant rhinorrhoea or haemorrhage

o Epistaxis implies mucosal disruption, increasing suspicion of fracture
o CSF leak is usually clear, unilateral, watery discharge
- Septal haemotoma can cause total nasal obstruction and cartilage necrosis, this is seen as a
boggy swelling of the septum
- Septal deviation or malposition
- Lacerations, ecchymoses, swelling and bruising
- Crepitus and instability
- Facial/mandibular fracture
- Opthalmoplegia, as tethering of eye muscles can occur in orbital fracture
- Facial anaesthesia
Investigations
The diagnosis of nasal fracture is generally made on clinical grounds, and imaging is not normally
necessary during the initial assessment
- X-ray can however be useful if other bony facial fractures are suspected, but not in nasal
fracture alone
Management
Septal haematoma should be immediately treated with surgical drainage
Management of the patient is dependent on clinical status
- Patients without significant swelling or deformity can be discharged for outpatient ENT
follow up and fracture reduction
- Where there is significant swelling there should be application of ice and simple analgesia
- If there is no swelling and it is possible to assess and manipulate the mobile nasal bones,
fracture reduction can be performed
o This is very rarely performed immediately, as there is almost always some swelling
present
- Antibiotics are indicated where there is a laceration overlying the fracture
If the fracture cannot be immediately reduced (most cases) there should be referral to ENT within 7
– 10 days of the injury, by which time swelling will have reduced and reduction is possible.
- Manipulation of the nasal bones and reduction of the fracture is only possible within 3
weeks of the injury, this may require general anaesthetic
If the fracture is not seen within the window of opportunity, later management can be with
rhinoplasty
Immediate referral to ENT should be made in the following circumstances
- Marked deviation
- Epistaxis that is failing to settle
- Septal haemotoma, as this requires incision and drainage to prevent abscess/necrosis
- CSF rhinorrhoea, as this implies fracture of the cribriform plate
- Facial anaesthesia, facial or mandibular fracture, or ophthalmoplegia
Maxillary Fractures
Maxillary fractures are assessed and resuscitated as above. Classification of maxillary fracture is by
Le Fort
- Le Fort I are horizontal inferior maxillary fractures of the nasal floor

- Le Fort II are pyramidal fractures
- Le Fort III are transverse craniofacial fractures, separating the facial bones from the cranial
base
Maxillary fractures present with facial oedema, epistaxis, loose teeth, and mobility of the facial
bones
Management is usually surgical, with open reduction and fixation
Orbit and Zygomatic Fractures
The most common orbital injury is a ‘blowout’ fracture, usually involving the orbital floor and medial
wall. Blowout fracture commonly damages CN V2, causing maxillary numbness
Assessment
Assessment should be as above
It is particularly important to closely examine the eye in these patients
- Subconjunctival haemorrhage
- Visual acuity, fields, pupil reflexes, and range of movement
- Diplopia
- Enopthalmos, proptosis, or hypoglobus
If there is any indication of damage to the eyeball itself, ensure to refer urgently to ophthalmology
Ensure to advise the patient to avoid blowing their nose
Investigations
A plain XR of the skill is important
- Views should include facial, occipitomental, and submento-vertical

o Assess for the tear-drop sign of orbital floor fracture and for fluid in the maxillary
sinus (if there is no fluid in the maxillary sinus there is no maxillary fracture)
CT scanning can be useful to indicate more about the disruption to anatomy
Management
Management differs dependent on the type of orbital/zygomatic fracture the patient has
- All patients should be referred to maxfax
Orbital floor fractures may or may not require surgery, dependent on entrapment of extra-ocular
muscle or significant enopthalmus
Medial and orbital roof fractures can usually be managed conservatively, but there should be close
monitoring of the patient for any evidence of CSF leak
Lateral orbital wall and zygomatic arch fractures usually follow a high-impact blunt trauma to the
cheek e.g. a punch
- If the fracture is undisplaced, conservative management is appropriate

- Surgery may be required and if the case is complex there may need to be both ENT and
maxfax involvement
Mandibular Fractures
Considerable force is required to fracture the mandible, therefore there should be assessment for
concurrent injuries
General assessment should be as above, check for blood in the mouth (indicating compound
fracture) and chin paraesthesia due to the risk of mandibular nerve branch (inferior alveolar/
mental) damage
- If there is a bilateral mandibular fracture, there is a risk that the tongue could fall back and
occlude the airway; these patients should have early airway intervention
Investigations
There are a number of plain XR views that give a good picture of the mandible
- A panoramic view is most useful; this is an orthopantomogram (OPG)

- TMJ dislocation and condylar fracture are best shown by condylar views
Management
Simple, undisplaced fractures are best treated with analgesia and soft diet, with outpatient follow-
up. If there is malocclusion or deviation on jaw opening, refer immediately to maxfax
Displaced fractures will require surgical fixation, this is usually with plates and screws. Mandibulo-
maxillary fixation may be required in some.
Burns
There are four main types of burn
- Thermal (including scalds - burns caused by contact with hot liquid or steam)
- Chemical
- Electrical
- Radiation
It is important to assess the extent and depth of burns, so that appropriate treatment can be
initiated
Extent of burns in adults is determined by the rule of 9s. The Lund-Brower chart can also be used,
and is more accurate but less practical
Head 9%
Each arm 9%
Each leg 18%
Front of trunk 18%
Back of trunk 18%
Extent of burns in children is determined by the rule of 5s
Head 20%
Each arm 10%
Each leg 20%
Front of trunk 10%
Back of trunk 10%
Depth of burns is through classification into degree

- First degree burns are superficial; these appear as painful, glistening blanching erythema
with no blisters
- Second degree burns can be futher sub-divided
o Superfical partial thickness (superficial dermal); these appear as painful, blanching
pale-pink erythema with blistering
o Deep partial thickness (deep dermal); these appear as painful or painless, non-
blanching, blotchy, red erythema with blistering
- Third degree burns are full thickness; these may be white, brown or black and look leathery.
They do not blister and have no sensation
Pre-Hospital First Aid
If the burn is severe approach the patient using an A to E assessment, ensuring that it is safe to
approach
Stop the burning process by removing all clothing
- Adherent synthetic clothing should be actively cooled with water, do not attempt to remove
Rinse the involved body surface areas with copious amounts of cold tap water for at least 10 – 30
minutes where possible. Do not use ice or refrigerated water.
Dress the burn using cling-film (layered over, not wrapped) to reduce pain from friction during
transfer to hospital
For chemical burns, establish what the caustic agent was. Remove any dry powder on the skin prior
to irrigation
- Irrigate with water for at least 20 minutes, and considerably longer in alkali burns
Assessment
Patients with severe burns should be assessed using an A to E approach
The airway may be compromised from associated inhalation injury (± airway burn). This can require
ET intubation and mechanical ventilation, particularly where there is any stridor
- This is suggested by face and neck burns, singed nasal hair, hoarseness, stridor, soot in the
nostrils or palate, soot in the sputum, and persistent coughing/wheezing
Breathing problems can occur due to inhalation injury, or circumferential chest burns leading to
contraction
- All patients with major burns should be given 15L non-rebreathe oxygen
- CO poisoning is common in patients burned in a fire in a confined space, SpO2 does not
indicate this so perform an ABG to assess for carboxyhaemoglobin or request co-oximetry
Circulation may be compromised due to hypovolaemic shock, therefore large-calibre IV access

should be established as soon as possible
- Fluid resuscitation should be carried out as required

- Fluid replacement should take place in all adults with >15% burns or children with >10%
burns, calculated by the Parkland formula
o In adults give 2 - 4ml/kg of Hartmann’s solution for each 1% of BSA that is burned
▪ 2 – 4ml x % burn surface area x weight
▪ Half of this volume should be given in 8 hours
▪ The other half should be given over the following 16 hours
o In children give replacement fluid as above, alongside maintenance fluids
(100ml/kg/day) with 0.45% saline with 5% dextrose solution
- Take routine bloods, ensuring to include U&Es and troponins in electrical burns due to the
risk of rhabdomyolysis and myocardial injury
o An exit site in an electrical burn is a poor prognostic sign, often there is deep muscle
damage
Ensure adequate analgesia and prevent hypothermia.
Focussed examination is assessment of the depth and extent of the burns
- % BSA burned does not include simple erythema
Where possible, further history should be obtained
- What was the burning material, and how long was the patient exposed to it?
- Has the patient been exposed to fire and smoke?
- Is there any history of LOC?
- When did the burn occur, this has implications on fluid replacement
Management of Minor Burns
Minor burns can be managed in primary care.
For epidermal burns, no dressing is required – advise simple analgesia and cold compress. For
superficial dermal burns clean with soap and water to remove any dead tissue, and assess the
blisters
- Blisters <1cm should be left to minimise the risk of infection

- Blisters >1cm are likely to burst, and should therefore be aspirated under aseptic technique
Dress the wound using a non-adhesive dressing with gauze padding or a biological dressing, with re-
dressing and re-assessment of the wound after 48 hours
- Dressings of superficial partial-thickness burns should then be re-applied, and changed after
3 – 5 days
If infection occurs clean the wound with 0.9% saline, swab the wound for culture, and start empirical
treatment with a 7-day course of flucloxacillin
- Daily wound inspection and dressing change is required
Referral to secondary care

Management of Major Burns
Major burns should be managed in secondary care
- This includes all deep-dermal and full-thickness burns, and all circumferential burns
All complex major burns should be referred to a specialist burns unit, particularly
- Patients aged <5 or >60

- Burns affecting the face, hands, soles of the feet, perineum, any flexure
- Circumferential deep-partial or full-thickness burns of the limb/torso/neck
- Inhalation injury
- Any electrical or chemical burn
- Large affected area
o <16 with >5% burns
o >16 with >10% burns
Analgesia and sedation are important in severely burned patients. Wound care is also essential to
prevent infection with non-adherent dressing
- Assess the need for tetanus prophylaxis
Full thickness burns will require further management
- Excision and grafting are used in burns >1cm in diameter, this should be within 3 weeks to
minimise scarring
- Full thickness circumferential burns may require escharotomy to alleviate circulatory/
ventilatory insufficiency
Inhalation Injury
Smoke inhalation causes three different forms of injury
1. Thermal injury to upper airways

2. Chemical injury to the tracheobronchial tree
3. Systemic poisoning due to CO or cyanide
It is important to determine peak flow, and perform an ABG, CXR and measurement of
carboxyhaemoglobin in all patients with suspected inhalation injury
Frostbite
Frostbite is a severe, localised, cold-induced injury that leads to freezing of tissue
- This is most common on the ears, nose, cheeks, chin, fingers, and toes
Patients may experience a throbbing/ burning pain alongside local signs e.g. pallor, firmness,
hyperaemia, necrosis, or gangrene
- Deep frostbite tends to have haemorrhagic blisters

Management is with A to E assessment alongside treatment of associated hypothermia. Rapid re-

warming with 37 fluids is used for the area, and must be preceded with adequate analgesia
Wound Care
Wound healing occurs in several defined stages
1. Inflammation takes place for the first 2 – 5 days. There is initial haemostasis from
vasoconstriction and clot formation, followed by histamine release and phagocytosis of
bacteria/debris
2. Proliferation occurs from 12 hours to three weeks. Epithelialisation and neovascularisation
precedes granulation tissue formation
3. Remodelling occurs from 6 to 12 months. The wound contracts and tensile strength is
achieved as new collagen forms
Assessment
History of a patient with a wound should include the following
- What was the mode/mechanism of the wound, particularly asking about any broken
glass/china
- What is the site of injury, are there multiple wounds?
- Did the wound occur in a contaminated or clean environment?
- How long ago did injury occur
o Wounds older than 12 hours are usually not suitable for primary closure (sutures are
not recommended after 8 hours, wounds can be closed up to 24 hours on the face)
Factors in the past medical and drug history can indicate potential problems with wound healing/
infection.
Social history is important in determining how able the patient is to care for the wound post-
discharge.
Examination of a wound should involve assessment of the following. It may be necessary to use local
anaesthetic for proper exploration of the wound
- Site (using diagrams where possible)

- Length, depth, and shape of the wound
- Contamination by dirt or other foreign bodies
- Injury to underlying structures
o Tendon injury should be assessed by testing movements of associated joints. Look at
the wound whilst moving the joint to bring structures to the surface
o Vascular injury should be assessed by checking distal pulses and capillary refill
o Neurological injury. Assume that any altered sensation reflects nerve injury
Investigations
X-ray is recommended where there is suspicion of associated fracture, risk of foreign body, or
involvement of a joint
- X-ray all wounds from glass that fully penetrate the skin
- Most metal (except aluminium) and glass objects >1mm will show up on x-ray
- Where there are radiolucent foreign bodies e.g. wood, USS can be used
Wound exploration under appropriate anaesthesia is the most important factor in investigation. X-
ray should be undertaken prior to exploration
- 1% lignocaine is usually sufficient (maximum 20ml in an adult, or 3mg/kg)
If there has been significant blood loss, the following lab tests may be appropriate
- FBC, U&Es, LFTs, clotting, G&S/ X-match
Management
All wounds should be thoroughly cleaned, irrespective of whether they are due to undergo closure,
this decreases the risk of infection
- Sterile 0.9% saline is best for this, but aqueous chlorhexidine can also be used
- Grossly contaminated wounds may require debridement alongside washing
There are three main forms of wound closure
1. Primary closure is physical closure of the wound soon after injury

2. Secondary closure is where the wound heals by granulation (secondary intention) and there
is no intervention
3. Delayed primary closure is physical closure 3 – 5 days after injury. This is recommended
where the wound is initially infected or grossly contaminated
There are several non-surgical methods of primary wound closure
- Steri-strips are useful for injuries where the skin in thin and inappropriate for sutures e.g.
pretibial lacerations
- Skin tissue glue is useful in scalp wounds
- Staples are useful in scalp wounds
Sutures are the most commonly used method to achieve primary closure, suture size and
appropriate use is summarised in the table below. Sutures with high memory are usually
monofilament and are more difficult to handle
Size Uses Recommended Duration

6/0 Face 5 – 7 days
5/0 Face, neck, hand dorsum 5 – 7 days
4/0 Mucosa, trunk, hands, feet 5 – 7 days
Back 7 – 10 days
3/0 Limbs, trunk, scalp Limbs 7 days
Back 7 – 10 days
2/0 Fascia, viscera, blood vessels Absorbable (used in surgery)
Tetanus prophylaxis is required in many wounds. High risk wounds are those that are heavily
contaminated, infected or >6hr old, bites, and wounds with devitalised tissue.
Immunisation Status Vaccine Human Tetanus Immunoglobulin

Fully immunise (5 doses None required Required if the wound is high risk*
of vaccine)
Primary immunisation None required (unless a booster Required if the wound is high risk
complete, no boosters is due soon, or is overdue)
Primary immunisation Give a reinforcing dose of Give one dose
incomplete vaccine, and further doses as
required to complete schedule
Not immunised, or Give an immediate dose of Give one dose
status unknown vaccine, and follow with further
doses to complete course
If a wound becomes infected after primary closure, remove all sutures etc. and thoroughly clean the
wound. Leave the wound open, cover with a dressing, and consider antibiotics.
Wound dressing may or may not be required, but dry non-adherent dressings are best. Advise
patients to keep the wound clean and dry for the first few days, and restrict movements of
associated joints to prevent suture lines opening
- Advise patients to be vigilant for signs of infection

- Tell patients to visit their GP to have sutures removed after an appropriate length of time
Referral
Consider referral of the following wounds to senior colleagues, as they may require surgical
intervention for closure or debridement
- Foreign bodies that cannot be removed

- Poor blood supply
- Grossly contaminated wounds e.g. bites
- Surgical debridement necessary
- Injury to underlying structures
Facial Wounds
Cosmetic considerations in facial wounds are significant
Certain facial structures require expert management
- Any damage to the parotid gland or facial nerve

- full thickness eyelid lacerations
- Injuries with tissue loss
- Injuries to ear/nose cartilage
- Lip lacerations that cross the vermillion border
Bite Wounds
Human and animal bite wounds have a significant infection risk. Investigation should generally
involve x-ray to assess for tooth fragments in the wound
- Cleaning and debridement is essential, this is best under anaesthetic as it must be thorough
- Primary closure is not advised, unless the wound is on the face

o The choice between delayed primary closure and secondary closure is dependent on
the size/extent of the wound
- Antibiotic prophylaxis is recommended
- Consider whether rabies PEP is required
Sixteen Key Presentations

Acute Abdominal Pain
The acute abdomen is a clinical syndrome with many medical and surgical causes
- Rupture of an organ (causing shock) and peritonitis usually require laparotomy

- Local peritonitis and colic may require laparotomy
The assessment and initial management of a patient presenting with acute abdominal pain should
follow an A to E approach
- Bloods to request when IV access is established should include

o FBC, U&Es, LFTs, amylase, clotting, group and save (or crossmatch if required),
cultures
o ABG should be performed to see lactate
- Following initial stabilisation, there can be brief history and examination
History
Clarify further details about the pain itself using the SOCRATES framework
- Character of pain is important to differentiate causes

o Colicky pain suggests an obstructed viscus
o Constant sharp pain worse on movement or coughing suggests peritonitis
o Constant dull ache suggests inflammation
- Specific associated symptoms to ask about include
o Vomiting
o Haematemesis, melaena or rectal bleeding
o Changes in bowel habit including flatus, colour, diarrhoea, and constipation
o Fever and rigors
o Urinary symptoms
o Weight loss
o Gynaecological symptoms
- Ask if they have experienced the pain before the current episode
Other important factors in the presenting complaint and past medical history include
- Bowel and urinary habit

- Menstrual history, last menstrual period
- PV discharge
- Last oral intake
- Recent surgery, due to the risk of adhesions
Drug history should cover the use of any anti-coagulants in preparation for complications in surgery,
and steroids, as these may change the nature of presenting complaint
Examination
Repeated examination is key to making the diagnosis of the acute abdomen

Inspection
- Evidence of anaemia, jaundice, or dehydration

- Patient lying still (board-like rigidity) with a positive cough test indicates peritonitis
- Restlessness indicates colic
- Visible peristalsis or abdominal distension
- Cullen’s and Grey-Turner’s signs
- Loss of abdominal breathing
Palpation
- Involuntary guarding (the reflex tensing of the abdominal muscles over the painful area) and
rebound tenderness (initial pressure does not cause pain but when the examining hand is
released, pain is felt) both indicate peritonitis
Percussion
- Percuss to distinguish distension due to bowel gas or ascites

- Percussion can also identify pneumoperitoneum by loss of hepatic dullness
- Tenderness to percussion indicates peritonitis
Auscultation
- Absent bowel sounds indicate generalised ileus, peritonitis, or full obstruction

- High pitched, tinkling bowel sounds indicate bowel obstruction
Investigations
Further investigations following A to E assessment in abdominal pain that may be useful, dependent
on history and examination, can include
- Urinalysis ± microscopy and culture, ± pregnancy test

- ECG
Imaging studies useful to order include
- Erect CXR and/or supine AXR

- Abdominal USS, Focussed Assessment with Sonography for Trauma (FAST) scan
- CT scan
In extreme cases, exploratory diagnostic laparoscopy can be used
Differential Diagnosis
The site of abdominal pain can often be a useful tool to distinguish different common causes,
however it is important to be mindful that all causes can present atypically
Epigastrium
- Intrathoracic: myocardial infarction, pericarditis, pleurisy, basal pneumonia, PE,

oesophagitis, oesophageal perforation
- Upper GI: peptic ulcer, GORD, pancreatitis
Upper quadrant (subcostal, upper flank and loin)
- Intrathoracic: myocardial infarction, pericarditis, pleurisy, basal pneumonia, PE

- Kidney: pyelonephritis, renal stones
- On the right, symptoms can be due to the liver or biliary tree: gallstone complications,
hepatitis, liver abscess/cyst, hepatic congestion
- On the left, symptoms can be due to the spleen: rupture, abscess, acute splenomegaly
Lower quadrant (lower flank and loin, iliac fossa) and central (umbilical, suprapubic)
- Bowel: mesenteric adenitis (viral lymphadenopathy of the mesentry), diverticulitis,

obstruction, hernia complications, perforation, colitis (IBD, ischaemia, pseudomembranous)
- Gynaecological: mittelschmerz, salpingitis, tubo-ovarian abscess, ruptured ectopic
pregnancy, ovarian torsion, PID, endometriosis
- Kidney: pyelonephritis, renal stones
- Musculoskeletal: psoas abscess
- On the right, symptoms can be due to: appendicitis, Meckel’s diverticulitis
Vascular causes can include AAA rupture and mesenteric thrombosis.
Medical causes can include DKA, septicaemia, shingles, sickle cell crisis, and infection.
Causes of acute abdomen categorised according to severity are listed below
1. Haemorrhage e.g. splenic rupture, AAA leak

2. Peritonitis e.g. perforation
3. Closed loop obstruction
4. Inflammation e.g. appendicitis, diverticulitis
5. Open loop intestinal obstruction
Referred Pain
Visceral pain is referred in a particular pattern due to the distribution of splanchnic nerves
- Foregut (oesophagus to 2nd duodenum, liver, pancreas) is epigastric

- Midgut (2nd duodenum to 2/3rd transverse colon) is umbilical
- Hindgut (2/3rd transverse colon to rectum) is suprapubic
Initial Management
Ensure that the patient has adequate pain relief, give fluids, and keep them NBM
- If the patient is not kept NBM they will have to fast for 6 hours for food and 2 hours for clear
fluids prior to surgery
Appendicitis
Appendicitis is commonest between the ages of 10 – 20. It occurs when gut organisms invade the
wall of the appendix after luminal obstruction, causing oedema and ischaemic necrosis, potentially
leading to perforation
- The appendix lumen can be obstructed by faecolith, parasitic worms, or lymphoid

hyperplasia
Presentation
Classically, patients will present with a colicky referred peri-umbilical pain that moves to the RIF
when the peritoneum becomes inflamed
- The classical site of pain is McBurney’s point: 2/3rd of the way from the umbilicus to ASIS
There will also be tachycardia, fever, anorexia, constipation, and (in some cases, after pain onset)
vomiting
On examination, the patient will be tender in the RIF and there is potentially rebound tenderness/
guarding
- Rovsing’s sign may be present, where pressing on the LIF elicits pain in the RIF
- There can also be psoas sign (pain on hip extension) and Cope sign (pain on flexion and
internal rotation of the hip)
Investigations
Patients should have a urine dip (including for -HCG in women) and SpO2. Routine blood tests
should all be performed
- There will be neutrophilia and raised CRP

Ultrasound scanning the appendix is useful. CT is rarely used due to delaying treatment, but has high
diagnostic accuracy where there is diagnostic uncertainty
- The Alvorado scoring system (out of 10) can indicate the likelihood of appendicitis, and the
investigation recommended dependent on score: <4 appendicitis unlikely, 5 – 6 ?CT, >7
operate
Clinical Criteria Score Lab Criteria Score
Pain migration 1 Rebound Tenderness 1
Anorexia 1 Temp >37 1
Nausea/ Vomiting 1 Neutrophils >75% 1
RLQ Tenderness 2 WCC >10 2
Management
Treatment is prompt appendicectomy, which can be laporoscopic or open
- Open appendicectomy can be Gridiron or Lanz. The Lanz incision is lower and more
horizontal)
- IV antibiotics are important, usually metronidazole and cefuroxime. These should be given
prior to surgery
Complications include perforation, appendix mass (inflamed appendix covered with omentum), or
appendix abscess (where an appendix mass is left unresolved)
- Appendix mass is best managed with initial conservative strategies e.g. analgesia, fluids and
antibiotics, with later appendicectomy after resolution
- Appendix abscess will require percutaneous drainage and antibiotics with later
appendicectomy
Meckel’s Diverticulitis
Meckel’s diverticulitis is a key differential diagnosis for appendicitis
- Meckel’s diverticulum is a congenital vestigial remnant of the vitellointestinal duct in the

distal ileum containing gastric mucosa
There are various complications of Meckel’s diverticulum, this will only occur in around 2%
- Intestinal obstruction, this may be due to intussusception or volvulus

- Diverticulitis
- Perforation
- Neoplasia
- Haemorrhage, typically painless fresh PR bleeding in a child <2
Where complications occur, resection is recommended. The diverticulum is usually identified intra-
operatively, but can occasionally be seen on CT
Bowel Ischaemia
Bowel ischaemia has been classified into three main types
1. Acute mesenteric ischaemia

2. Chronic mesenteric ischaemia
3. Ischaemic colitis (colonic ischaemia)
The arterial supply of the digestive system is through the branches of the abdominal aorta, which
lies anterior and to the left of the IVC.
The foregut is supplied by the celiac trunk
- The left gastric, hepatic and splenic arteries come directly from the trunk
- The splenic artery gives off the posterior gastric, short gastric and left gastro-omental
arteries (all to the stomach) before continuing to the hilum of the spleen
- The hepatic artery gives off the right gastric artery, gastroduodenal artery (which supplies
the duodenum, and gives off the superior pancreaticoduodenal artery and right gastro-
omental artery) and cystic artery (to the gall bladder) before branching into the left and right
hepatic arteries
- The left gastric artery gives off an oesophageal branch
The midgut is supplied by the branches of the superior mesenteric artery
- Branches include the jejunal arteries, ileal arteries, right (to the ascending colon) + middle
(to the transverse colon) colic and ileocolic artery (which gives off the appendicular artery)
- These lead into arterial arcades, which give off vasa recta into the mesentery
The hindgut is supplied by the branches of the inferior mesenteric artery
- The left colic (to the descending colon), sigmoid, and superior rectal arteries
Acute Mesenteric Ischaemia
Acute mesenteric ischaemia is an umbrella term to describe impaired blood flow to the intestine,
bacterial translocation to normally sterile tissue, and SIRS
- Mesenteric arterial embolus and thrombus

o Mural thrombus following MI, septic emboli from IE, AF
- Mesenteric venous thrombus
o Hypercoagulability disorders, tumours causing venous compression, infection,
venous trauma
- Non-occlusive mesenteric ischaemia
o Hypotension, vasopressive drugs (including cocaine)
Presentation
Patients usually present with moderate-to-severe colicky pain that is poorly localised
- Physical findings are out of proportion to the degree of pain, and there may be no features
of tenderness or peritonitis
- Hypovolaemia and shock occur rapidly
Investigations
A to E assess and stabilise the patient
- Give high flow oxygen through a non-rebreathe mask, the patient will be breathless due to
lactic acidosis (perform ABG)
- Gain IV access and commence fluid resuscitation
o Bloods to include FBC, U&Es, LFTs, coagulation profile, and G&S
o ECG
Further investigations should include urinalysis and further imaging
- Plain AXR and erect CXR can be used to exclude differentials, AXR may show thumb-printing
- Abdominal CT can show some features
- Angiography is the gold standard for diagnosis
- Echocardiogram can show valvular pathology leading to embolism
Management
There should be initial resuscitation with IV fluids and oxygen as per A to E approach. IV antibiotics
should also be used
- Where bowel appears viable on CT and there is no perforation, medical options can be used
o Thrombolytics can be infused through the angiogram catheter
o Heparin can be used for MVT
- Surgery may be required where bowel is viable

o Embolectomy
o Angioplasty
Where patients are septic following necrosis due to ischaemia there can be urgent laparotomy to
resect the dead bowel.
Chronic Mesenteric Ischaemia
Chronic mesenteric ischaemia occurs when there is atherosclerotic disease affecting the vessels that
supply the intestine
Presentation
Patients present with postprandial colicky pain due to claudication, this often leads to weight loss as
eating is uncomfortable
- Chronic mesenteric ischaemia is often called intestinal angina for this reason
- Patients will also often have associated vascular disease e.g. TIA, angina
On examination patients may have an upper abdominal bruit
Investigations
Routine bloods and ECG should be carried out to assess CVD risk factors and exclude malnutrition
Diagnostic investigation is imaging
- Angiography is gold standard
Management
Medical care is limited, and should only be used in patients not suitable for surgery; this is usually
with nitrates
Surgical care includes
- Transaortic endarterectomy of the coeliac or superior mesenteric artery

- Bypass grafting
- Angiography and stenting
Ischaemic Colitis
Ischaemic colitis is caused by compromise of the blood supply to the colon, most commonly
affecting the splenic flexure
- The most common cause is atheroma of the mesenteric arteries

- Certain factors can predispose to ischaemic colitis, these factors are similar to mesenteric
ischaemia
Presentation
Patients present with acute onset abdominal pain, usually in the LIF
- There is often nausea, vomiting, and loose stools containing dark or fresh blood
Investigations
Initial investigation should follow an A to E approach, bloods should be the same as in mesenteric
ischaemia. Following this there can be further imaging
- Erect CXR and AXR

- CT can indicate likely ischaemic colitis, further to this there can be either
o Colonoscopy can show blue, swollen mucosa with contact bleeding
o Barium enema shows thumb-printing with a similar appearance to UC and Crohn’s
Management
Bowel ischaemia often resolves once the cause of hypoperfusion has been alleviated, therefore it is
important to give IV fluids and rest the bowel
- Surgery is rarely required, and used to correct perforation, necrosis and strictures
Bowel Obstruction
Bowel obstruction can be divided broadly into dynamic and static causes. Dynamic bowel
obstruction is mechanical, whereas static bowel obstruction is due to failure of peristalsis e.g. ileus
or pseudo-obstruction (chronic bowel failure).
Both forms can affect the small or large bowel
- The two can be distinguished on investigation

- Small bowel obstruction can be identified by multiple dilated (>3cm) loops of central bowel,
completely traversed by valvulae conniventis
- Large bowel obstruction can be identified by dilated (>6cm or >9cm at the caecum) loops of
peripheral bowel, incompletely traversed by haustra
The causes of mechanical obstruction can be divided into intraluminal, transmural, and extraluminal
Intraluminal Transmural Extraluminal
Foreign body Neoplasm Adhesion (post-operative,

infection, inflammation,
congenital)
Faecal impaction Stricture (e.g. Crohn’s disease, Neoplasm

radiotherapy, diverticular
disease, post-operative)
Gallstone Fistula Pregnancy
Volvulus
Hernia
The commonest causes of small bowel obstruction are as follows
- Adhesions
- Hernias
- Other causes e.g. foreign bodies, tumours (most commonly benign polyps), strictures,
gallstone ileus
The commonest causes of large bowel obstruction are as follows
- Neoplasm (usually primary malignancy)

- Structures (usually diverticular)
- Faecal impaction
- Sigmoid or caecal volvulus
o Volvulus is rotation of the gut on its mesenteric axis, more commonly sigmoid
o This can produce a severe, rapid, strangulated obstruction
Closed-loop large bowel obstructions occur where the ileo-caecal valve remains competent,
therefore there can be no decompression of bowel contents into the small bowel. This is much more
dangerous, and likely to perforate
- Perforation occurs due to increasing pressure leading to decreased venous return, oedema,
and decreased arterial supply. This causes necrosis of the bowel wall
- Another effect of decreased venous return and oedema is bacterial translocation, risking
peritonitis in the absence of perforation
Paralytic ileus is where the bowel ceases peristalsis, there are many potential causes
- Post-operative
- Peritonitis or viscus perforation
- Trauma
- Metabolic and electrolyte disturbances e.g. uraemia, hypokalaemia
- Other acute abnormalities e.g. chest infection, MI, stroke, AKI, DKA, hypothyroidism,
pancreatitis
Presentation
There are four cardinal features of intestinal obstruction.
1. Vomiting, which may be faeculant

2. Colicky pain, this is usually diffuse and central. In paralytic ileus, pain is absent
3. Complete constipation i.e. no flatus or faeces
4. Distension
On examination there may be tenderness, highly active ‘tinkling’ bowel sounds on auscultation and
hyper-resonant percussion. It is important to check for hernias
Severe pain and tenderness suggests ischaemia or perforation
Investigations
The bowel secretes around 7L of fluid per day – leading to significant third space losses in
obstruction. Therefore fluid charts are essential to monitor intake and output, and catheterisation
may be needed for an accurate calculation of requirements
Further investigations should include
- Routine bloods including clotting, group and save, and cross match as surgery may be
required
- Plan erect AXR, looking for air-fluid levels and distention (>3cm in small bowel, >6cm in large
bowel, and >9cm in the caecum)
- Erect CXR where perforation is suspected
- CT scanning can be used where there is diagnostic uncertainty and to predict the need for
surgery
Management
It is essential to keep patients NBM and ensure they are catheterised
Management of bowel obstruction and ileus is usually conservative, using ‘drip and suck’ with
copious IV fluids and a nasogastric tube
- The NG tube decompresses the bowel and reduces the risk of perforation, but also alleviates
vomiting
- After initial NG placement there should be aspiration of fluid, and then the tube
should be left on free drainage
- IV fluids are vitally important due to third space losses, as fluid will not be absorbed from
the obstructed bowel it will either sit in the bowel or absorb to form ascites
Volvulus can be managed with conservative passage of a flatus tube
Urgent surgery is indicated where there is strangulation, perforation, or closed-loop large bowel
obstruction. For other cases, usually conservative measures will be trialled for 24 – 48 hours before
consideration of surgery to alleviate the obstruction. Endoscopic stenting can be used where
patients are not suitable for surgery
For ileus and pseudo-obstruction, there are no surgical options.
Diverticular Disease
Diverticulosis can be congenital or acquired
- Acquired diverticulosis is much more common, and associated with a Western diet and
lifestyle
o Incidence increases through age due to disordered motility, hyperelastosis, and
collagen abnormalities
It occurs as the lack of collagen weakens the muscularis propria, meaning that there are small
herniations of mucosa through the muscularis. This is typically adjacent to terminal arterial branches
and taenia coli
Presentation
Diverticulosis itself is asymptomatic, but presents when there is a complication
- Diverticular disease is diverticulosis with chronic symptoms e.g. colicky left lower abdominal
pain relieved by flatus, bloating, constipation, rectal bleeding
- Diverticulitis is inflammation of a diverticulum. This presents with fever, tachycardia, left
lower quadrant pain, nausea and vomiting, and change in bowel habit
o Diverticulitis can be further complicated by fistula formation, abscess formation,
perforation and peritonitis
o Fistulas include enterocolic, colovaginal, colovesical (pneumaturia, frequent UTI)
o Diverticular abscess is suggested by a swinging fever
- Diverticular bleeding can be minor or major, and presents with abrupt painless fresh PR
bleed
- Bowel obstruction
Investigations
Diverticular disease is typically an incidental finding on AXR, barium enema, or CT scan
Diverticulitis should be investigated with urgency
- FBC, U&Es, LFTs, clotting, and group + save

- Plain erect CXR and AXR to exclude perforation
- Contrast enhanced CT is the gold standard investigation
Investigation of diverticular bleeding is usually with colonoscopy, however angiography can also be
used
Management
Uncomplicated diverticular disease does not require active intervention, but dietary increase in fibre
is recommended. Mebeverine can be used
Diverticulitis can be treated at home with oral fluids and antibiotics. If pain is not controlled or the
patient cannot tolerate oral intake, there should be hospital management
- IV broad spectrum antibiotics (co-amoxiclav)

- Analgesia
- NBM
In complicated diverticulitis there may need to be surgery
- With perforation, Hartmann’s resection is generally used, as this enables colostomy reversal
- Fistulae can be treated with colonic resection
- Abscesses may require CT guided drainage
Diverticular bleeding usually resolves with bed rest ± transfusion
- It can be treated with endoscopic haemostasis in colonoscopy

- There may need to be operative intervention if bleeding continues
Hernias
A hernia is a protrusion of a viscus through its containing wall into an abnormal position
There are three main risk factors for abdominal wall hernias
1. An anatomical weakness where structures pass through the abdominal wall, muscles fail to
overlap, or muscle has been replaced with scar tissue
2. An acquired weakness following trauma
3. High intra-abdominal pressure from e.g. coughing, straining, abdominal distension, and
heavy lifting
All hernias occur at a weak spot, reduce on lying down or with direct pressure, and have an expansile
cough impulse
Presentation
The presentation of a hernia depends on its clinical state
- Reducible hernias are those in which the contents can be replaced completely into the
abdominal cavity, and are usually not painful
o Examination will show a reducible lump with a cough impulse
- Irreducible (incarcerated) hernias occur when there is adhesion of the contents to the wall
of the sac or between the contents, there is a narrow neck, or inspissated faeces within
bowel loops
o These hernias are painless, and cough impulse is absent
- Obstructed hernias contain intestine, in which the lumen has become occluded, this is
usually at the neck of the sac but can be due to adhesions
o Initially the blood supply is intact, but with time this will become impeded and
strangulation will result
Strangulated hernias occur where the contents of the hernia are constricted by the neck of the sac,
to such a degree that their circulation is cut off. Unless this is relieved, gangrene of the sac contents
will occur, leading to bowel perforation
- If this occurs there will be a sudden, severe pain in the hernia, colicky central abdominal
pain, and vomiting, distention and constipation
- The hernia will be irreducible, tender and tense with no cough impulse. The overlying skin
will be tense and oedematous. There will be bowel obstruction e.g. abdominal distension,
tenderness, and active bowel sounds
Examination
In order to inspect a hernia, the patient should stand up and the lump should be looked at from in
front
- The site and shape of the lump should be noted. Inguinal hernias bulge above the crease of
the groin, and femoral hernias bulge into the medial end of the groin crease (more lateral
than inguinal however)
- It should be noted whether the lump extends into the scrotum or not
Palpation of the lump should be from the front and from the side
- From the front, the scrotum and its contents should be examined. To ascertain whether a
lump is a hernia or a scrotal lump, one should try to get above it
- From the side the position, temperature, tenderness, shape and size, tension, composition,
cough impulse, reducibility, and control of the lump should all be ascertained
The lump should then be percussed and auscultated if possible. The other side of the groin should
then be felt, and following that, the abdomen examined.
- If there is bowel in the sac it will be resonant, and bowel sounds can be auscultated
- In abdominal examination, one should look for anything that may be raising the intra-
abdominal pressure. This includes a large bladder or prostate, ascites, chronic intestinal
obstruction, and pregnancy
Investigations
USS is the investigation of choice in most patients with abdominal wall hernias
- MRI and CT can also be used, particularly where the patient is obese
- Herniography is rarely necessary, but involves injection of x-ray contrast agent into the
peritoneum
Epigastric Hernia
The defect in an epigastric hernia is in the mid-line above the umbilicus in the linea alba, and there
may be multiple present
- A differential diagnosis for an epigastric hernia is a linea alba divarification (diatasis recti),
this can be distinguished as it does not appear on straining but only when the patient moves
to a sitting position from lying flat
Incisional Hernia
An incisional hernia is a risk of any abdominal surgery, and occurs when the wound fails to heal
correctly
- Patient and surgical factors both contribute
Umbilical Hernia
Umbilical hernias can be broadly classified into three groups
1. Congenital hernias (omphalocele)

2. Infantile hernias, these usually resolve spontaneously. If the hernia is >1.5cm in a child >4
years, surgery is usually required
3. Adult, associated with pregnancy, obesity and ascites
Femoral Hernia
A femoral hernia is a protrusion of preperitoneal fat, peritoneal sac and sometimes abdominal
contents through the femoral canal
- The femoral canal usually contains loose areolar tissue and the gland of Cloquet (a lymph
node)
- This is more common in women, particularly in the elderly
Hernias will be inferolateral to the pubic tubercle. Typically, they will present with a lump in the
groin, pain, discomfort, or obstruction
- Femoral hernias are prone to strangulation

Management of femoral hernia should be with urgent elective procedure. There are three classical
approaches to the femoral canal
1. Low (Lockwood)
2. Transinguinal (Lotheissen)
3. High (McEvedy)
Inguinal Hernia
The inguinal canal lies parallel to the inguinal ligament
- The internal ring is at the mid-inguinal point (above the femoral pulse). The inferior
epigastric vessels lie medially.
- The external ring is an inverted V shaped defect in the external oblique aponeurosis. This lies
superomedial to the pubic tubercle
In males, the inguinal canal should contain the spermatic cord (testicular artery, artery to the vas
deferens, genital nerve, ilioinguinal nerve, pampiniform plexus, vas deferens, lymphatics). In
women, the inguinal canal will contain the round ligament.
Presentation
Inguinal hernias can develop gradually or suddenly, sudden appearance of a hernia usually occurs
with an episode of heavy lifting
- The patient may complain of a pain or dragging sensation in the scrotum

Indirect inguinal hernias pass through the internal ring, along the inguinal canal and then emerge
through the external ring, descending into the scrotum. These are more common.
- Indirect hernias reduce upwards, laterally and backwards. After reduction, the hernia can be
controlled by pressure over the internal ring (1-2cm above the femoral pulse)
- If the internal ring is narrow, the hernia will be slow to appear and reduce, these are prone
to strangulation
Direct inguinal hernias push through the posterior wall of the inguinal canal in Hasselbach’s triangle
(between the rectus, inguinal ligament, and inferior epigastric artery), medial to the internal ring.
- These hernias will not pass into the scrotum and are always acquired. These are less likely to
strangulate
- Direct hernias reduce upwards and straight backwards. They are not controlled by pressure
over the internal ring
In physical examination the two types of hernia can usually be distinguished
- The hernia should be reduced and the patient asked to cough while the physician covers the
superficial inguinal ring, if there is a direct inguinal hernia it will protrude
Management
Management can be conservative; this is usually recommended in adults with small hernias.
Conservative advice includes weight loss and truss belts. Where the hernia is larger, recurrent, or in
a child, surgery may be indicated
- Herniotomy is removal of the hernia sac, and closure of the neck

- Herniorrhaphy restores the disturbed anatomy, increases the strength of the abdominal
wall, and constructs a barrier to resistance
There are two main laparoscopic surgical techniques to repair hernias, both use the Lichtenstein
technique using a mesh that becomes embedded with fibrous tissue and seals up the defect
- Totally extraperitoneal (TEP) seals the hernia outside the peritoneum, and the peritoneal
cavity is not entered
- Transabdo pre-peritoneal (TAPP) seals the hernia inside the peritoneum
Complications of hernia repair include urinary retention, scrotal haematoma, damage to the inguinal
nerve, ischaemic orchitis, and recurrence.
Gallstones
The gallbladder lies in the fossa for the gallbladder, on the posterior surface of the liver
- It is formed as a small part of the hepatic diverticulum in embryological development

The gallbladder has three parts
- The fundus is the wide blunt end that projects from the inferior border of the liver at the 9th
intercostal space
- The body is the main portion, it is in contact with the liver, transverse colon and duodenum
- The neck is end that joins into the cystic duct, this region has an outpouching known as the
Hartmann’s pouch where stones tend to collect
In cholecystectomy the cystic duct and cystic artery must be cut; there is no one cystic vein but
many small veins that drain to the HPV. The cystic artery is a branch of the right hepatic artery (from
the hepatic from the coeliac trunk). These structures must identified at the Calot’s triangle
(cholecystohepatic triangle), this can be difficult if it is inflamed
- Calot’s triangle is bordered by the common hepatic and cystic ducts and the cystic artery
The liver produces around 500ml – 1 litre of bile each day, this is not made at a continuous rate but
increased in response the fat in the duodenum stimulating CCK release. Some of this bile will pass
directly into the duodenum, however a lot will pass into the gallbladder for storage and
concentration
- The gallbladder can store around 50ml of bile at a time until stimulated by CCK and secretin
- The bile within the gallbladder consists of bile salts, conjugated bilirubin and water
The biliary tree is summarised in the diagram below. The common bile duct has a normal diameter
of 5mm.
Pathology
There are three main types of gallstones; cholesterol (80%), pigment (10%), and mixed (10%).
Cholesterol stones are typically larger and lighter than pigment stones
- Risk factors for stone formation include female, obese/overweight, middle aged (>40),
family history, ileal disease, diabetes and risk of complications increases with parity and
smoking
Most gallstones are asymptomatic, and can form in the gallbladder or biliary tree.
Complications
The complications of gallstones are dependent on where the gallstones lie within the biliary tree
Within the gallbladder
Biliary colic will cause a sudden onset of right upper quadrant colicky pain, which may radiate to the
shoulder blades. Typically the pain felt occurs after eating fatty food and generally passes after 4-5
hours; this may be associated with nausea and vomiting but not with fever
- There is no inflammation, and LFTs will be normal

Acute cholecystitis occurs where there has been an impaction of a gallstone within the Hartmann’s
pouch. This causes an accumulation of bile and build-up of pressure within the gallbladder
(increasing the chance of infection due to lack of irrigation). The patient will present with a gradual
onset of right upper quadrant pain, which will be continuous and severe
- Treatment is with broad spectrum antibiotics, pain relief, and cholecystectomy if the patient
presents within 72 hours of symptom onset (if not within 72 hours, should be elective after 6
weeks)
- The patient will be Murphy’s sign positive (stops inspiring when your hand is at the right
costal margin due to pain, keeps inspiring if hand is in the same position on the left). They
will have raised inflammatory markers and normal LFTs
Chronic cholecystitis has the same features and symptoms, however they develop slower over a
period of time. This is due to low level inflammation and irritation from the stones, causing fibrosis
over time
- Symptoms of acute and chronic cholecystitis include fever and constant tenderness in the
right upper quadrant (occasionally with referred shoulder pain)
Gallbladder empyema is a complication of cholecystitis, and is managed similarly. It may be possible
to have radiological drainage of the pus within the gallbladder for symptom relief.
Gallstone ileus occurs when a dislodged gallstone obstructs the small bowel (usually at the ileo-
caecal junction) this is due to the formation of a fistula between the gallbladder and duodenum
- Rigler’s triad will be present on imaging: small bowel obstruction, RIF opacity, and
pneumobilia
- Treatment is to remove the intestinal obstruction, but leave the gallbladder and fistula in
situ
There may be adenocarcinoma of the gallbladder (cholangiocarcinoma) if there are long-standing
gallstones leading to fibrosis and inflammation. CA 19-9 is a marker for this.
Within the common bile duct (Choledocholithiasis)
Obstructive jaundice occurs when a stone in the gallbladder is dislodged, and obstructs the biliary
tree at the level of the common bile duct or below. This is because bile contains conjugated bilirubin,
which backs up through the biliary tree and enters the blood stream
- This will present as biliary colic with jaundice (yellow skin, itching, dark urine, pale stools)
- There will be raised conjugated bilirubin, ALP and γ-GT. USS will reveal a dilated common
bile duct
- Treatment is with ERCP and later cholecystectomy
Cholangitis is obstructive jaundice with inflammation, typically due infection of the common bile
duct, this is due to a loss of normal bile irrigation. It presents similarly to acute cholecystitis with
jaundice
- Cholangitis is diagnosed through Charcot’s triad: fever/rigors, right upper quadrant pain, and
jaundice
- There will be raised conjugated WCC, CRP, bilirubin, ALP and γ-GT. USS will reveal a dilated
common bile duct
- Management is IV antibiotics (cefuroxime/ metronidazole), followed by ERCP and
sphincterotomy to remove the gallstone and cholecystectomy later
Biliary stricture can follow inflammation and fibrosis of the bile ducts due to the presence of a
gallstone
Within the pancreatic duct
Pancreatitis occurs when a gallstone is dislodged from the gallbladder and becomes lodged in the
pancreatic duct. This means that there can be no drainage of pancreatic juice and the enzymes it
contains
- Management is as for any cause of acute pancreatitis, followed by later cholecystectomy

Investigations
The first specialist investigation that is performed when symptoms of biliary colic or cholecystitis are
determined is ultrasound of the gallbladder and biliary tree
- Gallstones are visible on USS, and it will demonstrate any dilation of the biliary tree from
obstruction
MRCP can follow this (MRI imaging of the biliary tree) if there is diagnostic uncertainty.
Management
ERCP can be used to diagnose and treat gallstones that are impacted in the biliary tree through
sphincterotomy and stenting allowing the stones to pass
- Cholecystectomy should follow this after several weeks to prevent recurrence

Surgical management is recommended in symptomatic gallstone disease
- Early cholecystectomy is only used in emergency situations, this is usually open

- Laparoscopic cholecystectomy as an elective day-case procedure is the preferred treatment
- If surgery is contraindicated there can be medical dissolution of cholesterol stones using
MTBE (direct infusion to the gallbladder) or ursodeoxycholic acid (oral)
Acute Pancreatitis
Acute pancreatitis is a self-limiting inflammation of the pancreas, leading to SIRS
- This occurs due to the release and activation of digestive enzymes within the
pancreas, causing auto-digestion
Severe acute pancreatitis is associated with organ failure and/or pancreatic complications
Presentation
A typical history will describe a sudden onset of constant, sharp epigastric pain radiating to the back.
There is typically vomiting alongside this
- Past medical history and social history are key regarding known gallstones and
alcohol intake
On examination there may be several signs
- Basic observations can show fever, tachycardia, tachypnoea, hypotension (due to

SIRS)
- Upper abdominal tenderness, with or without guarding
- There may be paralytic ileus and absent bowel sounds
- Grey-Turner’s and Cullen’s sign may be present if there is haemorrhage
Investigations
Where there is suspected pancreatitis, several investigations should be carried out

- FBC, U&Es, glucose, CRP, LFTs, amylase/lipase, clotting, bone profile, and LDH. These
are largely to see baseline values to judge whether treatment will be tolerated, as
well as to risk stratify the pancreatitis
- USS should be used to check for gallstones. Where there are known gallstones, and
cholecystitis or obstruction suspected, ERCP should be used – ERCP runs the risk of
worsening the pancreatitis, so should only be used in this circumstance
- Erect CXR to rule out viscus perforation
- ABG
Amylase is the most widely used biochemical test to diagnose pancreatitis. The main issue with
amylase is that it is non-specific and can be raised in peptic ulcer disease, DKA, and renal failure
- In pancreatitis it will peak at around 18 hours of onset, and is diagnostic at >3x the
upper limit of normal (reference range 50 – 120, in pancreatitis it will be >360)
- Where patients present late, amylase may have normalised. Usually amylase will
normalise after 36 hours of symptom onset
Lipase is the alternative test to amylase, and is much more sensitive and specific. The issue with
lipase is that it is not widely available
Risk stratification is essential in pancreatitis as it determines what treatment options should be used.
The main tool used for this is the Glasgow score (remember the anagram PANCREAS), each factor
below is worth one point
- PaO2 < 8kPa

- Age > 55
- (Neutrophils) WWC > 15
- Calcium < 2
- (Renal) Urea > 16
- (Enzymes) ALT > 200, LDH > 600
- Albumin < 30
- (Sugar) Glucose > 10
Mild pancreatitis = 0 – 1. Moderate pancreatitis = 2. Severe pancreatitis >3
If there is diagnostic uncertainty, CT scanning is used.
Management
Management should first cover ABC principles as the patient is acutely ill. Risk stratification and
investigations should follow. Treatment is largely supportive
- Give analgesics, usually morphine and an anti-emetic

- IV crystalloid fluids, 2L in 2 hours. It is essential to perform input output fluid
monitoring (it may be necessary to catheterise) and maintain fluid balance
- Give oxygen
- Enteral nutrition is used where possible, but in severe disease TPN may be needed
- If the aetiology is alcohol, it may be important to commence alcohol detox and

provide chlordiazepoxide and prabrinex
- Antibiotics (meropenem) should only be used in cholecystitis and severe pancreatitis
Complications in acute pancreatitis are relatively common, and can be very severe (death is a
complication at all stages). Usually conservative management of complications is used, but in some
cases surgery can be indicated e.g. necrosis or infection
Immediate 5 – 7 Days Delayed

Hypoglycaemia Acute haemorrhage (nb. Grey- Pseudocyst
Turner and Cullen signs)
Hypocalcaemia Pancreatic necrosis Chronic pancreatitis
AKI Pseudocyst Diabetes mellitus
ARDS Pancreatic abscess
Sepsis
VTE
Dyspepsia and Peptic Ulcer Disease
Dyspepsia describes pain or discomfort in the upper abdomen, excluding those with GORD and IBS.
Peptic ulceration is the term applied to both gastric and duodenal ulcers
- Gastric ulcers are more likely in women, and duodenal ulcers more common overall and in
men
There are many potential causes of peptic ulceration
- H.pylori infection is the commonest cause of peptic ulcers, particularly duodenal ulcers
- Medications e.g. NSAIDs, steroids, SSRIs
- Smoking and alcohol
- Stress
- Zollinger-Ellinson syndrome (gastrinoma)
Presentation
Dyspepsia commonly presents with epigastric discomfort, fullness or bloating, flatulence, nausea
and intolerance of fatty foods
- It is diagnosed where symptoms have been present for at least 12 weeks in the last year
Symptoms of peptic ulceration are non-specific, and often cannot distinguish between gastric and
duodenal ulceration
- Epigastric pain, and often epigastric tenderness on palpation

o With duodenal ulcers this is usually 1 – 3 hours postprandial, worst at night and
alleviated by food
o With gastric ulcers pain occurs soon after meals, is not relieved by eating, and is
often associated with weight loss
Investigations
Perform routine blood tests, particularly looking at the FBC for anaemia
Endoscopy should only be performed if there are any red flags for upper GI cancer (iron deficiency
anaemia, if the patient is over 55, dysphagia, UGIB, weight loss) this is largely to rule out malignancy
through biopsy of ulcers
- Follow-up endoscopy where there is no malignancy is common after two months’ therapy to
ensure ulcers have healed
Testing for H.pylori is important in all patients that have not improved following 4 weeks of
conservative management
- Carbon-13 urea breath test is the most reliable test but stool antigen testing can also be
used. Patients swallow urea labelled with the isotope carbon-13, their breath is then
analysed in the following 30 minutes for isotope labelled carbon dioxide
o A positive test indicates that the labelled urea has been split by urease (an enzyme
produced by H.pylori) in the stomach to release labelled CO2
o The patient needs to be off PPI treatment for at least 2 weeks prior to the test
- Confirmation of H.pylori eradication is usually with urea breath test 6 weeks after
completion of eradication therapy
Management
Review medications for potential causes e.g. NSAIDS, steroids, or bisphosphonates; stop the
medication and prescribe 8 weeks of PPI therapy.
Lifestyle advice such as reducing stress, smoking cessation, regular meals with smaller portion size,
and decreasing alcohol consumption can reduce symptoms
- Patients can be advised to try over the counter antacids

Where patients are H.pylori negative, there can be the following
- Full dose PPI can be prescribed for 4 – 8 weeks

- If this is ineffective H2 antagonists (ranitidine) can be trialled for the same amount of time
Where H.pylori is present it should be eradicated to prevent future development of atrophic
gastritis, gastric adenocarcinoma and gastric lymphoma
- Eradication of H.pylori is with PPI triple therapy for 7 days (1g amoxicillin BD/ 500mg
clarithromycin BD, 500mg metronidazole BD, and lansoprazole 30mg BD)
Surgery is used very rarely due to the wide availability of medications
- In bleeding ulcers, perforated ulcers, and gastric outlet obstruction there can be
gastrectomy
- Ulceration that is refractory to medical management can be treated with patching and
highly selective vagotomy
Complications
Complications of peptic ulceration can be life-threatening
- Haemorrhage
- Perforation
- Penetration, this can lead to fistula formation with the biliary tree or penetration of the left
liver lobe
- Obstruction
Where a patient experiences perforation of a peptic ulcer, there will be acute epigastric pain
progressing to peritonitis and generalised rigidity
- Examination will show that the patient may be in shock, and will have a generalised
peritonitis
- Paralytic ileus will also occur, causing a silent abdomen
- There is usually associated vomiting
Renal Colic
There are several risk factors that can predispose a patient to urinary tract calculi
- Anatomical anomalies in the kidneys and/or urinary tract

- Previous calculi or family history of calculi
- Hypercalcaemia
- Hyperuricaemia (CKD/gout)
- Dehydration
- Inherited conditions such as homocysteinuria
The composition of renal stones varies; most are calcium based (either calcium oxalate or calcium
pyrophosphate), other forms include urate, cysteine (familial), infection stones and struvite
- Formation of stones occurs due to increased concentration of precipitant factors, therefore

increased load or decreased solute will predispose to precipitation or crystallisation
Presentation
Stones are commonest in males in their early to middle adulthood. Most patients with renal stones
will present with ureteric colic
- This typically sudden onset unilateral sharp colicky pain, migrating from loin to groin with
potential radiation into the genitalia
- There may be associated rigors and fever, vomiting, macroscopic or microscopic haematuria
on urine dip, and long-standing aching pain at the renal angle
Many stones are asymptomatic and discovered incidentally
On examination there is usually no significant finding, but patients may have tenderness in the
affected iliac fossa or renal angle
Investigations
Urinalysis should include
- Dipsticking for RBCs, WBCs and nitrates, and pH

- MSU for MC&S
Blood tests should include
- FBC, CRP, ESR can check for signs of infection

- U&Es can show normal/decreased GFR and increased creatinine
- Group and save and clotting screen are essential, as patients with renal colic may be surgical
Imaging studies can include
- USS to detect evidence of obstruction

- Non-enhanced CT scanning (CT KUB) is the imaging modality of choice
- Plain abdominal x-rays can be used to watch the passage of radio-opaque stones
Stone analysis is recommended for patients on their first presentation. This may require the patient
to catch a stone for analysis by urinating through a tea strainer or filter paper
Management
Management of patients with renal colic is dependent on their clinical status
- Initially, there should always be ABC stabilisation, prompt analgesia (with opioids or strong
NSAIDs), and rehydration
If the patient is stable and there are no significant changes in the blood results they can be
discharged with pain management and anti-emetics, and followed up as an outpatient in urology. An
exception to this is patients in which pain/vomiting is intractable, these patients should be admitted
for pain management
- The majority of stones will pass in 3 – 4 weeks. Symptomatic patients or those that have not
passed the stone in 4 weeks should be monitored with CT KUB weekly to check the progress
of the stone
- Medical expulsive therapy can be used to facilitate the passage of the stone e.g. nifedipine,
tamsulosin
If the stone does not pass spontaneously, the surgical management depends on where the stone
impacts
- If there are bladder stones (formed within the bladder) treatment is cystoscopy and stone
extraction
- If the stones are in the ureter (most likely at the PUJ, PVJ, or where the ureters cross the
pelvic brim) there can be ureteroscopy ± stone extraction ± JJ stent placement ± laser
lithotripsy
- If the stone is in the kidney there are several treatment options
o Percutaneous nephrolithotomy (PCNL), this is common for staghorn calculi
o Open nephrolithotomy
- If the stone is 1 – 1.5cm there can be extracorporeal shockwave lithotripsy (ESWL)
Complications
If the patient shows any signs of sepsis, the sepsis 6 pathway must be followed and the patient
admitted
- There should be urgent CT KUB and then decompression of the kidney with percutaneous
nephrostomy
- Definitive management will follow this after a few weeks
If the patient has obstructive uropathy and AKI, there needs to be urgent CT KUB. Emergency
ureteroscopy and stent placement should follow this
Urgent referral should also be made where there are bilateral obstructive stones, or where the
patient only has one kidney
Urinary Tract Infections (UTI)
UTI is the inflammatory response to bacterial infection of the urinary tract, most bacteria cause
infection by ascending up the urethra (more likely to ascend up to the kidneys where the organism
has P pili), but can also cause infection by haematogenous spread or infection via lymphatics. UTI
can be diagnosed in the following situations
- >105 bacteria/mL of MSU specimen in asymptomatic patients

- >102 bacteria/mL of MSU specimen in symptomatic patients
Most UTIs are caused by faecal-derived bacteria that are facultative anaerobes; the majority are
caused by E.coli, S.saprophyticus, and P.mirabilis
- Less common organisms are more likely to cause infections in the immunosuppressed or
catheterised
o Klebsiella, P.vulgaris, Candida albicans, pseudomonas
The inflammatory response to bacteriuria is indicated by pyuria
General risk factors for UTI include female gender, increasing age, pregnancy, diabetes, indwelling
catheters, voiding dysfunction, and genitourinary tract malformation
Atypical UTI is one that occurs with poor urine flow, bladder mass, raised creatinine, septicaemia,
failure to respond to suitable antibiotic treatment within 48 hours, and infection with non E-coli
organisms
Recurrent UTI is defined as >2 episodes of UTI with pyelonephritis, or >3 episodes of cystitis in a year
(>2 within 6 months)
Presentation
Cystitis presents with classical UTI symptoms
- Frequent small volume voids with urgency, urine can be offensive and cloudy
- Suprapubic pain
- Dysuria ± haematuria
Pyelonephritis may develop following this, presenting with fever, rigors, malaise, and loin pain.
Patients with pyelonephritis may develop SIRS
- Temperature >38 or <36

- Heart rate >90
- Respiratory rate >20 or PaCO2 <4.3 kPa
- WBC >12 or <4
A complicated UTI is one occurring in the presence of underlying anatomical or functional

abnormality, this is more common in men. Complicated UTIs usually take longer to respond to
antibiotics, and are more likely to recur
Investigations
Urine dipsticking is first line

- UTI will be positive for nitrites and/or leukocytes, and may also show microscopic
haematuria
- Nitrite positivity is more sensitive than leukocyte positivity
There should also be MSU in all patients other than symptomatic non-pregnant women where there
is no suspicion of pyelonephritis
Where the patient presents with symptoms of pyelonephritis, there should be the following
additional investigations
- Bloods should include FBC, CRP/ESR, U&Es, and blood cultures

- Imaging may be useful; this is usually with CT KUB and renal USS to look for infection stones
in the kidney and perinephric abscess
Where UTI is recurrent there can be further investigation with USS of the full and empty bladder to
look for scars and VUJ reflux and CT KUB to check for stones
Management
Acute, uncomplicated cystitis is managed with oral antibiotics
- Nitrofurantoin for 50mg QDS for 3/7

- Alternatives include trimethoprim (200mg BD for 3/7), and co-trimoxazole
Uncomplicated pyelonephritis where patients are systemically well is usually managed with oral
antibiotics in the outpatient setting, these should be started as an empirical treatment while
awaiting the results of MC&S
- Ciprofloxacin 500mg BD for 1/52 is first line
Where patients are systemically unwell there should be resuscitation with crystalloid fluids,
adequate analgesia, and IV antibiotics
- IV aminopenicillin ± aminoglycoside (gentamycin) or IV cephalosporins
Surgery may be required to treat obstruction by infection stones or to drain perinephric abscess/
pyelonephritis. These complications are suggested by lack of response to IV antibiotics, and can be
confirmed on CT KUB
Childhood UTI
UTI is more difficult to diagnose in children due to non-specific symptoms, and difficulty in obtaining
urine samples (adhesive plastic bags applied to perineum, clean catch of urine into a pot,
catheterisation)
UTI in children is important as many patients will have a structural abnormality of the urinary tract.
Potential urinary tract abnormalities leading to recurrent UTI include
- Vesicoureteric reflux, due to anatomical abnormalities of the VUJs meaning that urine
refluxes during micturition. This can be very severe, leading to dilatation of the renal pelvis
and calyces, causing renal scarring
- Incomplete bladder emptying due to dysfunctional voiding
- Obstruction
Children <6 months with a typical UTI should have USS within 6 weeks, but not during the acute
infection. Further investigation is indicated in children with atypical or recurrent UTIs.
- USS during the acute infection

- Micturating cystourethrogram (MCUG) to assess for reflux if the child is <6 months
- DMSA radionuclide scan of the kidneys to assess for scarring
- MAG3 scanning can also be undertaken to assess for obstruction, but is not routine
Scarring risk is increased in certain cases
- Obstruction
- Reflux with dilation
- Young age with UTI
- Delay in treatment
- Number of episodes of pyelonephritis
- Unusual (non-E.coli) bacteria
Aneurysm
An aneurysm is an abnormal localised dilation of a vessel of over 50% of the normal diameter,
involving all three vessel layers
- Up to 50% of normal is known as ectasia

- Where <3 of the vessel layers are involved, it is a pseudo-aneurysm and less likely to rupture
There are two types of aneurysm, summarised in the pictures below
Fusiform aneurysms are much more common. Sacular aneurysm is usually in younger people, and
associated with infection (aortitis leads to weakening)
Risk factors for aneurysm include hypertension, family history, smoking, increasing age, male
gender, and connective tissue disorders (Ehler’s Danlos and Marfans)
- Aneurysm occurs due to a loss of collagen and elasticity in the vessel wall, as the vessel is
weakened, over time the effects of the pressure of blood will dilate the wall. There is
typically associated blockage of the vasa vasora
One of the commonest aneurysms is the AAA (abdominal aortic aneurysm), as the normal aortic
diameter is 2cm, therefore an aneurysm is anything 3cm or above
- These typically arise at the level below the renal arteries

Presentation
Typically, AAA is asymptomatic, however it can cause retroperitoneal pain (radiating to the back,
loin, or groin). Patients will usually present where there has been a complication of the AAA
Complications include rupture, leak, embolization, and direct pressure effects
- Rupture is where the vessel bursts anteriorly, there is no compression to blood loss and the
patient is likely not to survive
- Leak is where the vessel bursts posteriorly, as there is some compression from the vertebral
column there is more time to intervene
- Embolization causes femoral artery thrash and acute limb ischaemia
- Direct pressure effects include compression of the duodenum, ureters, or IVC.
The aneurysm may be palpable as an expansile, pulsatile mass above the umbilicus (T12 – L2/3).
There may be an associated abdominal bruit
Investigations
There is a screening program for AAA, where males >55 can elect to have an abdominal ultrasound
- Where AAA is detected, management depends on size and rate of growth

- <5.5cm will have annual or 3 monthly USS to monitor growth. Typically, an
aneurysm will grow by <0.5cm per year
- >5.5cm in men, >5cm in women, or growth >0.5cm/yr will have elective surgery.
This is because the risk of rupture outweighs the risk of surgery
Patients should have routine bloods, ECG and CXR to detect associated co-morbidities and to look at
suitability for surgery
USS, CT, and MRI angiography can all be used to characterise the aneurysm. Gold standard imaging
is with CT angiography.
Management
Elective AAA repair is usually with EVAR, but it can be open
- Open repair involves a midline laparotomy, and movement of the intact peritoneum to the
side to expose the aorta. The aneurysm sac is then opened, and a graft is inserted and
stitched in place
- With open repair there is a significant risk of AKI and bowel ischaemia
- Endovascular repair is more common, and involves the placement of multiple stents
(forming a trouser graft) from both femoral arteries
- One issue with this is endoleak; the leakage of blood from the aorta into the
aneurysm sac around the stents. This blood can leak from the join points of the
stents, or from the lumbar arteries/ inferior mesenteric
- EVAR cannot be used where the aneurysm is within 1.2cm of the renal arteries
Where patients have aneurysms too small for surgery, the focus should be in reducing risk factors –
particularly blood pressure control
Ruptured AAA
In rupture, there will be a severe sudden onset retroperitoneal pain
- Pain can be intermittent or continuous

- Shock and collapse will occur soon after pain in many cases
- Grey-Turner’s (haematoma around flanks) and Cullen’s (haematoma around umbilicus) signs
may be present
75% of patients will die (50% outside of hospital, 25% in theatre)
Perform an urgent cross-match of at least 4 units, and activate the major haemorrhage protocol to
give O- blood, whilst arranging surgery. When wide-bore IV access is secured, take routine samples
in addition to cross-match
- If IV access cannot be secured, use intra-osseous or saphenous cut-down to give fluid

- Investigation should never delay treatment, and is usually with portable USS
- If the patient is stable enough there can be CT scanning
Catheterise the patient, and give O- blood. Urgent surgical repair is essential, and usually open repair
is used
- Aim to keep SBP<100 and MAP>80

Chest Pain
When a patient presents with chest pain it is essential to give an urgent assessment, so that life
threatening causes of the symptoms can either be excluded or promptly treated
A to E assessment should be the first step in care. It is essential to ensure haemodynamic stability
- Blood pressure should be taken from both arms, and there should be comparison of
peripheral-to-peripheral and peripheral-to-central pulses
- When IV access is established, the following bloods should be taken
o FBC, U&Es, LFTs, CRP, amylase, coagulation screen, cardiac enzymes, group & save
(or crossmatch where appropriate)
- 12 lead ECG should be performed, and continuous cardiac monitoring established
- When the patient is adequately stabilised, there should be brief history and focussed
examination
History
Clarify further details about the pain using the SOCRATES framework
- The character of the pain can give an indication as to its cause

o Somatic chest pain (pericardium, pleura, chest wall) is sharp and localised
o Visceral chest pain is dull, aching, or heavy in nature
- Specific associated symptoms to ask about include
o Dyspnoea
o Cough and haemoptysis
o Nausea and vomiting
o Sweating
o Palpitations, dizziness, and syncope
- Exacerbating and alleviating factors to ask about include
o Exercise or rest
o Eating
o Breathing
o Medications such as GTN spray
- Ask if they have experienced the pain before the current episode
In the social and family history it is important to clarify if the patient has any cardiovascular risk
factors
- First-degree male relative with MI <55, or female relative with MI <65

- Smoking, exercise, diet, diabetes, hypertension, hyperlipidaemia
Examination
Focussed examination should be of the respiratory, cardiovascular and abdominal systems
Inspection
- Patient looking grey, clammy, and unwell indicates ACS

- Patient looking dyspnoeic and cyanosed points more towards a respiratory cause
Palpation
- Check for epigastric tenderness

- Assess for chest expansion, if reduced unilaterally think respiratory cause
- Check for chest wall tenderness, more of an indication of MSK pain
Percussion
- Assess for hyper-resonant or dull percussion, indicating respiratory cause
Auscultation
- Gallop rhythm indicates heart failure, which may be precipitated by ACS

- Reduced air entry
- Consolidation
Chest pain could potentially be cardiac, vascular, musculoskeletal, respiratory, or gastrointestinal
In terms of cardiac chest pain
- There could be ACS

- Pericarditis; this would be pleuritic chest pain worse on lying down. ECG changes include
saddle ST elevation and PR depression, on examination there may be pericardial rub
- Stable angina; the pain here would not be sustained and it would be relieved by GTN
- Others include arrhythmia, myocarditis, aortic stenosis, and HCM
A vascular cause could be aortic dissection; this would be sudden onset and radiate to the back.
There would also be radio-radial delay and unequal blood pressure, CXR may show mediastinal
widening
Musculoskeletal causes would typically have a defined traumatic onset, or have come on very
suddenly during activity. There would be no abnormality of investigation. The pain would most likely
be exacerbated with movement and relieved in certain positions
- Specific musculoskeletal causes include costochondritis (Tietze’s syndrome), and trauma and
rib fracture
Respiratory causes include
- PE, the pain here would be more pleuritic in nature and there may be history of
immobilisation or DVT risk factors. It would be important to Well’s score if this was
suspected
- Pneumonia this would be pleuritic chest pain coupled with shortness of breath and cough
with purulent sputum, there may also be fever
- Pneumothorax would present with sudden pleuritic chest pain and shortness of breath
Gastrointestinal causes could be GORD or oesophageal spasm
- GORD would be more of a burning pain, related to meals and positioning

- Oesophageal spasm is difficult to differentiate from angina as it is relieved by GTN

- Others include oesophageal rupture, and referred pain from upper GI pathology e.g.
cholecystitis, pancreatitis, peptic ulcer disease
Other causes include panic disorder and shingles.
Investigations
Further investigations following A to E assessment can include
- Serial cardiac enzymes (troponin I or T)

- D-dimer
- Serial 12 lead ECG
- CXR
Acute Coronary Syndrome (ACS)
ACS is a term used to describe symptoms that result from acute myocardial ischaemia, usually due
to rupture of atheromatous plaques. An ACS resulting in myocardial injury is termed myocardial
infarction (MI). There are three main forms of ACS
- ST segment elevation MI (STEMI). This is usually caused by a totally occlusive thrombin rich
clot, causing transmyocardial ischaemia and necrosis
- Non-ST segment elevation MI (NSTEMI). This is usually caused by a non-occlusive lesion
- Unstable angina (UA). This is usually caused by a non-occlusive platelet rich lesion
Presentation
Typical symptoms in ACS include
- Retrosternal chest pain (or epigastric pain), characteristically described as a central crushing
sensation with radiation to the jaw and left arm. Onset is usually at rest
- Associated symptoms of shortness of breath, sweating, nausea, and palpitations also occur
On examination the patient may have a dyskinetic apex beat, and may have a third and fourth heart
sound
Investigations
12 lead ECG should be performed as soon as possible (within 10 minutes), this will distinguish STEMI
from other forms of ACS
- STEMI ECG changes include

o Within seconds there will be enlargement of T waves
o Within minutes there will be ST segment elevation. Criteria for thrombolysis are
>2mm ST elevation in adjacent chest leads, or >1mm in adjacent limb leads, or new
LBBB
o Pathological Q waves, loss of R wave progression, and T wave inversion occur
following myocardial necrosis, and are long term ECG changes not seen acutely
- ECG changes in other forms of ACS can include
o ST segment depression
o T wave inversion
Artery Affected ECG Change

Anterior MI LAD V1, V2, V3, V4 ST elevation. Reciprocal ST depression in III
and aVF
Lateral MI Circumflex I, aVL, V5, V6 ST elevation. Reciprocal ST depression in III
and aVF
Inferior MI Right Coronary II, III, and aVF ST elevation. Reciprocal ST depression in I and
aVL
Posterior MI Right Coronary V1, V2, V3: ST depression, tall + wide R wave, and high T
wave in V2
It is important to note that ST elevation can also be caused by other factors
- Pericarditis, myocarditis
- Hyperkalaemia
- Brugada syndrome
- Massive PE
- Aortic dissection
- lV aneurysm
- Subarachnoid haemorrhage
- Early repolarisation/ normal variant
- FBC as there may be anaemia and as baseline in view of anticoagulant use

- U&Es as a baseline for renal function given the possible use of IV contrast
- CRP to indicate underlying infection
- LFTs and clotting profile as there may be vascular intervention and bleeding risk
- Troponin T and Troponin I
o The upper limit of normal for troponin is <25ng/L, MI is indicated as anything this
o If it is not elevated >1000 (convincing as MI) there should be serial measurement,
with >20% change positive for MI. If there is no >20% change after 6 hours then
potentially the diagnosis of MI is not appropriate
Cardiac markers are released into the bloodstream following myocardial necrosis
- Cytosolic enzymes include creatine kinase (CK), aspartate aminotransferase (AST), and
lactate dehydrogenase (LDH)
o These are only raised for a short time following MI, and can therefore be a good
indication of a re-infarct where troponins remain raised
- Structural proteins include troponin T and troponin I (part of the actin-myosin crossbridge)
o Troponins are raised in the serum for several days (~14) following MI
o Troponins are not specific and can be raised in arrhythmia, heart failure, pericarditis,
myocarditis, cardiomyopathy, following heart surgery or chest trauma, sepsis, right
heart strain from pulmonary disease, and end stage renal disease
There should be CXR to rule out alternative diagnoses.
Initial ACS Management
All patients with suspected ACS should be placed in resus, and given 300mg aspirin to chew and one
other antiplatelet drug e.g. 60mg prasugrel/ticagrelor in STEMI or 600mg clopidogrel in NSTEMI
- There should be contraindication of any IM injections

IV access should be secured as soon as possible, and medications should be administered
- Oxygen, only if the patient has a low SpO2

- Diamorphine 2.5 – 10mg IV PRN for pain relief
- Metoclopramide 10mg IV for nausea
- GTN spray (this is typically not effective in STEMI)
If the patient degenerates to VF at any point there should be immediate defibrillation
In STEMI, the patient should be on serial BP, ECG, and SpO2 monitoring and be transferred to a
rescuss setting. Defibrillation pads should be attached as a precaution and IV access gained as soon
as possible (ideally with a pink or green cannula)
- The cath lab team should be contacted as soon as possible. This includes an interventional
cardiologist, radiographer, and cardiac physiologist
STEMI Management
Patients experiencing STEMI must undergo reperfusion therapy on presentation with the aim of re-
opening any blocked vessels to re-perfuse the myocardium before there is necrosis
- Re-perfusion is a time dependent benefit, and patients need to be treated as quickly as

possible
The mainstay of treatment for STEMI is primary PCI. There should be immediate transfer of any
patient with ST segment elevation to the cath lab
- Primary PCI should ideally be within 90 minutes (door to balloon time 90 minutes) but
should be given up to 12 hours of symptom onset. The pPCI team should be notified as soon
as the ECG is reviewed
- In primary PCI access is via the femoral, radial, or brachial artery. Under fluoroscopy a guide
wire is passed into the coronary artery and across the stenosis, the balloon is then inflated
over it leaving the stent (usually a drug-eluting stent) in place. Thrombectomy prior to stent
insertion is no longer universal
Anti-thrombotic drugs are given alongside PCI in STEMI
- Pre-PCI there is usually dual anti-platelet therapy e.g. aspirin and

clopidogrel/prasugrel/ticagrelor
- During PCI there is an additional anticoagulant given e.g. heparin/fondapurinox and/or
bivalirudin
- If there are problems during angioplasty, GP2a/3b inhibitors are used
In the acute phase, if PCI fails, there can be CABG
If PCI is not available within 2 hours of presentation there should be immediate thrombolysis
- tPA is used e.g. streptokinase or alteplase

- There should then be transfer to a PCI centre for possible rescue PCI following this
NSTEMI and Unstable Angina Management
All patients with UA and NSTEMI should receive dual anti-platelet therapy. This is usually with aspirin
and clopidogrel
There should then be risk stratification of death within 6 months using GRACE scoring. The GRACE
score combines features of the patient’s status prior to the ACS event as well as the ACS event itself
- Age, heart rate, blood pressure, peripheral vascular disease, creatinine, cardiac arrest, ST
deviation, elevated serum cardiac marker, signs of CCF
Higher risk patients (>3% chance of death in 6 months) should receive full medical therapy, and then
be offered coronary angiography within 72 hours
- Following angiography there can be PCI or CABG

Low risk patients should be managed with conservative medical therapy and later ischaemia testing
e.g. stress ECG, myocardial perfusion scintigraphy
Complications of MI
Acutely there can be left ventricular failure, revascularisation is key in the management of this
complication
- Pulmonary oedema should be treated with high flow oxygen and IV loop diuretics,
diamorphine, and nitrates
- Cardiogenic shock should be managed with intensive monitoring, optimisation of filling
pressures and possible use of inotropes and vasodilators
- Arrhythmia is common in the acute phase following MI
A few days following MI there is necrosis of tissue, leading to weakening of the myocardium and
rupture
- Acute mitral regurgitation due to papillary muscle rupture

- Ventricular septal defect
- Cardiac tamponade
- Mural thrombosis and embolization
- Dressler’s pericarditis
- Ventricular aneurysm
In the long term, complications include mitral regurgitation and CCF
Assessment of LV function is essential for all patients before discharge, this is with
echocardiography. Where LV function is found to be impaired there should be further management
- Aldosterone antagonist e.g. spironolactone

- Warfarin if there is evidence of thrombus formation
- ICD
If there are no complications, patients can be discharged after 3 to 4 days following
echocardiography
Secondary Prevention
Lifestyle changes
- Cardiac rehabilitation programmes should be encouraged, starting around 1 month post

discharge and continuing for ~12 months. This involves structured exercise and education
about lifestyle
- A Mediterranean diet should be encouraged, and alcohol limited to 14 units per week
- Smoking cessation is essential
- Patients should not drive for 4 weeks. Unless there is successful angioplasty, in which case
the patient can drive after 1 week
Drug therapy should be with
- Beta blocker
- Ace inhibitor
- Aspirin
- Clopidogrel for 12 months (prasugrel and ticagrelor can also be used)
- Statin
Gastro-Oesophageal Reflux Disease (GORD)
GORD is the presence of prolonged or excessive reflux of stomach acid into the lower oesophagus
- The spectrum of disease ranges from endoscopy negative GORD (NERD) through to
oesophageal ulceration and stricture formation
Potential causes of GORD can include
- Increased intra-abdominal pressure e.g. obesity, pregnancy

- Inadequate gastro-oesophageal sphincter tone or anatomical abnormality e.g. oesophageal
dysmotility, hiatus hernia, previous treatment for achalasia
- Increased gastric pH, reflux of bile or pepsin
- Medications e.g. SSRIs, anti-cholinergics, NSAIDs, bisphosphonates
Longstanding GORD can lead to metaplasia of the lower oesophageal epithelium from stratified
squamous to columnar (Barrett’s oesophagus), and predispose to oesophageal adenocarcinoma
Presentation
Patients will usually complain of retrosternal discomfort and heartburn, this is a burning feeling that
rises from the stomach to towards the neck
- The pain is usually exacerbated by meals, lying down, bending over, and straining
There may be additional odynophagia (pain on swallowing) due to oesophagitis, hoarseness of voice,
and chronic cough
Investigations
Endoscopy is the gold-standard investigation in GORD, and enables grading of disease. This is
indicated in the following situations
- Symptoms >4 weeks or despite medical treatment

- Any red flags for upper GI cancer e.g. haematemesis, >55, dysphagia or odynophagia, weight
loss, anaemia
Findings on endoscopy include
- Grade 1: erosions on a single fold

- Grade 2: multiple erosions on multiple folds
- Grade 3: multiple circumferential erosions
- Grade 4: ulcer, stenosis, or oesophageal shortening
- Grade 5: Barrett’s epithelium
Further investigations can be used where endoscopy is normal
- Barium swallow can be indicated to show hiatus hernia

- Oesophageal pH monitoring and manometry can also be used
o Diagnosis of GORD is made where pH is <4 for more than 4% of the 24 hours
Management
Lifestyle advice is the first step in GORD management, this includes weight loss, smoking cessation,
reduction in alcohol intake, raising the head of the bed, eating smaller portions, and not eating
within 3 hours of going to bed
- Conservative treatment is generally not effective

Pharmacological treatment is used to lower or neutralise gastric acid
- OTC antacids act to neutralise gastric pH e.g. aluminium hydroxide and magnesium trisilicate
- Foaming agents (alginates)
- Histamine H2 receptor antagonists e.g. cimetidine and ranitidine
- Proton pump inhibitors e.g. omeprazole and lanzoprazole. These are the mainstay of
treatment and can be prescribed long term, a therapeutic trial of PPI can also be used in
diagnosis of GORD
Most patients with GORD will not require surgery, however in refractory cases surgery is indicated
- Endoscopic gastroplication
- Laparoscopic fundoplication is used in hiatus hernia
- Laparoscopic insertion of magnetic bead bands can also be used
Pneumothorax
Pneumothorax is air in the pleural space. There are two main forms of pneumothorax; tension and
spontaneous
Tension Pneumothorax
Tension pneumothorax is caused mainly by trauma, but can also occur after central venous catheter
insertion. A one-way valve forms in the chest wall, sucking in more air with every breath and not
releasing it. This raises pressure in the chest, displacing and compressing the mediastinum
- Movement of the mediastinum kinks the great vessels, decreasing venous return and cardiac
output
In tension pneumothorax the patient will be in acute respiratory distress
- Tachycardia, pulsus paradoxicus, hypotension (and other signs of shock) can occur
- Tracheal deviation and raised JVP are key features
This is a medical emergency that must be immediately treated
- Give high flow 100% oxygen

- Insert a wide-bore IV cannula into the pleural space in the 2nd ICS MCL
After there is relief of tension pneumothorax, there should be chest drain insertion immediately.
CXR should be obtained after the drain is in place.
Open Pneumothorax
An open pneumothorax occurs where there is a pneumothorax associated with a chest wall defect,
hence the pneumothorax communicates with the exterior
- The chest wall defect offers less resistance to flow than the trachea, therefore air
preferentially enters through the chest wall resulting in inadequate oxygenation and
ventilation
Cover the defect with a bandage taped on 3 sides to create a one-way valve. Definitive management
is with 100% oxygen and chest drain insertion
Spontaneous Pneumothorax
Spontaneous pneumothorax can be a primary spontaneous event, or be secondary to some other

pathology
Primary spontaneous pneumothorax is commonest in tall, thin, young males
- This can be associated with Marfans

- Features include aortopathy (mitral valve prolapse, dilattion with risk of
dissection/rupture), upward lens dislocation, aracnodactyly and pectus excavatum
- There is a ~40% recurrence rate with primary spontaneous pneumothorax, particularly if the
patient is a smoker
Secondary spontaneous pneumothorax is due to underlying lung disease e.g. COPD, CF, cancer,
pneumonia, TB, interstitial lung disease, or HIV
Symptoms in primary spontaneous pneumothorax tend to be more minimal than in secondary

spontaneous pneumothorax, but can include
- Sudden onset pleuritic chest pain

- Dyspnoea
Assessment
Patients should be assessed using an A to E approach
- Measure oxygen saturations and give oxygen as required

- Establish IV access and take routine blood tests
- FBC, U&Es, LFTs as baseline
- Clotting, as a chest drain may be required
- CRP to see if there is underlying infection
- ABG should be performed if oxygen saturations are low
On examination, the following signs may be present
- The affected side will have reduced expansion, and is hyper-resonant to percussion, with
reduce breath sounds and vocal resonance
Further Investigations
CXR is the most important imaging study
- USS and CT can be used where CXR is not diagnostic

- CXR enables estimation of pneumothorax size by measurement of interpleural difference at
the level of the hilum
- 1cm = 27%
- 2cm = 50%
- >2cm = Large
Management
In treatment, the size of the pneumothorax is not as important as the patient’s clinical picture and
differs between primary and secondary pneumothorax
For primary pneumothorax
- If it is <2cm, and the patient is not breathless they can be discharged and followed up as an
outpatient as the pneumothorax will naturally resolve at 2% every 24 hours
- If it is a primary pneumothorax, >2cm, and/or the patient is breathless they should have the
air aspirated and put on high flow oxygen
- High flow oxygen increases resorption rate, but be wary of absorption atelectasis
- Most of the alveolar space is usually nitrogen, therefore when it is replaced with
oxygen the oxygen can be absorbed into the blood – collapsing the alveolus
- If symptoms do not improve after aspiration, a chest drain is indicated
For secondary pneumothorax
- All patients should be admitted and put on high flow oxygen (unless oxygen sensitive)
- >1cm should be aspirated, and if there is no improvement there should be chest
drain insertion
- Chest drain is indicated first line if >2cm, >50 years old, or breathless
Any bilateral pneumothorax should be admitted
Treatment is at >2cm as here the risk of damage from needle insertion is less than the risk of
hypoxia
When aspirating air (thoracocentesis) this should be in the triangle of safety. Aspirate a maximum of
2.5L, or to the point of pain or resistance
- Aspiration of >2.5L can lead to re-expansion pulmonary oedema due to changes in capillary
endothelium in collapse
- The triangle of safety is between the latissimus dorsi, pectoralis major, and the 5 th
intercostal space
Chest drains (small bore <14F) should be inserted using the Seldinger technique. A bubbling chest
drain (when the patient coughs) indicates there is still air in the pleural space, a swinging fluid level
(when the patient breathes) indicates there is no blockage of the tube
- The Seldinger technique involves puncturing the cavity with a trocar (hollow needle) and
then feeding a guidewire through the trocar, withdrawing the trocar, and then passing a
cannula over the guidewire into the cavity, and then withdrawing the guidewire. The chest
drain has a three way tap, which should be closed at this point. The drain is sutured in place,
and its positioning is confirmed by imaging
- A bubbling chest drain should never be clamped, as this will cause a tension pneumothorax
- Complications include pain, intrapleural infection, drain dislodgement, and drain blockage.
There can also be surgical emphysema and direct organ damage
The drain should be flushed daily with saline to prevent infection.
Surgical intervention is indicated where there is recurrent pneumothorax or a persistent air leak
- Primary spontaneous has a ~50% recurrence rate, and it is recommended that there is
intervention after first recurrence
Chemical pleurodesis can be used where patients are not suitable for surgery
- This involves the instillation of sterile talc into the pleural cavity, causing formation of
adhesions between the pleural layers
- The talc is instilled via a chest tube
Open thoracotomy and VATS (video assisted thorascopic surgery) aim to resect any bullae and
create a symphysis between the two pleural surfaces. It is common in secondary pneumothorax,
aiming to staple any subpleural blebs/bullae or in primary pneumothorax to staple any air leaks
- This combines pleurectomy and pleural abrasion

- VATS can be done under local anaesthetic and has a faster recovery time than open
thoracotomy
- There can also be thoracoscopic talc poudrage, which is similar to chemical pleurodesis but
has better outcomes
Venous Thromboembolism (VTE)

Deep Vein Thrombosis (DVT)
DVT typically arises in the deep veins of the legs of pelvis
Major and minor risk factors are summarised in the table below, these can also be summarised in
terms of Virchow’s triad
- Stasis of blood flow

- Hypercoagulability
- Endothelial injury
Major RF Minor RF
Surgery (particularly orthopaedic) Congenital heart disease (paroxysmal emboli
from VSD/ASD)
Pregnancy, particularly third trimester OCP/HRT use
Advanced malignancy Nephrotic syndrome
Reduced mobility e.g. hospitalisation Dialysis
Lower limb disease e.g. varicose veins, fracture MPN or pro-thrombotic disease
Previous VTE Long distance sedentary travel
Presentation
Clinical diagnosis of DVT is difficult, but symptoms occur as a result of obstruction to venous
drainage
- Pain and tenderness along the line of deep veins

- Unilateral swelling of the calf or thigh with increase in skin temperature and
erythema/cyanosis/purple discoloration
- Distension of superficial veins
- Pitting oedema
Homan’s sign can be present. This is a discomfort behind the knee on forced dorsiflexion of the foot
Investigations
Well’s scoring is used to risk stratify patients with possible DVT. DVT is likely if >2 and unlikely if <1.
Subtract 2 points if an alternative cause is suspected
- Active malignancy – 1.0 points

- Immobilisation – 1.0 points
- Localised deep vein tenderness – 1.0 points
- Swelling – 1.0 points

- Pitting oedema – 1.0 points
- Collateral superficial veins – 1.0 points
- Previous DVT – 1.0 points
Where the Well’s score indicates likely DVT there should be a proximal leg vein duplex USS. Where
the score indicates unlikely DVT there should be D-dimer test, and if positive, proximal leg vein
duplex USS
- Contrast venography is the gold-standard for diagnosis, but is rarely used

Management
As for PE (see below)
Pulmonary Embolus (PE)
PE is an obstruction within the pulmonary arterial tree, emboli can be caused by
- Thrombosis, this is the commonest cause usually arising from a distant vein (typically lower
limbs or pelvis)
- Fat, following long bone fracture or orthopaedic surgery
- Amniotic fluid
- Tumour
- Air, following neck vein cannulation of bronchial trauma
The haemodynamic effects of PE can cause compromise
- Large PE (occluding >50% of the vascular bed e.g. saddle embolus) causes the pulmonary
arterial pressure to rise, increasing right ventricular afterload and causing right ventricular
failure. Pulmonary blood flow then decreases, reducing left ventricular filling and cardiac
output
o A PE causing haemodynamic compromise is defined as a massive PE
o Sub-massive PE is branch/saddle not causing haemodynamic compromise
o Segmental and sub-segmental PEs do not cause compromise
- Hypoxia develops as there is reduced cardiac output and VQ mismatch at the lungs
Presentation
Acute PE presents in three main ways
1. Pulmonary infarction and haemoptysis (with pleuritic pain)

2. Isolated dyspnoea
3. Circulatory collapse with loss of consciousness. 25% of patients will present with sudden
death, but is a reversible cause of cardiac arrest
Assessment
Initial assessment should use an A to E approach
- Give supplemental oxygen and perform ABG according to SpO2

- Establish IV access, fluid resuscitation may be required
- Baseline bloods should include FBC, U&Es, LFTs, and clotting
- Cardiac troponins are indicated to exclude MI, however it can be raised due to RCA
compression
For massive PE causing haemodynamic compromise thrombolysis is indicated, this is with alteplase
or streptokinase
On focussed examination there may be signs of DVT, hypotension, tachypnoea, tachycardia,

decreased oxygen saturation, and raised JVP. There may also be a pleural rub on auscultation
- Other signs of right heart strain may also be present e.g. right parasternal heave, gallop
rhythm
Further history should clarify risk factors and symptoms
- Typical symptoms include dyspnoea, pleuritic pain, cough and haemoptysis, symptoms
suggesting DVT, and light-headedness
ECG and CXR should take place in all
- ECG can show different features dependent on severity

- Sinus tachycardia
- Right heart strain: right bundle branch block, right axis deviation, T-wave inversion
in anterior leads
- Acute right heart strain can be seen as the S1Q3T3 pattern. Prominent V1 S wave, Q
wave in V3, T wave inversion in V3
- CXR is usually normal, but can show linear atelectasis (localised collapse), raised
hemidiaphragm, small pleural effusion, and a wedge shaped defect (localised infarction)
The modified Well’s score is used to judge the risk of PE in a patient. A high score is >4, and does not
require a D-Dimer before additional scanning is performed
- Clinically suspected DVT – 3 points

- Alternative diagnosis is less likely than PE – 3 points
- Tachycardia (HR>100) – 1.5 points
- Immobilisation in the past 4 weeks – 1.5 points
- History of DVT/PE – 1.5 points
- Haemoptysis – 1.0 points
- Malignancy – 1.0 points
Further investigation is with imaging, this is diagnostic
- Gold standard is CTPA, but this requires high volumes of IV contrast. If there is delay in
obtaining CTPA and the patient has a high Well’s score there should be parenteral LMWH in
the interim
- VQ SPECT and/or leg USS-Doppler is an alternative to CTPA in patients with impaired renal
function or contrast allergy
- Echocardiogram can assess for right heart failure and pulmonary hypertension
In patients with a low Well’s score there should be D-dimer testing
- Negative D-dimer (degradation product of fibrin) is very sensitive for excluding acute DVT or
PE
- This is not a specific test, therefore if positive it should be followed with CTPA
Management
Initial definitive management should follow stabilisation through A to E
- The commonest measure is to commence LMWH (enoxaparin or fondapurinox)

- A loading dose of 15mg BD rivaroxaban can also be used for 3/52 before moving to
maintenance dose of 20mg OD
Longer term management of PE is with anticoagulation; target INR is 2 – 3
Warfarin should be commenced within 24 hours of diagnosis
- Continue LMWH alongside warfarin for 5 days, ensuring INR >2 for at least 48 hours
- For patients with a temporary provoking risk factor there should be 3 months of
anticoagulation with warfarin followed by review
- For an unprovoked PE there should be 6 months of anticoagulation with warfarin/ NOAC
followed by review
- For patients with malignancy there should then be treatment with LMWH for 6 months,
potentially continuing with warfarin longer term
NOACs can also be used as an alternative to warfarin, the duration of treatment is the same as
warfarin
- For dabigatran continue LMWH alongside for 5 days

- For apixaban and rivaroxaban, stop LMWH and give the dose of NOAC when the next dose of
LMWH would have been due
Embolectomy is used in CTEPH (chronic thromboembolic pulmonary hypertension), this is due to
fibrotic organisation of the clot, meaning that it cannot be broken down with anticoagulation
Management in Pregnancy
Where PE is suspected in pregnancy there are some differences in treatment. D-dimer cannot be
used as a diagnostic marker in pregnancy as it will be raised
- Where leg symptoms are present there should be USS-Doppler of the leg before any
radiation exposure is considered. If DVT is identified, management can commence from this
point
- Where there is suspicion of PE, arrange CXR
- If CXR is normal arrange USS-Doppler of the leg
- If all investigations are normal arrange V/Q scan. This is preferable to CTPA
LMWH should be used as warfarin is contraindicated
An obstetrician should be consulted
Pleuritic Chest Pain (Pleurisy)
Pleuritic chest pain is sharp, well localised, and worse on inspiration. There are many potential
causes
Cardiac MI, pericarditis

Respiratory PE, pleural effusion, pneumothorax
Gastrointestinal IBD
Rheumatological Lupus pleuritic, rheumatoid pleuritic, Sjögren’s syndrome
Infectious Viral (commonest cause), pneumonia
Investigations
Investigations in the hospital setting should include
- Routine bloods, including troponins and D-dimer where indicated

- ECG
- CXR
Management of Viral Pleurisy
Reassure the patient that the condition is not worrying and self-limiting
- Prescribe pain killers as per the analgesic ladder
Pleural Effusion
Pleural effusion is defined as an abnormal accumulation of fluid (>20ml) in the pleural space
between the parietal and visceral pleural layers
Assessment
Use an A to E approach
- Measure SpO2 and titrate need for oxygen according to this

- Order CXR
- Gain IV access and take the following bloods from the cannula
o FBC, raised WCC could indicate infection
o U&Es and LFTs as both liver and renal failure can lead to effusion
o CRP and ESR to indicate infection or inflammation
o Clotting screen as chest drain may be indicated
o Amylase
o Protein and LDH as per Light’s criteria
- Perform an ABG if the patient has reduced SpO2
- Order an ECG
Focussed examination and history will establish likely diagnosis, and can give an indication of the
underlying cause
- Symptoms of pleural effusion will differ dependent on the size of the effusion as well as the
underlying cause. Typical history includes
o Shortness of breath, particularly on exertion
o Dry cough and pleuritic pain
- On examination pleural effusion has several key signs on the affected side
o Decreased expansion, stony dull percussion, diminished breath sounds, and
decreased vocal resonance
o With a large effusion there may be tracheal deviation away from the affected side
Causes
Commonest causes of pleural effusion in the UK are as follows
- Cardiac failure, pneumonia, malignancy, PE

Other causes are summarised below, separated into transudative and exudative forms
Transudates (3 failures) Exudates (infection, inflammation, malignancy)

Left ventricular failure Parapneumonic effusion
Cirrhosis Pleural malignancy
Nephrotic syndrome TB
Peritoneal dialysis PE (more commonly exudate)
Hypoalbuminaemia Rheumatoid arthritis

Atelectasis Other autoimmune diseases
Hypothyroidism Pancreatitis
Ensure that chest X-ray is undertaken. This is the most important imaging study and can be a PA or
lateral view
- Blunting of the costophrenic angles with a meniscus is indicative

If there is high clinical suspicion of malignancy there should be CT thorax
- Malignant pleura is thickened, nodular, and thickened mediastinally

- If malignant pleura is seen on CT, biopsy is indicated for diagnosis
VATS or medical thoracoscopy can also be used to assist with diagnosis
If clinical judgement suggests that the effusion is transudative, it may not require further
investigation. If not there should be pleural aspiration of at least 50ml (this may be under US
guidance), fluid should be sent for
- Cytology to test for malignancy

- Biochemistry to test protein level, LDH, pH, glucose
- Microbiology culture and sensitivity as well as AAFB stains
Management
Effusions are classified into transudates (<25g/L of protein, due to increased hydrostatic pressure) or
exudates (>35g/L of protein, due to altered capillary permeability)
-If the protein level is between 25 and 35, Light’s criteria are used
- It is an exudate if pleural:serum protein >0.5, pleural:serum LDH >0.6, or if
pleural LDH is >2/3 the upper limit of normal serum LDH
- If LDH is >1000 this indicates empyema, rheumatoid arthritis, or malignancy
- If glucose <3.33 this indicates rheumatoid arthritis, empyema, malignancy, TB, or
oesophageal rupture
Management of pleural effusion should be aimed at the underlying cause
After pleural aspiration has taken place, if the patient is symptomatic, the next stage of treatment is
pleural tap and removal up to one litre of fluid
- One litre is the maximum amount of fluid that should be removed, or re-perfusion
pulmonary oedema may occur (sudden expansion of the lung stimulates stretch
receptors, blood vessels then release vasoactive factors into the lung parenchyma)
Simple pleural effusions will resolve naturally after pleural tap
- Complicated effusions (pH <7.2, turbid, culture positive, or gram stain positive) and
empyema will need a chest drain
Malignant pleural effusion often recurs, therefore there should be consideration of pleurodhesion
- This can be with medical or surgical intervention

- Intercostal tube drainage and sterile talc pleurodesis
- VATS with pleurectomy and pleural abrasion
- If there is trapped lung (cannot expand due to pleural disease) a long-term indwelling
pleural catheter can be used
Empyema
Empyema is the presence of pus in the pleural space, this can occur in the absence of preceding
infection (primary empyema) or secondary to other causes
- The fluid in empyema may be free-flowing or multiloculated and requires drainage

The commonest cause of empyema is parapneumonic effusion, where bacteria gain access to the
effusion from the lung parenchyma
- Initially parapneumonic effusion is a clear, sterile, exudative fluid

- Complicated parapneumonic effusion develops where the fluid is infected, but not yet
purulent. It appears cloudy/turbid
- Empyema is the final stage
o Fluid is yellow, with a pH <7.2, low glucose, and raised LDH
Other secondary causes include TB, bronchiectasis, lung abscess, and abdominal abscesses
(subphrenic, hepatic, perinephric)
Primary empyema can occur due to aspiration, bronchial obstruction, and oesophageal rupture
If untreated, empyema will develop a thick pleural peel due to fibroblast growth (organisation).
Treatment at this stage becomes difficult
Presentation
Empyema presents similarly to pneumonia with fever, productive cough, chest pain, and
breathlessness
- Anaerobic empyema may present less acutely, with weight loss and absence of fever
Investigation
Measure oxygen saturations, and if low perform an ABG alongside routine blood tests
- FBC, raised WCC could indicate infection

- Blood cultures
- U&Es and LFTs as both liver and renal failure can lead to effusion
- CRP and ESR to indicate infection or inflammation
- Clotting screen as chest drain may be indicated
- Amylase
Chest X-ray is the most important imaging study, this can be a PA or lateral view
- Blunting of the costophrenic angles with a meniscus is indicative

Diagnostic pleural tap of at least 50ml (this may be under US guidance), fluid should be sent for
- Cytology to test for malignancy

- Biochemistry to test protein level, LDH, pH, glucose
- Microbiology culture and sensitivity as well as AAFB stains, pleural infection is usually
polymicrobial
Contrast-enhanced pleural-phase CT scan is useful in supporting diagnosis as well as visualising the
distribution of fluid
- Bronchoscopy is indicated if an obstruction is suspected

Management
All patients with pleural infection should be prescribed antibiotics for at least 3 weeks
- Community acquired empyema should be treated with a β-lactam (co-amoxiclav) or

cephalosporin (cefuroxamine) combined with metronidazole for anaerobic cover
- Hospital acquired empyema should be treated with broad spectrum cover, including MRSA.
Meropenem and vancomycin is common
Chest tube drainage is indicated in all cases of empyema. There should also be anti-coagulation.
If symptoms persist after 7 days of treatment there can be surgery. This includes VATS, thoracotomy
and decortication, or open thoracic drainage
Pericardial Disease
Acute Pericarditis
Acute pericarditis is inflammation of the pericardial sac. There are many potential causes
- Primary idiopathic disease is commonest

- Secondary causes include
o Infection e.g. coxsackievirus
o Metastatic neoplasm
o Systemic autoimmune disorders e.g. SLE, sarcoidosis, RA
o Dressler’s syndrome post-MI
o Uraemia
o Iatrogenic causes e.g. radiation, hydralazine, procainamide
Presentation
Acute pericarditis usually presents with pleuritic chest pain that is exacerbated by lying flat and
relieved by leaning forward
- Pain may be described as dull, sharp, burning or pressing

- A pericardial rub on auscultation is highly specific
Pericarditis can characteristically follow viral infection and flu-like illness
Investigations
Blood tests should include FBC, ESR and CRP, U&Es, and cardiac enzymes
- These can help exclude differentials and identify the underlying cause
- If symptoms persist for >1 week then there should be rheumatological studies, antibody
testing, and pericardial biopsy in some
ECG in pericarditis shows a PR depression, T-wave inversion, and diffuse saddle-shaped ST elevation.
ECHO can show a small pericardial effusion, this does not usually cause haemodynamic compromise
Where there is pericardial effusion, CXR may show an enlarged globular heart
Management
Most patients can be managed out of hospital. Admission to hospital should occur in patients with
fever, large pericardial effusion, immunosuppression, acute trauma, or failure to respond to NSAIDs.
Treatment of acute pericarditis should be directed at the underlying cause
- High dose NSAIDs (naproxen 250mg QDS) for 7 to 14 days, alongside PPIs will usually resolve
symptoms. Dose should then be tapered according to CRP
o Colchicine can also be used
- Glucocorticoids should only be used in refractory cases
- The patient should avoid strenuous exercise for one month after resolution
Pericardiocentesis or surgical pericardotomy/pericardial window are indicated where there is
tamponade or the aetiology is neoplastic
Constrictive Pericarditis
Constrictive pericarditis is a consequence of scarring of the pericardium following injury. This results
in stiffness and loss of distensibility
- The most common origin is idiopathic or viral

- Neoplastic, purulent or tuberculous pericarditis are likely to result in constrictive pericarditis
Presentation
It presents with congestive right heart failure and reduced cardiac output
- JVP will rise paradoxically with inspiration

- Heart sounds are quiet
Investigations
CXR, CT and MRI can show calcification and thickening. Haemodynamic studies with cardiac
catheterisation will show increased diastolic pressure and collapsing ventricular pressure.
Management
It may be reversible with NSAIDs for several months, but pericardectomy is usually required.
Cardiac Tamponade
In cardiac tamponade an accumulation of fluid in the pericardial sac leads to an increase in intra-
pericardial pressure that compromises cardiac output and ventricular filling
- This can be caused by pericarditis, aortic dissection, ventricular rupture (blunt or (usually)
penetrating chest trauma, post-MI), or iatrogenically
Presentation
Patients will be haemodynamically unstable and in shock. Signs on examination include
- Beck’s triad: falling BP, rising JVP, muffled heart sounds

- Tachycardia
- Pulsus paradoxus, where the pulse drops during inspiration
Investigations
Investigation is as for pericarditis
- CXR may show a big globular heart

- ECG may show low QRS amplitude or alternation of QRS complexes
In trauma, FAST scan should be the investigation of choice as formal echocardiography is rarely
available immediately
Management
Management and assessment should follow A to E principles
- Venous return and cardiac output can be improved by raising the legs and giving positive
inotropic drugs
If possible, theatre thoracotomy should be performed to drain the pericardial fluid, as this has better
outcomes. However, this is often not available rapidly
- Echocardiogram-guided pericardiocentesis in the ED may have to be the definitive therapy in

unstable cases, particularly traumatic cases
- Pericardiocentesis may be ineffective due to clot formation, therefore thoracotomy in ED
may be required
Oesophageal Rupture
Oesophageal rupture is most common after vomiting (Boerhaave syndrome)
- This differs from a Mallory-Weiss tear, as the disruption is through all oesophageal layers
leading to perforation
Other causes include
- Iatrogenesis: endoscopy, gastroscopy, surgery

- Ingestion of caustic substances
- Trauma
- Foreign body
- Carcinoma
Presentation
Perforation of the oesophagus should be suspected in patients complaining of severe chest pain,
pain may also be in the neck or upper abdomen
- Dysphagia, odynophagia, and pyrexia are also features
On examination there may be surgical emphysema felt in the supraclavicular area. The patient may
be cyanosed and tachycardic
Investigations
Blood tests should include FBC (raised WCC), ABG (acidosis), and other routine surgical bloods.
Imaging studies are diagnostic
- CXR shows pleural effusion with gas in the mediastinum

- Barium swallow
- CT scanning
- Upper GI endoscopy can be considered when there is a high suspicion of perforation but
there is negative imaging and the patient is unable to swallow contrast agent
Management
It is essential to keep patients NBM from the point of diagnosis for at least 5/7, give parenteral
nutrition and NG suction
- When contrast swallow confirms healing, oral feeding can re-commence
There should be drainage of the pleural space through chest-drain insertion and IV antibiotics
In some patients, surgery is necessary. It is best done early, as delayed repair increases mortality
Aortic Dissection
An aortic dissection is a disruption of the medial layer of the wall of the aorta due to intramural
bleeding
- Blood separates the layers of the aortic wall (either intima and muscularis, or muscularis and
serosa), forming a false lumen for blood to travel through
Risk factors include
- Modifiable risk factors: hypertension, smoking, dyslipidaemia, cocaine

- Aortic valve disease
- Vascular inflammation
- Connective tissue disorders such as Ehlers-Danlos and Marfan’s syndrome
There are two forms of aortic dissection (Stanford Classification)
- Type A involves the ascending aorta. These will require cardiothoracic surgical input as soon
as possible due to risk of proximal spread causing MI/tamponade
- Type B does not involve the ascending aorta
Presentation
Aortic dissection presents with a sudden onset of severe sharp/tearing chest pain, radiating to the
back. The pain will be maximal at onset, and can change dependent on position
- Alongside chest pain, it can present with angina due to coronary artery involvement,
paraplegia due to spinal artery involvement, limb ischaemia, renal failure, and neurological
deficit
- If dissection moves proximally there can be aortic valve incompetence, inferior MI, or
cardiac arrest
On examination there are several key findings
- Difference in blood pressure in the limbs (>15mmHg systolic), patients are generally
hypotensive
- Radial-radial delay or pulse deficit
- Cap refill may differ between arms
Investigations
Measurement of SpO2 and blood pressure is essential. Routine blood tests should all be performed,
including troponins to differentiate ACS and cross-match of several units of blood (>4)
- ECG may be normal, or may show signs indicating myocardial infarction/ischaemia, or PR

prolongation due to aortic root dilation
o It is essential to check for other signs indicating aortic dissection in MI, as
thrombolysis will be fatal in these patients
- CXR can show mediastinal widening
Diagnostic investigations are imaging
- Transthoracic or transoesophageal USS can show the site and extent of dissection
- MRI angiography is gold-standard, but CT with contrast is an alternative
Management
Management should follow an A to E assessment, and patients should be placed in an ITU setting
and kept NBM
- Ensure good IV access and analgesia

- Aim for a systolic pressure 100 - 120 by using medications where required, or permissive
hypotension with inadequate fluid resuscitation
o Medications can include IV beta-blockers e.g. labetalol ± vasodilators (e.g. sodium
nitroprusside)
- When in ITU insert an arterial line, central venous line, and urinary catheter
o Catheter insertion and AVPU help to monitor perfusion
Surgical intervention with endovascular/open aortic repair and graft insertion is generally required
in type A dissections. Type B dissections can be initially managed medically with aggressive BP
control
Acute Confusional State

Delirium can be defined as a state of mental confusion that develops quickly and usually fluctuates
in intensity. There are four DSM-IV criteria required to make the diagnosis
1. Disturbance of consciousness (attention and/or arousal)

- This may be hypoactive, hyperactive or mixed – hypoactive delirium has the worst
prognosis as it is more likely to be missed
2. Worsening confusion
3. Acute onset with fluctuating course
4. Due to a medical condition, substance intoxication and/or substance withdrawal
There may also be emotional distress and disturbed psycho-motor behaviour
Assessment
It is important to first carry out an A to E assessment of the patient
- Ensure to measure SpO2, BM, and temperature as part of the assessment

- Specific bloods to assess when IV access is established include
o FBC, CRP/ESR for signs of infection
o Glucose
o Confusion screen
▪ U&Es to look for electrolyte imbalance or dehydration
▪ LFTs
▪ TFTs
▪ B12 and folate
▪ Calcium, magnesium and phosphate
▪ Syphilis serology
o VBG (or ABG if oxygen saturation <92%)
- Carry out a 12 lead ECG
History
If possible, collateral history should be obtained, as the patient may not be able to provide an
adequate account of events
- The onset and course of confusion should be established as well as any previous episodes
- There should be exclusion of head injury/falls
- Full systems review to indicate possible cause
Try to establish past medical history and medication history early
Examination
Tilmus (playing with bedclothes) is quite a specific sign of delirium. Focussed examination should
include
- Assessment of conscious level with GCS

- Assessment of cognition e.g. AMT, MMSE or clock-drawing test
- Focussed physical examination on evidence of infection (lung, abdomen, skin) and focal
neurology
- Palpate for a bladder as well as PR for constipation
Diagnosis follows confusion assessment method (CAM), this can be determined following GCS and
AMT. This requires the presence of items 1 and 2, and either 3 or 4
1. Acute onset and fluctuating course

2. Inattention (easily distracted, difficulty keeping track of conversation – assessed as part of
AMT with counting backwards from 20 to 1)
3. Disorganised/ disordered thinking (ask patients if anything odd or strange has been going
on)
4. Any altered level of consciousness (GCS <15, vigilant, hyper-alert, drowsy, difficult to arouse)
4-AT can also be used, and tends to be more reliable.
There should be urinalysis (+ MC&S) in all delirious patients regardless of history, often UTI
presentation is atypical in elderly patients
Drug levels can be useful dependent on what the patient is taking, and the risk of toxicity
- CXR, as part of an infection screen

- Head imaging
- EEG
Specific cultures should be carried out as indicated e.g. blood, urine, sputum, lumbar puncture
CT head should be considered if indicated
Delirium is often multifactorial, and it is not always possible to determine the cause, but it is
essential to attempt to identify it. Common causes include (mnemonic delirium(+3p))
- Drug intoxication or withdrawal (anticholinergics, anxiolytics, antidepressants,

anticonvulsants, opiates, alcohol)
- Electrolyte imbalance (hypo-/hypernatraemia, hypercalcaemia)
- Liver failure, Low oxygen
- Intracranial pathology (intracranial haemorrhage, stroke, space occupying lesion, epilepsy)
- Renal failure, Retention (urinary retention, constipation)
- Infection (chest, UTI, intra-abdominal, or cellulitis)
- Uraemia and fluid imbalance
- Metabolic (endocrine imbalance: hypo-/hyperglycaemia, hypo-/hyperthyroidism, Addisonian
crisis)
- Pain, Postoperative, Psychiatric
Delirium can have long term consequences such as increased mortality, institutionalization, and
dementia
Management
Conservative measures to help improve delirium include
- Provision of a quiet environment with a clock/window to aid orientation

- Ensure the patient has adequate spectacles and hearing aids
- Reassure the patient frequently and encourage relatives to visit
- Cot sides to beds can be very dangerous in these patients and should be avoided
If patients are agitated and not responding to conservative measures, one can try a dose of
paracetamol as analgesia for any pain that they are not communicating
Physical restraint should only be used in extreme circumstances e.g. severe aggression for
administration of parenteral drugs. Use of sedative drugs should also be kept to a minimum and only
used where the patient is a danger to themselves or others
- Rapid tranquilisation with haloperidol is first line, ideally this should be 0.5mg PO every 30
minutes to 2 hours. It can also be given 1 – 2mg IM every 4 hours
o Maximum 5mg in 24 hours
- Second line is lorazepam, ideally PO 0.5 – 1mg every 2 hours (maximum 3mg in 24 hours)
o Lorazepam is used in patients with Parkinson’s disease, Lewy body dementia,
alcohol intoxication/withdrawal, or severe cardiovascular disease
- As an F1, always discuss with a registrar before giving rapid tranquilisation.
The underlying cause should be addressed
- Removal of offending medications, in line with STOPP/START criteria

- Treatment of infection
- Correction of hypoxia and metabolic derangements
Symptoms of delirium may last longer than the underlying condition, therefore some patients will be
discharged with persisting abnormalities and will therefore require support from family/carers
Electrolyte Imbalance
Disorders of Sodium Balance
Homeostasis of sodium is linked with water homeostasis, and is regulated by two main hormonal
axes
- ADH is released in response to fluid depletion, increased plasma osmolarity (>288mOsm),

and physiological stress that is sensed in the AV3V region of the hypothalamus. ADH release
corrects osmolarity by stimulating thirst and increasing renal water reabsorption through
insertion of AQP2 in the collecting ducts
- Protection of circulating volume overrides control of osmolality, therefore in
haemorrhage there will be low osmolality initially that will be corrected later
- Aldosterone is released when fluid depletion causes a fall in blood pressure. This is sensed in
the JGA of the kidney, triggering renin release and downstream production of aldosterone.
Aldosterone will increase Na reabsorption in the distal tubule, promoting reabsorption of
water
Plasma sodium concentration in health must remain between 133 – 146mmol/L
Hyponatraemia
Hyponatraemia is defined as serum [Na] < 135mmol/L
The rate at which hyponatraemia develops is critical to the symptoms and risks. If there is rapid
hyponatraemia water will move intracellularly, this causes cerebral oedema. Where the onset is
slow, the brain will compensate by losing solutes and oedema will not occur
- Below 125mmol/L this becomes symptomatic presenting with headache, nausea, vomiting,
muscle cramps, lethargy, restlessness, and disorientation
- Below 120mmol/L there is a risk of seizure, coma, brain damage, and brainstem herniation
Hyponatraemia can either be caused by sodium loss or water excess. There are several
investigations that need to be carried out to differentiate the causes when there is hyponatraemia
identified
- Measure urinary [sodium] and osmolality

- Assess the patient clinically to see if there is evidence of fluid overload or hypovolaemia
The differential diagnoses of hyponatraemia and investigation findings are summarised below
- Where the patient is clinically dehydrated there should be measurement of urine [Na]
- Urine [Na] > 20 indicates that there is high sodium loss from the kidney. This can be
due to salt-wasting nephropathy, adrenal insufficiency, diuretic excess (thiazides),
diuretic phase of renal failure
- Urine [Na] < 20 indicates that there is extra-renal sodium loss. This can be due to
diarrhoea, vomiting, GI fistulae, burns, villous adenoma, bowel obstruction
- Where the patient is oedematous the likely cause is renal failure, cardiac failure, or liver
failure
- Where the patient is normovolaemic, there should be measurement of urine osmolality and
[Na]
- Urine osmolality >100mmol/kg or urine [Na] >20 indicates SIADH
- Urine osmolality <100mmol/kg or urine [Na] <20 can be due to severe polydipsia,
hypothyroidism, or glucocorticoid insufficiency
Treatment of hyponatraemia is to replace sodium and water at the rate they were lost
- The patient can be given dietary salt or IV normal saline (no faster than 15mmol/L/day or
1mmol/L/hr increase in serum [Na])
- Where the patient is oedematous, fluid restriction is important
In an emergency situation where the patient is having seizures, hypertonic 1.8% saline can be used
with caution
It is essential not to correct hyponatraemia rapidly, as rapid correction causes intracellular

dehydration and pontine myelinosis – this can cause permanent spastic paraparesis, seizures, and
coma
SIADH is an important differential diagnosis of normovolaemic hyponatraemia, and occurs when

there is inappropriate ADH secretion for the osmolality of the ECF. Causes include
- Tumours, particularly small cell lung carcinoma

- Chest disease such as TB, pneumonia, abscess, pneumothorax
- CNS disorders such as pituitary adenomas, infections, head injury, Guillain-Barre
- Iatrogenesis with drugs such as chemotherapy agents, MAOIs, phenothiazines,
carbamazepine
- Metabolic disorders such as hypothyroidism and porphyria
Diagnosis of SIADH comes where there is hyponatraemia with hypotonic plasma, high urine
osmolality (higher than plasma osmolality), high urine sodium, and normovolaemia. There must be
exclusion of renal, adrenal, and thyroid disease.
Treatment is of the underlying cause alongside fluid restriction and increased salt intake. If there is a
long-term problem demeclocycline (600mg OD) can be used to induce nephrogenic DI, and in the
future vasopressin antagonists (tolvaptan) may be used
Hypernatraemia
Hypernatraemia is defined as serum [Na] > 145mmol/L typically presents with lethargy, thirst,
weakness, irritability, confusion, and other signs of dehydration. In extreme states ([Na] >
160mmol/L) it can lead to seizure and coma
- Signs may include orthostatic hypotension and tachycardia

Hypernatraemia can either be caused by water loss in excess of sodium loss, or sodium excess. This
includes
- Fluid loss without water replacement e.g. dehydration, burns, diarrhoea, vomiting
- Diabetes insipidus
- Osmotic diuresis e.g. hyperglycaemia, use of osmotic diuretics like mannitol
- Primary hyperaldosteronism
- Iatrogenesis from excessive use of saline
Investigation into hypernatraemia should begin with physical examination to determine whether
there is fluid excess or fluid deficit
- High circulating volume occurs in hyperaldosteronism

- Low circulating volume occurs in most other states
Baseline laboratory investigations should include U+Es to see the extent of the hypernatraemia and
also to assess for other electrolyte abnormalities (e.g. hypokalaemia in hyperaldosteronism). There
should also be measurement of urinary osmolality
- Urine will be hypertonic where there are extra-renal fluid losses and lack of fluid intake
- Hypotonic urine indicates diabetes insipidus (<300mOsm/kg)
- Isotonic urine can be seen with osmotic diuresis and salt wasting
Treatment of hypernatraemia is to give water orally where possible, or give IV 5% dextrose solution.
Fluid administration should be guided by urine output and plasma sodium level.
Diabetes insipidus is a rare but important cause of hypernatraemia. It will typically present with
polyuria and polydipsia, resulting in hypernatraemia if the patient cannot compensate with
adequate fluid intake
- DI can be classified as central or nephrogenic

- Central DI is due to a deficiency in circulating ADH. This can develop following
trauma, tumours, infection, or can be idiopathic
- Nephrogenic DI is due to renal resistance to ADH. This can be congenital or due to
lithium toxicity, metabolic disease, or chronic renal disease
Investigation into DI includes 24 hour measurement of urine volume (>3L/day), and exclusion of
osmotic diuresis leading to this large urine output. There is then fluid deprivation testing to
distinguish DI from psychogenic polydipsia
- The patient is deprived of fluids for 8 hours or until loss of 5% of body weight, during this
time the plasma osmolality is measured every 4 hours and urine osmolality is also measured.
The patient has DI, their plasma osmolality will rise >305mOsm/kg and they will continue to
produce large volumes of urine
- To distinguish central and nephrogenic DI, the patient is then given IM desmopressin. In
central DI there will be an increase in urine osmolality to >800mOsm/kg
- There is then investigation of the cause of DI, including MRI head
Treatment of DI is maintenance of adequate fluid input as well as the ADH analogue desmopressin
(oral or intranasal). Where there is nephrogenic DI it is important to treat the underlying cause, but
high dose desmopressin can be effective and thiazide diuretics can also be used
- It is very important to regularly monitor serum sodium and osmolality to detect if there is
any development of hyponatraemia
Disorders of Calcium Balance
Calcium is in a dynamic exchange between the bone and cellular/extra-cellular fluids. At any one
time, the vast majority of the calcium will lie in the bone, creating a readily accessible store that can
be converted to soluble calcium through bone turnover
- Bone turnover is coordinated by osteoclasts and osteoblasts, breaking down and building up
bone respectively
In the blood calcium can be free ionised calcium or ultra-filterable (bound to protein or complexed
with other ions). Ionised free calcium is the physiologically important part as it regulates the
negative feedback mechanisms and should be 2.10 – 2.60 mmol/L
- If there is a hypoalbuminaemia, total calcium levels will decrease, but free calcium levels will
remain the same
- As total calcium levels are measured, calcium correction can be used to indicate whether
free calcium will be within normal range. For every g albumin <40g/L multiply by 0.02 and
add to measured calcium, for every g albumin >40g/L multiply by 0.02 and subtract from
measured calcium
The endocrine control of extracellular calcium homeostasis is largely coordinated by the parathyroid
glands. The parathyroid glands are stimulated to secrete PTH in response to low serum calcium or
high serum phosphate, whereas there is negative feedback from 1,25(OH)2vitamin D and calcium
- PTH increases serum calcium by promoting renal calcium resorption, activating vitamin D in
the kidney to promote intestinal calcium absorption, and stimulating osteoclasts to increase
calcium release from bone
- PTH will also decrease renal phosphate reabsorption to lower serum levels
Hypercalcaemia
Acute hypercalcaemia has a typical presentation, common to all causes of the condition
- Renal symptoms include polyuria, polydipsia. Gastrointestinal effects include anorexia,

vomiting, constipation, and abdominal pain. The effect on the CNS results in confusion,
lethargy and depression
- In chronic hypercalcaemia there may also be bone pain or fracture and renal stones
Causes of hypercalcaemia include
- Primary or tertiary hyperparathyroidism

- Hypercalcaemia of malignancy due to lytic bony metastases, ectopic PTHrP secretion, or
multiple myeloma
- Vitamin D intoxication
- Familial hypocalcuric hypercalcaemia (FHH). This is an autosomal dominant asymptomatic
condition due to a mutation reducing the sensitivity of the parathyroid calcium sensing
receptor. It is benign in the heterozygous state (may cause pancreatitis), however it requires
parathyroidectomy in the homozygous state
- Sarcoidosis and other granulomatous disorders, as there is production of active vitamin D
within the granulomas. This is treated with steroids as in vitamin D intoxication
- Rarer causes such as lithium toxicity, thiazide diuretics, immobilisation, hyperthyroidism,
renal failure, Addison’s disease, milk alkali syndrome (taking calcium supplements alongside
alkali-based antacids), and vitamin A intoxication
Where a patient has confirmed hypercalcaemia (corrected for albumin level) there are several
investigations that can identify the mechanism of the hypercalcaemia, indicating what the causative
underlying condition may be. Calcium > 3.0 is almost always malignancy
- Measure U+Es to assess renal function and look for dehydration

- Measure corrected calcium, vitamin D, and phosphate
- Phosphate will be low in hyperparathyroidism
- Phosphate will be raised myeloma, vitamin D excess, bony malignancy, and
sarcoidosis
- Measure LFTs looking specifically at ALP and albumin
- ALP will be raised in bone metastasis, sarcoidosis, lithium toxicity
- Measurement of serum PTH
- PTH levels will be increased in parathyroid overactivity (hyperparathyroidism, FHH,
lithium) and suppressed in other states
- Urine calcium to determine calcium:creatinine excretion ratio
- This will be low in FHH and high in primary hyperparathyroidism
It is always essential to do an ECG in hypercalcaemic patients as they may have a short QT interval
Other investigations can include plasma electrophoresis to identify myeloma, isotope bone scan to
assess for malignancy, parathyroid USS, and CXR to assess for lung malignancy
Treatment of severe hypercalcaemia is with rehydration (usually around 6L 0.9% saline over 24
hours), and following this an IV bisphosphonate (zoledronate 4mg) is given. If the patient is resistant
to the bisphosphonate, there should be IM calcitonin or PO steroids.
Hypocalcaemia
Hypocalcaemia typically presents with symptoms related to increased neuromuscular excitability.

This includes numbness and tingling, muscle cramps, spasm (carpopedal spasm, laryngospasm), and
seizures
- Chvostek’s sign (tap facial nerve in front of ear = spasm of corner of mouth) and Trousseau’s
sign (inflate sphygmanometer cuff = carpopedal spasm) may also be present
Causes of hypocalcaemia include
- Hypoparathyroidism. This may be due to iatrogenesis, infiltration, failure of development

(DiGeorge syndrome, X-linked hypoparathyroidism), hypomagnesaemia causing failure of
PTH secretion
- Vitamin D deficiency
- Conditions that prevent calcium release from bone e.g. sclerotic bony metastasis,
osteomalacia, some chemotherapy medications, hungry bone syndrome (this occurs in bone
that is deficient in calcium following longstanding hyperparathyroidism that is treated with

parathyroidectomy)
- Acute pancreatitis
- CKD
- Respiratory alkalosis
Investigation into hypocalcaemia should include the following
- Measure corrected calcium, as this is most commonly an artefact of low albumin

- Phosphate, vitamin D and magnesium levels
- Phosphate is raised in CKD, hypoparathoidism, vitamin D deficiency, and
hypomagnesaemia
- Phosphate is low in pancreatitis, respiratory alkalosis, and bone disease
- PTH, even normal PTH in the presence of hypocalcaemia indicates hypoparathyroidism
It is always essential to do an ECG in hypocalcaemic patients as they may have a prolonged QT
interval
Acute symptomatic hypocalcaemia should be treated with IV calcium gluconate, this is normally
20ml 10% calcium gluconate diluted in 100ml 0.9% saline given over 10 minutes
- The patient should then be given a continuous calcium infusion, with regular adjustment of
dose dependent on plasma calcium concentrations. When the patient is able, there should
be oral calcium and vitamin D metabolites given.
Treatment of chronic hypocalcaemia is dependent on the cause
- In hypoparathyroidism the aim of treatment is not normalisation of calcium levels (as this
will likely cause renal stones) but rather reduction of symptoms. Most patients are given
vitamin D analogues e.g. calcitriol, and some will require additional calcium supplementation
Disorders of Potassium Balance
Hyperkalaemia
The normal reference range for potassium is 3.5 – 5.3 mmol/L
- Acute hyperkalaemia becomes dangerous when >6.0 mmol/L, particularly in the elderly or
those with pre-existing cardiac disease
- Urgent treatment is required when K+ >6.5 mmol/L
Hyperkalaemia has four main causes
- Renal: AKI, CKD, Addison’s disease, medications interfering with the renin-angiotensin axis
(ACE inhibitors, ATII blockers, NSAIDs, spironolactone)
- Increased circulation of potassium: tumour lysis, rhabdomyolysis, potassium
supplementation
- Shift from intracellular to extracellular space: DKA
- Pseudohyperkalaemia: lysis of cells in the blood sample
Raised K+ results in decreased membrane excitability in all excitable tissues, this leads to cardiac
dysrhythmias and neuromuscular depression
- Patients present with muscle weakness and absent reflexes

Investigation should include routine bloods and ABG, alongside ECG
- A typical ECG in hyperkalaemia can show tenting of T waves, flattening of P waves,

prolonged PR interval, widening of QRS complexes, and can progress through sine wave
pattern to VF and cardiac arrest
If K >6.5 or there are ECG changes, urgent treatment is required
+
- 10ml 10% calcium gluconate (or 5ml 10% calcium chloride) solution should be given over 5
minutes, this is cardioprotective and stabilises the myocardium. This should be repeated
every 20 minutes until ECG normalises
- 10 - 15 units of insulin in 50ml of 50% glucose should be given over 30 minutes to lower
serum K+
If the former is not effective, there can be nebulised salbutamol (10mg over 30 minutes) or IV
sodium bicarbonate.
Further management should include ridding the body of excess potassium
- Restricting potassium intake

- Avoidance of and stopping all potassium sparing diuretics (spironolactone, amiloride), ACEi,
ARBs, medications/fluids containing potassium, and potassium supplements
- Consider stopping digoxin and beta-blockers
- Give calcium resonium with lactulose to remove potassium from the GI tract
- Dialysis is used in resistant cases
Hypokalaemia
Hypokalaemia is serum potassium <3.5mmol/L, this can be sub-classified
- Mild 3.1 – 3.5

- Moderate 2.5 – 3.0
- Severe <2.5
Most cases are either due to GI loss (diarrhoea, vomiting) or consumption of thiazide/loop diuretics.
Other causes include
- Renal losses: thiazide or loop diuretics, hyperaldosteronism

- Transcellular shift: metabolic or respiratory alkalosis, salbutamol overdose
- Decreased potassium intake: TPN, malnutrition, anorexia
- Non renal losses: diarrhoea, vomiting, burns, fistula
Presentation is similar to hyperkalaemia, but can also involve tetany. Investigations are the same as
in hyperkalaemia
- ECG changes include flat T waves, ST depression, and prominent U waves (following T
waves)
For mild-moderate hypokalaemia treatment can be with oral potassium replacement e.g. bananas,
avocados, potatoes. KCl supplements can also be used.
For severe hypokalaemia or hypokalaemia with ECG changes, treatment should be in the inpatient
setting
- 20 – 40mmol oral potassium (sando K) QDS

- KCl slowly infused IV in normal saline, not exceeding 10mmol/hr alongside regular ECG
monitoring
Alcohol Dependence, Intoxication and Withdrawal

Alcohol Intoxication
Alcohol intoxication results in disinhibition, euphoria, incoordination, ataxia, stupor and coma
- Obtain a collateral history from a less/none intoxicated friend or relative

- Examine the patient for signs of chronic liver disease, trauma, or infection
Complications
There are many potential complications to alcohol intoxication
- Acute gastritis causing nausea and vomiting, abdominal pain, and GI bleeding
- Respiratory depression, inhalation of vomit (with ARDS), and hypothermia may accompany
profound sedation
- Hypoglycaemia
- Alcoholic ketoacidosis
- Accidental injury, particularly head injury and subdural haematoma
- Rhabdomyolysis and acute kidney injury
- Infection
Investigations
Where patients are comatose following ingestion of alcohol, measurement of blood alcohol level can
indicate if their GCS is due to the alcohol itself
- 80mg/100ml is the legal drink-drive limit

- Alcohol level >300mg/100ml is extreme intoxication leading to drowsiness and coma
- Levels >400mg/100ml may be fatal
Other investigations should blood tests
- U&E, glucose, amylase, lactate, and ammonia are essential. Other routine bloods should also
be taken
- ABG
Management
Management should follow A to E assessment, ensure the airway is clear of vomitus and nurse in the
recovery position.
For mild to moderate intoxication there may be a need to admit for IV rehydration and observation
- Ipecacuanha, gastric lavage, or charcoal are not indicated
Alcohol Dependence
There are many factors that can contribute to the likelihood of a person developing a substance
misuse or dependence disorder
- Genetic factors are key

- Childhood experiences such as abandonment, bereavement, abuse, and conditions like

ADHD
- Adolescent experiences such as learning or conduct disorders, family breakdown, and the
actions of peers
- Environmental factors such as the economic and physical availability of the substance,
stress, loss events, and the actions of peers
Dependence on a substance tends to follow an initial social use, followed by the development of
problematic use. This transforms experimental/casual substance use through a more regular pattern
of use into a compulsion
The states of change model for understanding motivation and action towards change in harmful
patterns of drug use can be used to tailor treatments to the individual
- Pre-contemplation: the user does not recognise that the problem exists
- Contemplation: the user accepts that there is a problem, and begins to weigh up the positive
and negative aspects of continued drug use
- Decision: the user decides whether to continue using the drug
- Action: the user attempts change
- Maintenance: this is a stage of maintaining gains made and attempting to improve those
areas of life that have been harmed by drug use
- Relapse: a return to previous behaviour, but with the possibility of gaining useful strategies
to extend the maintenance period on the user’s next attempt
Assessment of Dependence
Brief screening tools such as CAGE can be used to indicate if a patient is at risk of alcohol
dependence
- Have you ever considered cutting down on alcohol?

- Does it ever irritate you when people suggest you reduce your alcohol intake?
- Do you ever feel guilty for drinking alcohol?
- Do you ever need to have a drink in the morning?
AUDIT-C or full AUDIT questionnaires can also be used
Try to quantify how much alcohol the patient is drinking in a day/week, what situations they are
drinking in, if they are drinking every day, and whether they have tried to stop drinking before
- The recommended alcohol intake for men is 3 – 4 units per day, and women 2 – 3 units per
day. Everyone should have at least 2 alcohol-free days per week
- Binge drinking is defined as >8 units for men >6 units for women in one sitting
Dependence syndrome has several key features which should be assessed. Be aware that denial is a
common defence mechanism used by alcoholics, and therefore history may not be accurate
- Salience (a change in life priorities to primacy of drug seeking behaviour)

- Tolerance, the patient will be drinking more alcohol than they did previously to achieve the
same effect
- Impaired control of consumption, the patient is unable to stop drinking alcohol when they
have started
- Compulsion, even when the patient wants to resist drinking they will feel compelled to do so
- Withdrawal syndrome, the user will learn to anticipate and avoid withdrawals alongside
relief use
- Continued drug use despite harm
- Reinstatement of the previous pattern of drug use after abstinence
Physical examination of patients does not usually reveal any findings. However, there may be signs
of chronic liver disease, parotid enlargement, rhinophyma, peripheral neuropathy, or signs of
alcohol withdrawal.
Investigations
There are also several investigations that can be used to estimate recent alcohol consumption
- Breath or blood alcohol levels

- FBC, as MCV is typically raised in alcoholism
- LFTs can give a good indication of alcoholic liver disease
o Gamma-GT will be raised in chronic alcohol abuse, but also following binge drinking
o AST and ALT are both raised, but AST:ALT >2
- Clotting screen
- U&Es
- Fasting glucose, as chronic pancreatitis can lead to diabetes mellitus
Management
Encouraging abstinence in alcohol dependence can be with brief intervention (low intensity short
interventions in primary care) and motivational interviewing (the interviewer aids the patient in
explaining why they should change their behaviour and how to change it)
Some patients may benefit from controlled drinking rather than abstinence
Controlled Drinking Abstinence

<40 >40
Early detection Long duration
Minimal dependence Dependence evident
No medical/psychiatric comorbidities Medical/psychiatric comorbidities
Social stability Poor social support
Compliance Poor attendance
Patient preference Patient preference
Management of alcohol withdrawal is with detoxification, see below. Following detoxification, there
needs to be support to maintain sobriety
Psychological interventions include
- Brief interventions and motivational interviewing, as above

- Cognitive behavioural therapies can include relaxation training, assertiveness, drink refusal
skills, and developing alternative coping strategies
- Relapse prevention
- Alcoholics anonymous, this is a 12 step programme that takes place in a group setting
There are also pharmacological interventions available to aid abstinence
- Disulfiram inhibits ALDH, leading to a build-up of acetaldehyde causing unpleasant

symptoms of flushing, headache, nausea and vomiting, and hypotension. The dose is titrated
to the level that creates the reaction when drinking
o It is important to emphasise the danger of drinking when taking disulfiram
- Acamprostate enhances GABA transmission, reducing cravings
- Naltrexone is opioid antagonist that decreases the pleasurable effects of drinking alcohol
Withdrawal from Alcohol
Withdrawal begins 6– 72 hours after the last drink, and therefore should be considered in all in-
patients with acute confusion a few days after admission
- Signs include hypotension, tachycardia, and those of delirium tremens
The severity of alcohol withdrawal symptoms is assessed with the CIWA tool, this looks at the
intensity of several symptoms, indicating the likelihood of delirium tremens
- Nausea and vomiting

- Coarse tremor
- Paroxysmal sweats (diaphoresis)
- Anxiety
- Agitation
- Tactile disturbances
- Auditory disturbances
- Visual disturbances
- Headache
- Orientation and clouded sensorium
Withdrawal from alcohol passes through several stages
6 – 24 Hours Insomnia, tremor, anxiety, GI upset, headache, diaphoresis, palpitations,

anorexia
24 – 72 Hours Withdrawal seizures (generalised tonic-clonic)
>72 Hours Delirium tremens: hallucinations, disorientation, tachycardia, hypertension,
fever, agitation, diaphoresis
Delirium Tremens
Delirium tremens (DTs) is a medical emergency, and can occur in complete or partial withdrawal.
There is a triad of features associated with DTs
1. Delirium. This is fluctuating and associated with clouding of consciousness and

disorientation in time, place and person
2. Hallucinatory experiences. These are usually vivid, chaotic, bizarre and can affect any
modality, but visual hallucinations are commonest and classically frightening
3. Tremor
The symptoms are fluctuant, and tend to be worse during the night. The condition generally lasts
around 3 – 5 days, and recurrent attacks are common once the initial attack has occurred.
Investigations
Alcohol withdrawal is a clinical diagnosis, but investigations can help to assess associated medical
problems
- FBC, LFTs, clotting, blood glucose, blood alcohol levels, U&Es, amylase
- ABG should be performed to look for metabolic acidosis
CXR should be considered as co-existing pneumonia is common. ECG should be performed to

exclude arrhythmia
Detoxification
This involves medication to reduce withdrawal symptoms, nutritional supplementation, and

psychological support
Where patients are uncomplicated, and there is a low risk of seizure/DTs there can be detox in the
outpatient setting
- There is usually chlordiazepoxide 20 – 30mg QDS gradually reduced over 5 – 7 days,

alongside 100mg thiamine TDS for 4 weeks
Admission for detox is recommended in patients with severe symptoms. Where patients present
with alcohol withdrawal, A to E assessment is essential
- Chlordiazepoxide or diazepam are used to ease withdrawal symptoms, these should also be
used in delirium tremens at an adequate dose to control agitation
- If there are alcohol withdrawal seizures there should be use of diazepam 10mg IV, alongside
a 100mg loading dose of chlordiazepoxide
- 500mg IV pabrinex TDS should be given in all patients to prevent Wernicke-Korsakoff’s
syndrome for three days
o Pabrinex contains B vitamins (thiamine (B1), riboflavin (B2), pyridoxine (B6)),
nicotinic acid, folate, vitamin C and vitamin E
o Patients can then be switched to oral thiamine 100mg TDS and vitamin B co-strong
TDS
Alcohol Related Syndromes
Pathological Intoxication
Pathological intoxication is incredibly dangerous, and can follow ingestion of only a small amount of
alcohol. This is the murder or injury of another person, followed by complete amnesia of the event
- The patient is observed to be in a trance-like state (automatism), and EEG abnormalities

support this
It can be used as a defence in murder cases “mania a potu”, but is incredibly rare.
Alcohol Related Amnesia
Transient amnesia related to intoxication is relatively common, the amnesia stems from inability to
recall memories rather than register them. Once experienced it is more likely to become a regular
occurrence
- This can be total with abrupt onset and when the patient recovers from intoxication there is
no subsequent recall of events
- It can also be patchy amnesia, where there are indistinct boundaries with islands of memory
An example of this is journey syndrome, where patients regain awareness and they are in a strange
place and cannot recall how they arrived there
Alcoholic Hallucinations
Transient hallucinatory experiences are common in alcoholism, and are fleeting experiences of
varying perceptual disturbances. They are usually intermittent, lasting for weeks to months
- Auditory hallucinations are commonly unformed noises or snippets of music/voices

- Phonemes (running commentary or 2nd person voices) are typical, these may be favourable
or derogatory
These hallucinations do not cloud consciousness and are not related to any form of formal thought
disorder.
Alcoholic hallucinations can occur while the patient is intoxicated or sober, but will slowly fade on
long-term cessation of drinking. Antipsychotics may be considered if this fails
Wernicke-Korsakoff’s Syndrome
10% of chronic alcoholics will develop W-K. The condition develops due to thiamine deficiency,
which occurs as the primary source of energy in alcoholism is ethanol and the patient’s thiamine
absorption is impaired
- Thiamine is a cofactor for the breakdown of glucose by the Kreb’s cycle, meaning that when
the patient is given IV glucose/ eats a meal they quickly deplete their remaining thiamine
stores
- Thiamine deficiency leads to petechial haemorrhages of the floor of the third ventricle,
mammillary bodies, brain stem, and thalamic nuclei
Wernicke’s presents acutely with 6th nerve palsy and nystagmus, clouding of consciousness and
ataxia. If untreated Wernicke’s has a high mortality, and of the patients that survive the majority will
go on to develop Korsakoff’s psychosis
- Korsakoff’s psychosis is a devastating anterograde loss of short term memory, visuospatial

impairment, and reduced insight with preservation of other functions
- Patients attempt to compensate for their loss of memory by confabulating
Alcoholic Organic Brain Damage

There is a decrease in the volume of white matter and an increase in ventricular size in alcoholics,
therefore the vast majority will show some form of cognitive impairment. This includes
- Impairment of judgement, dementia, cerebellar degeneration, and alcoholic amblyopia
Pathological Jealousy
Pathological jealousy is also known as Othello syndrome. These are delusions of infidelity combined
with excessive ruminations over the delusions
- This is a dangerous condition for the partner of the affected person
Hypothermia
Hypothermia is a core (rectal or tympanic) temperature <35, it should be suspected where

peripheral temperature <36.5. The patient may be elderly and not initially appear to be cold
- If the patient is shivering, the hypothermia is not severe. Alongside shivering there is usually
lethargy, confusion, and loss of motor coordination
- Symptoms and signs of more severe hypothermia include agitation/delirium, reduced GCS,
slowed reflexes, bradycardia, hypotension, and arrhythmias
There are many potential causes of hypothermia, that can be divided into primary and secondary
groups
- Primary hypothermia is due to environmental exposure with no underlying medical

condition causing disruption of temperature regulation
- Secondary hypothermia can include
o Decreased heat production: hypothyroidism, hypoadrenalism, malnutrition
o Increased heat loss: vasodilation, burns, erythroderma
o Impaired thermoregulation: CNS trauma, stroke, sepsis, pancreatitis
Investigations
ECG may show J-waves (small upward deflections after the QRS). Other investigations can include
- U&Es, plasma glucose, amylase, TFTs, FBC, coagulation studies (DIC is a complication), and
blood cultures
Management
Treatment should follow an A to E approach, but with minimal exposure
- Aim for a temperature rise of 0.5C per hour using warm IV fluids, warm oxygen, and
blankets
o If temperature increases too quickly there can be peripheral vasodilation and shock
- Where a patient is in cardiac arrest, warming should occur as quickly as possible
o In order to raise temperature quickly, warmed fluids should be infused into all
orifices with access e.g. IV, through a catheter or NG tube
Patients should not be pronounced dead until they are re-warmed sufficiently.
Transient Loss of Consciousness

Differential diagnosis for a blackout or ‘funny turn’ can be summarised in the following flow chart
Patients should be stabilised first with an A to E assessment
- Specific blood tests when IV access is established should include

o FBC, U&Es, and glucose
- It is essential to take a 12-lead ECG
History
History in transient LOC should take a before, during, and after format
- Before the collapse

o Pre-syncope symptoms and warning signs
o What was the patient doing at the time
o Any focal neurological signs or aura
o Any palpitations
- During the collapse
o Any LOC
o Did anyone notice a change in colouring
o Any seizure movement, tongue biting, or incontinence
- After the collapse

o How long did it take the patient to recover
o Any residual symptoms e.g. weakness, confusion
o Any injury
- A witness account of the episode can be very useful
There should also be discussion of whether the patient has had LOC before, how frequently this
occurs, and the duration of LOC
Examination
Focussed examination should be of the cardiovascular and neurological systems
Investigations
Other, more specific, investigations can include
- Lying-standing blood pressure, tilt-table testing

- Echocardiography
- For suspected epilepsy CT or MRI may be appropriate, but are not usually undertaken in the
acute phase
Cardiogenic Causes
In syncope there is a brief (<20 seconds), complete loss of consciousness
- Light-headedness, preceding nausea, sweating and blurred vision are common pre-syncopal
symptoms
- Recovery from syncope is usually spontaneous and total following a few seconds of
disorientation
Psychogenic Causes
Anxiety disorder, if severe, can lead to blackout. This is suggested by the following features
- History of anxiety, and feeling of emotional distress

- Situational triggers
- Difficulty breathing, chest tightness, and globus hystericus
- Blurred vision, light headedness, tingling
Non-epileptic attack disorder (NEAD) is a syndrome of recurrent dissociative seizures
- Features suggesting NEAD include: long duration, gradual onset, fluctuating course, violent
thrashing movements, side-to-side head movement, recall
- Video-electroencephalogram (VEG) is the gold standard for diagnosing NEAD, with the EEG
showing no epileptiform activity during seizure
Neurogenic Causes
Epilepsy is suggested by the following features
- Lateral, deep, tongue biting

- Head turning to one side, unusual posturing

- No memory of abnormal behavior before event, and confusion for >2 minutes following the
event
- Déjà vu and jamais vu
Vertebrobasilar insufficiency is caused by atherosclerosis
- Symptoms occur when changing head position due to temporary occlusion of one vertebral
artery
- Vertigo, nausea and vomiting, headache
- Symptoms of posterior circulation stroke e.g. ataxia, visual field defects, diplopia, nystagmus
Diarrhoea
Acute Diarrhoea
There is no universally agreed definition for diarrhoea, but it can be defined as the abnormal
passage of loose or liquid stools (types 6 + 7) more than three times daily and/or a volume of stool
>200g/day
- Acute diarrhoea lasts for less than two weeks

Diarrhoea can be a cause of severe dehydration and hypovolaemic shock, features of dehydration
are described below
Mild Moderate Severe

Lassitude Apathy Profound apathy
Anorexia Tiredness Weakness
Nausea Dizziness Confusion (leading to coma)
Light-headedness Muscle cramps Shock
Postural hypotension Dry tongue/ sunken eyes Tachycardia
Reduced skin turgor Peripheral shut down
Postural hypotension SBP <90
Tachycardia Anuria
Oliguria
The initial assessment of a patient presenting with acute diarrhoea should therefore follow an A to E
approach
- Stabilise airway and breathing as required

- Assessment of circulation is key in these patients
o IV access and fluids are generally required
o Bloods to send should include: FBC, U&Es, CRP, LFTs, TFTs, VBG and where
there are signs of sepsis there should be blood cultures
o Catheterisation may be required in the very unwell
- Assess conscious level in disability
- Expose the patient to see if there is any evidence of PR bleeding, rash, or further
signs of dehydration
Following stabilisation there can be history and focussed examination
Assessment
It is important to consider the underlying cause, which may be different in newly presenting patients
and in-patients
- Other symptoms such as fever, abdominal pain, nausea, and vomiting

- Stool frequency
- The nature of the stool should be discussed
o Bloody (see below)

o Mucus: IBS, colorectal cancer, polyps, IBD
o Pus: IBD, diverticulitis, abscess
o Watery
o Steatorrhoea
- Recent travel
- Contact with other people with similar symptoms
- Possible sources of food poisoning
- Recent changes in medication, or use of antibiotics
Clarify in the past medical history whether the patient is immunocompromised, or taking any
medications that could lead to immunocompromised
- Ensure in the social history that the patient’s job is not a public health risk e.g. chef
Incubation periods can indicate a potential cause
- Viruses are usually incubated for around 1 day, bacteria for a few hours to a few
days, and parasites up to two weeks
It is also important exclude any symptoms associated with the diarrhoea that may warrant
admission
- Persistent vomiting
- Painless, watery, high-volume diarrhoea as this is a risk of dehydration
Lower GI red flags include
- Age >50
- Rectal bleeding
- Recent change in bowel habit
- Nocturnal symptoms
- Unexplained or unintentional weight loss
- Iron deficiency anaemia
- Family history of colorectal cancer or IBD
Focussed examination should be abdominal with a PR examination
- Assess for masses, PR bleeding, or impacted faeces

- Oral ulcers, clubbing, and signs of anaemia are also very important to assess
Osmotic Secretory Motility Combined

Hypolactasia Toxins (c diff) IBS IBD
Drugs Peptides (vipoma, ze, Diverticular Colon cancer
carcinoid)
Malabsorption Drugs
Causes of Acute Diarrhoea without Blood

Infection (gastroenteritis) is a common cause of acute diarrhoea in both adults and children.
Common pathogens include
- Clostridium difficile infection often follows treatment with clindamycin or broad

spectrum antibiotics, it can cause pseudomembranous colitis
- Cholera presents with profuse watery diarrhoea without abdominal pain or fever
- Parasites such as giardia, entamoeba, cyclospora, and cryptosporium will cause a
prolonged diarrhoea for >14 days usually without vomiting
- Rotavirus is very common in young children and is self-limiting within 1 week
- Norovirus is predominantly a vomiting illness, but is accompanied by watery non-
bloody diarrhoea for 1 – 2 days
Many different medications can cause diarrhoea as a side effect. This includes magnesium antacids,
NSAIDs, PPIs, antibiotics, metformin, and thyroxine
Other non-infective causes include
- Hyperthyroidism
- Malabsorption
- IBS
- Crohn’s disease
- Lymphocytic colitis
o This is associated with medications, coeliac disease, older people
o This leads to a profuse non-bloody diarrhoea with a normal mucosal
appearance but intraepithelial lymphocytes on biopsy
o It responds well to budesonide, or other systemic steroids
- Constipation with overflow diarrhoea
Non-bloody diarrhoea tends to be from the small bowel. This is larger in volume and typically
painless.
Causes of Acute Diarrhoea with Blood
Infection (gastroenteritis) is a common cause of acute bloody diarrhoea in both adults and children.
Common pathogens include those that target the large bowel
- Campylobacter jejuni, this causes profuse watery bloody diarrhoea with fever and
cramps. There is often a 24-hour prodromal flu-like illness
- Salmonella (particularly serogroup D), this causes bloody diarrhoea with fever and
cramps that last from 4 – 7 days
- E.coli 0157, this usually causes a mild self-limiting diarrhoea for <72 hours. VTEC
E.coli can lead to haemorrhagic colitis and haemolytic uraemic syndrome
- Shigella, this causes an acute watery diarrhoea that may accompanied by mucus, pus
or blood for around 3 days
- Schistosomiasis
Other non-infective causes include
- Diverticulitis
- Ischaemic colitis
- Ulcerative colitis
Bloody diarrhoea tends to be from the large bowel. This is smaller in volume and painful
Stool sample for MC&S and OCP should be sent (3 samples on 3 different days) if the patient is
systemically unwell, immunocompromised, the diarrhoea is prolonged or following foreign travel, or
if there is blood or pus in the stool
- Pathogens routinely looked for include campylobacter, cryptosporidium, E.coli,

salmonella, and shigella
- There may be red or white blood cells in the stool, particularly in shigella and
campylobacter
If the patient is systemically unwell there should be AXR to rule out toxic megacolon
- Further imaging with flexible sigmoidoscopy can be used if there is a high suspicion
of IBD.
Management
Mild diarrhoea is managed supportively, with attention to fluid balance and electrolyte depletion
- Anti-secretory medications e.g. racecadotril can be used alongside rehydration

treatment
- If the patient is severely dehydrated, shocked, or unable to retain oral fluids it may
be necessary to admit to hospital for IV fluids
Symptomatic treatment may be beneficial, but should only be used where there is a clear diagnosis
of the underlying cause of the diarrhoea
- Antimotility agents e.g. loperamide 2mg after each loose stool (max 16mg/24hr),
codeine phosphate 30mg TDS. These should be avoided where the cause is
infectious
- Antispasmodics e.g. mebeverine, hyoscine butylbromide
Antibiotics can be used in certain cases of infectious diarrhoea
Public Health Reporting
Advice should be sought from the local health protection unit regarding the need for investigations if
- The patient is a suspected public health hazard e.g. food handlers, healthcare
workers, elderly residents in care home
- There is an outbreak of diarrhoea where isolating the organism may help pinpoint
the source of the outbreak.
- The patient is infected with certain organisms that may cause serious clinical
sequelae e.g. E. coli O157
Food poisoning is a notifiable disease
Chronic Diarrhoea
Chronic diarrhoea is the passage of abnormally large volumes of loose stools for >14 days
- Persistent diarrhoea tends to suggest a non-infectious pathology
Colonic
- Diverticular disease
- Colon cancer
- Colitis: ulcerative colitis, Crohn’s disease, microscopic colitis, ischaemic colitis
Small bowel
- Malabsorptive conditions: coeliac disease, bile salt malabsorption (ileal resection,

cholecystectomy), Whipple’s disease, tropical sprue, small bowel bacterial overgrowth,
chronic pancreatitis, cystic fibrosis
- Lactose intolerance
- IBS
Endocrine
- Hyperthyroidism
- Autonomic neuropathy from diabetes
- Addison’s disease
Chronic infection e.g. cryptosporidium, giardiasis
Assessment
Red flags for chronic diarrhoea include
- Weight loss
- Rectal bleeding
- Diarrhoea persisting >6 weeks in patients >60
- Family history of bowel or ovarian cancer
- Abdominal or rectal mass
- Anaemia in a man or post-menopausal woman
- Raised inflammatory markers
Where colorectal cancer is suspected there should be urgent two-week wait referral for further
investigation
Investigations
Blood tests can include
- FBC, LFTs, TFTs, ESR/CRP

- Tests of malabsorption: calcium, B12, folate, iron studies
- Antibody tests for coeliac disease e.g. EMA, TTG
Stool for MC&S and OC&P may be appropriate
- There can be additional testing for faecal elastase, chymotrypsin, and fat
Further investigation where malabsorption is suspected can include
- Endoscopy and small bowel biopsy

- Barium follow-through
- Pancreatic CT scanning or ERCP/MRCP
Flexible sigmoidoscopy or colonoscopy are important where colonic or terminal ileal disease are
suspected.
Gastroenteritis
Gastroenteritis is the term used to describe a condition in which there is diarrhoea ± vomiting from
an infectious origin
- Common viral causes include norovirus, rotavirus, adenovirus

- Common bacterial causes include campylobacter, E.coli, salmonella, and shigella
- Common parasitic causes include cryptosporidium, entamoeba, and giardia
Presentation
A to E assess patients initially to stabilise before any further assessment
- Treat dehydration early

- Exclude any severe abdominal pathology e.g. appendicitis
Features of infection with common organisms are summarised below
Organism Clinical Features Incubation

Salmonella Bloody diarrhoea with fever and cramps 8 – 24 hours
Norovirus Predominantly vomiting, with watery 12 – 48 hours
diarrhoea
Rotavirus Diarrhoea in young children 1 – 7 days
Campylobacter Profuse watery bloody diarrhoea with fever 2 – 5 days
and cramps
E.coli Usually mild self-limiting diarrhoea for <72 12 – 72 hours

hours
VTEC E.coli can lead to haemorrhagic colitis
and haemolytic uraemic syndrome*
Shigella Acute watery diarrhoea that may 2 – 3 days
accompanied by mucus, pus or blood. Fever
and abdominal pain
C.difficile Diarrhoea following antibiotics 1 – 7 days
Cholera Profuse watery diarrhoea without abdominal 2 – 5 days
pain or fever
Cryptosporidium HIV/immunocompromised, prolonged 4 – 12 days
diarrhoea
Giardia Prolonged diarrhoea 1 – 4 weeks
*Haemolytic uraemic syndrome is a condition characterised by AKI, haemolytic anaemia, and

thrombocytopaenia
The setting which infective diarrhoea should be managed is dependent on presentation
- If the patient has no systemic signs, is not immunocompromised, and has not had
any recent foreign travel stool culture is not needed
o The patient should receive symptomatic treatment
- If the patient is systemically unwell there should be hospital admission
o IV fluids and empirical antibiotics (ciprofloxacin) should be given
o Stool culture is required
Investigations
The results of stool culture indicate the likely infectious cause of diarrhoea. Stool culture only
routinely looks for campylobacter, E.coli, salmonella, shigella and cryptosporidium – if another
organism is suspected, it must be requested
- Polymorphs seen on direct faecal smear indicate shigella, campylobacter, or E.coli

- No polymorphs seen on direct faecal smear indicate salmonella, E.coli or C.difficile
In patients that have severe diarrhoea and dehydration, there should be blood tests
- FBC, U&Es, CRP/ESR, LFTs

- In severe cases, ABG should be considered to quickly assess electrolyte levels
Where there is evidence of electrolyte imbalance, there should be ECG
Management
In-patients that develop diarrhoea should be isolated in a side-room, and the consultant in infectious
diseases notified
- Barrier nursing should be introduced for the patient

Hydration should be maintained with oral/IV fluids, and oral rehydration solutions can also be
considered
Where patients have severe symptoms, there can be symptomatic management. This is not
recommended in all cases, as it slows clearance of the pathogen
- Prochlorperazine 12.5mg QDS PRN

- Loperamide 2mg after each loose stool (max 16mg/24hr) or codeine phosphate
30mg TDS
Antibiotics can be used in certain cases of infectious diarrhoea
- Traveller’s diarrhoea can be treated with ciprofloxacin 500mg BD for 3/7 or

azithromycin 500mg BD for 3/7
o These can also be used in prophylaxis
- In parasitic infections, metronidazole is most effective
In most cases, the use of antibiotics is only in the immunocompromised or those with
severe/prolonged infection
Clostridium Difficile
C.difficile (gram positive rod) is a common cause of diarrhoea in in-patients treated with broad-
spectrum antibiotics
- Common antibiotics leading to C.diff infection include clindamycin and meropenem

Identification of C.diff infection is not with stool culture, but with C.dif toxin (A+B toxins) stool
analysis. Where C.diff infection is confirmed in a patient, the following management plan is
appropriate
- Isolate the patient in a side room and introduce barrier nursing

- Moderate disease can be treated with metronidazole PO 500mg TDS for 10/7
- Severe disease can be treated with vancomycin PO 125mg QDS for 10/7
Where antibiotic therapy is proving ineffective, faecal transplantation can be considered
A potential complication of C.diff infection is pseudomembranous colitis, in its severe form this can
lead to toxic megacolon and bowel perforation
- Where patients have abdominal distension there should be urgent ABG (to check
lactate) and AXR
o Urgent colectomy may be required
- Flexible sigmoidoscopy can identify pseudomembranous colitis through the
appearance of yellow adherent plaques on an inflamed mucosa
Irritable Bowel Syndrome (IBS)
IBS is a relapsing functional bowel disorder that has a significant negative impact on quality of life
and social functioning
- IBS is not associated with development of serious disease or increased mortality

- There is an association between IBS and psychiatric distress
- Onset is more common in middle age
Three sub-classes of IBS have been described, with equal prevalence of each
- IBS-C is constipation dominant

- IBS-D is diarrhoea dominant
- IBS-M is mixed disease
Presentation
The Rome III Diagnostic criteria for IBS should be used
- >6 month history of intermittent or continuous abdominal pain/discomfort, bloating, and

change in bowel habit
IBS can also be diagnosed by the Manning criteria
- Abdominal pain relieved with defaecation and altered stool frequency/form alongside 2 of
o Altered passage of stool e.g. straining, urgency, tenesmus
o Bloating
o Aggravation of symptoms by eating
o Passage of mucus PR
Additional symptoms can include fatigue, nausea, backache, and dyspareunia
It is essential to rule out any GI cancer red flags, and refer urgently if these are present
Investigations
IBS is no longer considered a diagnosis of exclusion, however in diagnostic uncertainty there should
be investigation to rule out significant pathology e.g. colon cancer and IBD
All patients should have the following investigations, all of which will be negative/normal in IBS
- FBC
- ESR and CRP
- Coeliac antibody screen (EMA, TTG)
- Faecal calprotectin
- CA-125 if there is any suspicion of ovarian cancer
Additional investigations are not routine, but can be indicated in certain patients
- TFTs
- Imaging with USS, sigmoidoscopy, or barium enema
- FOBt
- Faecal OCP and MC&S
- Hydrogen breath test
Management
Reassurance and explanation of the condition are essential. Conservative management can be
effective in many patients
- Reduction in stress and increased physical activity

- Drink plenty of fluids, reduce/increase fibre as per diarrhoea/constipation, reduce
consumption of lactose
- Introducing probiotics to the diet can be beneficial

Pharmacological treatments in IBS are thought to potentially be creating a placebo effect to relieve
symptoms
- Loperamide can be used for diarrhoea

- Antispasmodics should be used for abdominal pain and spasm e.g. mebeverine, hyoscine
butylbromide, peppermint oil
- Laxatives may be required for constipation, lactulose should be avoided
- Antidepressants may be of benefit e.g. low dose TCA, SSRI
Complementary therapies such as acupuncture can also be highly effective in IBS patients
Inflammatory Bowel Disease

Inflammatory bowel diseases are idiopathic immune mediated chronic disorders
- Peak incidence is 15 – 40 years, and are often associated with other autoimmune disorders
The cause is unknown but thought to be multifactorial, potentially related to vitamin D or bacterial
antigen triggers
- Smoking increases the risk of Crohn’s disease but is thought to decrease the risk of
ulcerative colitis
- pANCA antibodies are more associated with UC, and ASCA antibodies are associated with
Crohn’s
The main differences between the two are summarised below
Crohn’s Ulcerative Colitis

Small and Large Bowel (not rectum) Only large bowel, rectum is always involved
Inflammation is not continuous (skip lesions) Continuous inflammation
Bowel wall is thickened, with a cobblestone The bowel wall will be thin with a loss of
appearance vascularisation
Strictures and deep fissures, fistulae No strictures, fissures or fistulae
Granulomatous formation No granuloma
Inflammation is through the mucosa to the Inflammation is symmetrical and confined to
muscle the mucosa
Increased WBC count Increased WBC count
Crohn’s Disease
Crohn’s disease is an inflammatory bowel disease that can affect any part of the GI tract. Typically,
the proximal colon and terminal ileum are particularly affected
- The inflammation in Crohn’s is transmural, granulomatous, and occurs in skip lesions

- Crohn’s can be complicated by the formation of strictures, fissures, and fistulae
Presentation
Patients will typically present with chronic diarrhoea (>6 weeks), this may be bloody or associated
with mucus, and abdominal pain
- Weight loss is common, and in children there may be poor growth and delayed puberty
- Systemic symptoms of fatigue, malaise, anorexia, and fever may also occur
On examination there may be extra-intestinal manifestation of disease visible
- Apthous ulcers of the mouth

- Signs of anaemia
- Anal and perianal lesions e.g. skin tags, abscesses, fistulae
- Clubbing, erythema nodosum, pyoderma gangrenosum
- Conjunctivitis, episcleritis, uveitis
- Enteropathic arthritis, this can present as ankylosing spondylitis
- Perineal scarring
Investigations
Laboratory investigations should include FBC, CRP, U&Es, LFTs, and stool culture (OC&P, C.Diff toxin)
- High CRP indicates active disease

Diagnosis is made primarily on endoscopic and histological investigation
- Ileocolonoscopy with biopsy from the terminal ileum and any affected colonic segment is
first-line to establish diagnosis
o The mucosa may be bleeding and friable, and have a cobblestone appearance with
ulceration and skip lesions
Where Crohn’s disease is confirmed there should be further investigation to examine the location
and extent of disease in the small bowel. These investigations can also show strictures, fistulae, and
abscesses
- Barium studies or small bowel follow-through

- CT and MRI enterography
Management of Flare
In flare of Crohn’s there should be A to E assessment and stabilisation of the patient
- IV fluids and monitoring of stools with a Bristol stool chart

- Bloods should include inflammatory markers and electrolytes
AXR to rule out toxic megacolon is important
Ensure to give prophylactic LMWH due to the risk of VTE
Induction of remission is essential where patients are suffering flares of disease, and this can be with
IV or oral corticosteroids
- If the patient has had >2 flares within 12 months they should be offered azathioprine or
mercaptopurine in addition to steroids. TPMT activity should be measured prior to
prescribing these medications, low activity is a contraindication
Where patients do not respond to the above therapy, they should be offered infliximab or
adalimumab (continue for 12 months and then review)
- If anti-TNF fails, the patient may require surgery

Management of Stable Disease
Maintenance therapy in Crohn’s is given to prevent relapse of disease, smoking cessation is very
important
In patients where remission was induced by steroids, systemic maintenance therapy can be with
azathioprine or 6-mercaptopurine monotherapy (5-ASA are not effective in Crohn’s)
- Where these are not tolerated, methotrexate (and folate) can be used
- Some patients will require continuation of anti-TNF treatment
3 monthly monitoring of renal, liver, and bone marrow function is important where patients are
taking 5-ASA, immunomodulatory drugs or biological agents. Patients should be made aware of their
increased risk of osteoporosis
Ulcerative Colitis
Ulcerative colitis is a chronic inflammatory disease of the colon; it may be solely distal (proctitis/
proctosigmoiditis) or more extensive (pancolitis)
- The inflammation in UC is mucosal, continuous, and symmetrical. It always starts distally and
extends proximally
Presentation
Patients will usually present with bloody diarrhoea. There may be associated symptoms of colicky
abdominal pain, urgency, or tenesmus
- Proctitis can present with constipation and rectal bleeding

- There may be additional malaise, fever, weight loss, and extra-intestinal manifestation
o Related to disease activity: erythema nodosum, aphthous ulcers, episcleritis,
pyoderma gangrenosum, uveitis
o Not related to disease activity: sacroilitis, enteropathic arthritis, PSC
There can be abdominal tenderness on palpation, distension, or abdominal mass
Mild disease is <4 stools/day, moderate is <6 bloody stools/day, and severe is >6 bloody stools/day
with features of systemic upset (temperature >38, HR >90, anaemia, raised ESR/CRP)
Investigations
Laboratory investigations should include FBC, LFTs, U&Es, ESR and CRP, vitamin B12 and folate, and
stool culture
- Faecal calprotectin can also be used to indicate diagnosis of IBD

Diagnosis usually follows colonoscopy with multiple biopsies (at least two biopsies from five sites),
usually this is flexible sigmoidoscopy
- This will usually show a friable, ulcerated mucosa. Histology usually shows cryptitis and crypt
abscess
Management of Flare
In flare of UC there should be A to E assessment and stabilisation.
- IV fluids and monitoring of stools with a Bristol stool chart

- Bloods should include inflammatory markers and electrolytes
It is also important to AXR and rule out toxic megacolon
Ensure to give prophylactic LMWH due to the risk of VTE
Induction of remission in UC can be achieved by several different means
- Where people have mild procitis they can be offered topical ASA ± oral ASA e.g. mesalazine,
if this is not tolerated oral corticosteroids can be used
- Where people have mild colitis they can offered oral ASA, if this is not tolerated oral
corticosteroids can be used
- Where people have moderate to severe disease they should be offered IV corticosteroids. If
this is not effective biological agents (infliximab) can be used as rescue therapy
- Surgery can be curative in UC, but is seen as a last resort
o This includes proctocolectomy and temporary loop ileostomy with ileo-anal pouch
formation later
Management of Stable Disease
Maintenance therapy in UC is given to prevent relapse and flare of disease
- Oral or topical 5-ASA is the commonest maintenance therapy

- In more severe disease immunosuppressant agents e.g. azathioprine, 6-mercaptopurine are
used
Coeliac Disease
Coeliac disease is an autoimmune inflammatory condition that can be known as gluten sensitive
enteropathy
- Gluten is formed of gliadins and glutenmins and is found in barley, rye, and wheat
In coeliac disease, gluten causes a T-cell mediated inflammation of the bowel due to antibody
formation against TTG (the enzyme that breaks down gluten). This leads to enterocyte damage
resulting in malabsorption
The aetiology of coeliac disease is multifactorial, but there is a strong familial tendency that has
been associated with HLA-DQ2 and HLA-B8
Presentation
Coeliac disease can present at any age, but has peak incidence in the 50s and is more common in
women
- In children there will be failure to thrive, diarrhoea or constipation, and irritability

- In adults, there are usually mild symptoms: malaise, prolonged fatigue, diarrhoea, bloating
and abdominal discomfort, weight loss, anaemia, osteoporosis, psychological conditions
- Mouth ulcers in coeliac disease are common and recurrent
Dermatitis herpetiformis rash may be present on the skin
Testing for coeliac disease should be offered to patients with autoimmune thyroid disease, IBS, type
1 diabetes, and those with first degree relatives suffering with the condition.
Investigations
- FBC (generally with iron or folate deficiency), biochemistry (albumin, calcium, phosphate,
B12, folate, and ferritin may all be low), and LFTs (transaminases may be raised)
- Coeliac antibodies (EMA, IgA TTG, DGP) are generally sensitive and specific
In patients with positive antibodies there should be referral for endoscopy and duodenal biopsy
while the patient is taking a diet containing gluten
- Histological examination classically shows villous atrophy, intraepithelial lymphocytosis and

crypt hyperplasia
DEXA scanning can be used in older patients to exclude any associated osteoporosis.
Due to differential causes of the same histological findings, in children <2, diagnosis of coeliac
disease can follow a gluten-challenge
- This involves giving the child gluten, and repeating the intestinal biopsy to see worsening
Management
Treatment is with a gluten free diet, and the patient should have an appointment with a dietician to
manage this soon after diagnosis
Supplements should be added to the diet as necessary
- This can include fibre, folic acid, iron, calcium, and vitamin D
Sustaining a gluten free diet reduces rates of complications such as splenic atrophy, intestinal
lymphoma, ulcerative jejunitis, and GI tumours
Malabsorption
Malabsorption is the inability to fully absorb nutrients from the GI tract, this results in malnutrition
Carbohydrates are starches, sucrose, and lactose
- Starch is a polysaccharide broken down by salivary and pancreatic amylase, and further
hydrolysed to monosaccharide (glucose, fructose, galactose) at the brush border
Fats are triglycerides, cholesterol, and fat soluble vitamins
- Fats are emulsified in the stomach and hydrolysed by pancreatic lipases, the fats form
micelles when they come into contact with bile in the duodenum. The lipid from the micelle
is absorbed, and the monoglycerides re-esterified to form fatty acids that are placed in
chylomicrons and transferred to the lymph. The bile from the micelle is absorbed at the
terminal ileum
Proteins are digested by pepsin from the stomach and zymogens from the pancreas to form
oligopeptides
- Further breakdown of oligopeptides occurs at the brush border, where they are absorbed as
amino acids
Vitamins and minerals have a complex route of absorption. Hydrochloric acid in the stomach will
solubilse calcium and iron for absorption
- Folate is absorbed at the jejunum only

- B12 is absorbed at the terminal ileum, only after complexing with gastric IF
- All other vitamins and minerals are absorbed preferentially at the jejunum, but also along
the small bowel
Presentation
Regardless of the cause of malabsorption, there are multiple common presenting symptoms
- Weight loss, lethargy and fatigue and common in adults

- Children are more likely to present with failure to thrive
- Chronic diarrhoea and/or steatorrhoea
Family history may be indicative of causes such as IBD, coeliac, and CF
On examination there may be signs of deficiency

- Oedema from protein malnutrition

- Purpura due to bleeding from vitamin K deficiency
- Signs of IDA
Investigations
- FBC, B12 and folate level, iron studies, serum albumin, clotting screen (for vitamin K
deficiency), calcium, and magnesium
- ESR and CRP to look for any inflammatory cause
- Coeliac antibody screen
In terms of iron studies
IDA ACD
TIBC ↑ ↓
Transferrin saturation ↓ ↓
Ferritin ↓ ↑
Assessment of stool samples can also indicate potential causes
- Faecal fat
- Faecal elastase or chymotrypsin
Imaging studies can include abdominal USS, barium follow-through for structural abnormalities, and
ileocolonoscopy + biopsy
Breath hydrogen test can be used if there is a suspicion of small bowel bacterial overgrowth
Potential Causes and Management
Mucosal diseases include
- Coeliac disease
- Isolated specific disorders
o Disaccharidase deficiency e.g. lactose/sucrose intolerance
o Glucose/galactose malabsorption
o Fat transport defects
o Micronutrient malabsorption e.g. pernicious anaemia
- Infection
o Giardiasis
o Whipple’s disease
o Tropical sprue
o Small bowel bacterial overgrowth
- IBD
Intraluminal causes include
- Pancreatic insufficiency
o Chronic pancreatitis
o Cystic fibrosis
- Defective bile salt secretion
o Cholestasis
o Terminal ileal disease
Other causes
- GI fistulae leading to small bowel syndrome

- Thyroid disorders
Chronic GI Tract Infections
Giardia
Giardiasis is due to protozoan infection
- It typically presents with diarrhoea, weight loss, and abdominal pain + bloating
Diagnosis is with OCP analysis of stool sample, treatment is with metronidazole
Whipple Disease
Whipple disease is an uncommon chronic systemic bacterial disease, caused by gram negative rod
shaped bacilli
- There can be effects in all tissues, but typically the GIT and CNS
Biopsy will show clubbing of the villi and PAS positive macrophages
It can present with weight loss, chronic cough, lymphadenopathy, hyperpigmentation, abdominal
distention, steatorrhoea, fever, arthralgia, neurological abnormalities, and heart murmur
Treatment is with antibiotics
Tropical Sprue
Tropical sprue causes chronic diarrhoea and malabsorption of fat and vitamins, leading to nutritional
deficiency, steatorrhoea and weight loss
- It is caused by an overgrowth of coliforms, and therefore treatment is antibiotics and folate

Diagnosis is with jejunal biopsy, showing partial villous atrophy – this differentiates it from coeliac
disease
Treatment is with fluid and vitamin replacement. Tetracycline is given over 6 months to reduce the
bacterial load in the gut
Small Bowel Bacterial Overgrowth
Small bowel bacterial overgrowth is characterised by nutrient malabsorption. The overgrowth of

bacteria can be due to many different causes
- Intestinal stasis
- Abnormal connections between proximal and distal GIT
- Hypochlorhydria
- Immunodeficiency
- Age
It is diagnosed by breath hydrogen test (following lactose ingestion), where there will be two peaks
of hydrogen as the food reaches the small and then large bowel – in normal people there is only one
peak
- There can also be aspiration and culture of small bowel contents

Treatment is with correction of cause and antibiotics
Chronic Pancreatitis
Chronic pancreas occurs as a result of chronic inflammation, leading to atrophy
- The commonest cause is recurrent acute pancreatitis from alcoholism

- Hereditary pancreatitis is a rare autosomal dominant condition, and presents similarly to
chronic pancreatitis but at a younger age
- Autoimmune pancreatitis can also lead to chronic pancreatitis
Presentation
Patients can present with episodes of exacerbation with intervening remission, or may be
continuous
- Abdominal pain is usually epigastric and radiates to the back. It may be relieved by bending
forward
- Malnutrition, decreased appetite, and diabetes mellitus are all common. The patient may
have steatorrhoea
- Nausea and vomiting
Chronic pancreatitis is commonest following recurrent acute episodes, and the patient will therefore
usually have a history of acute pancreatitis
Investigation
Diagnosis is difficult as there are no biochemical markers
- Faecal elastase test may be positive if there is exocrine dysfunction. Faecal chymotrypsin
may also be positive
- USS, CT scanning, or plain AXR can show pancreatic calcification
- ERCP, MRCP, or EUS can all be used
- Pancreatic biopsy is rarely used, but can show chronic inflammation and fibrosis
Management
Management is an MDT approach
- Pain management is commonly with opiates, but there can be coeliac plexus block
- Nutritional support, including CREON enzymes to help reduce malabsorption
- Diabetic control
- Alcohol abstinence
- Surgical management can include duct dilation with ERCP and complete/partial pancreatic
resection
Complications
Biliary obstruction can occur due to oedema, pseudocyst formation, fibrosis, or malignancy
- This is treated if it persists for >3 weeks. If the patient is fit there can be biliary
reconstruction surgery (hepatico-jejunostomy), but if they are not sufficiently fit there is
stenting via ERCP
Chronic pseudocysts are a common complication and are unlikely to resolve. They can become
infection, cause local compression, or bleed/rupture
- Treatment can be with endoscopic drainage, percutaneous drainage, or surgical removal

Splenic vein thrombosis can be treated with distal pancreatectomy and splenectomy
Pseudoaneurysm can occur due to erosion of arteries with pancreatic enzymes, this is commonest in
the splenic artery and can lead to GI bleeding
- Treatment is with angio-embolisation or distal pancreatectomy

Pancreatic ascites can be caused by rupture of a pseudocyst or pancreatic duct
- Ascitic tap will show fluid rich in amylase

- Treatment is with paracentesis and endoscopic stenting of pancreatic ducts
Pancreatic cancer should be suspected if the patient develops weight loss or jaundice
- If inoperable there can be palliation with stenting

- If operable there can be pancreatico-duodenectomy (Whipple’s procedure)
Bile Salt Malabsorption
Bile salts are synthesised in the liver and re-cycled through the gut after absorption at the terminal
ileum
- If there is a failure of re-absorption the excess bile acids escape into the colon where the
stimulate electrolyte and water secretion, leading to diarrhoea
Presentation
Bile salt malabsorption presents with a chronic, non-bloody, watery diarrhoea
- Diarrhoea can be continuous or intermittent

The patient may have a history of ileal disease (e.g. Crohn’s) or cholecystectomy
Investigations
Generally, the diagnosis of bile salt malabsorption is made after a trial of bile acid binder. However,
there are other methods of diagnosing the condition
- 75SeHCAT test, to assess for retention of radiolabelled bile acids

- Measurement of stool bile acid level
- Increased C4 levels
Management
The main goal of management is to control diarrhoea
- Low fat diet and oral bile acid binders are usually sufficient
o Bile acid binders include: cholestyramine, colestipol and colesevelam
Diabetic Ketoacidosis (DKA)

DKA is defined as the presence of three biochemical abnormalities, and typically occurs in T1DM
1. Ketonaemia >3mmol/L or >2+ ketonuria

2. Blood glucose >11mmol/L or known diagnosis of diabetes mellitus
3. HCO3– <15mmol/L or venous pH <7.3
DKA can be the first presentation in undiagnosed diabetes, or can be a complication of established
diabetes. Any physiological stress has the potential to initiate DKA, this includes
- Infection
- Inadequate insulin or non-compliance
- Medical illness e.g. pancreatitis, PE, hypothyroidism, MI, stroke
- Medications e.g. corticosteroids, thiazides, sympathomimetics, tacrolimus, anti-psychotics
Assessment
It is important to initially assess and stabilise patients in DKA using an A to E method
- IV access should be established at two sites where DKA is suspected, as two cannulas will be
required to deliver treatment
- Take the following bloods from the cannula:
o Plasma glucose and ketones if available
o FBC, as raised WCC can indicated infection
o U+Es to assess if there is any electrolyte abnormality, particularly hyperkalaemia
(extracellular K+ will be high, but overall K+ will be low due to loss in urine)
o VBG to see the extent of metabolic acidosis
- Give IV fluids as soon as possible
- ECG to look for evidence of ACS or arrhythmia from electrolyte imbalance
Brief history should then be obtained. Patients with DKA typically present similarly to those first
being diagnosed with T1DM
- Polydipsia and polyuria

- Weight loss
- Nausea, vomiting, and non-specific abdominal pain
- Lassitude, weakness, and fatiguability. This can progress to confusion and coma
- Breathlessness (tachypnoea or Kussmaul’s respiration)
It is important to enquire about symptoms of the common precipitating conditions, as well as recent
insulin and dietary patterns
On examination the patient will typically appear dehydrated and there may be the smell of ketones
on their breath. It is important to perform respiratory, cardiovascular (including BP), and abdominal
examinations to identify any obvious precipitant
Further investigations following A to E should include
- Urinalysis (dipstick for glucose and ketones, and send for MC&S)
- Further blood tests including TFTs, amylase, cardiac enzymes, and blood cultures as
suspected
There should also be an ECG and CXR if not already performed
Key differential diagnoses of a high anion gap metabolic acidosis (same presentation and ABG)
include
- Alcoholic ketoacidosis
- Lactic acidosis
- Metabolic acidosis due to e.g. aspirin overdose, ingestion of ethylene glycol/ methanol
- Starvation ketoacidosis
Management in Adults
Management of DKA should follow trust protocol, it is important to do this otherwise there may be
insulin dosing errors and electrolyte imbalances can develop
- DKA protocol is a pro-forma that is national, but its layout is unique to the individual trust
- It takes a stepwise approach to investigation and management, leading down different paths
as necessary
The main aims of treatment are replacement of lost fluids, resolution of hyperglycaemia and
acidosis, and correction of electrolyte abnormalities
- Following this, there can be treatment of precipitating cause
Ensure that assessment of the severity of DKA is underway to determine the management setting.
There should be admission to ITU in the following circumstances
- Ketones >6
- HCO3– <5
- pH <7.1
- Hypokalaemia
- GCS <12
- Tachycardia or bradycardia
- SBP <90
- Oxygen saturation <92%
- Heart failure, kidney failure, or other significant co-morbidity
Fluid replacement is essential, and should begin as early as possible
- Initial management depends on SBP

o SBP <90 give 500ml 0.9% saline boluses
o SBP >90 give 1000ml 0.9% saline over 60 minutes
- There should then be continuous 0.9% saline infusion at a rate of 0.5L/hr, decreasing to
0.25L/hr after four hours
- Potassium replacement is indicated where potassium is <5.5
o 3.5 – 5.5 (20 mmol) or <3.5 (40 mmol, and seek senior input)
o This should be added to the 0.9% saline
- When serum glucose reaches 14mmol/L, there should be 10% glucose at 0.125L/hr
alongside the saline as insulin dosing needs to continue until resolution of ketosis
The patient should be started on fixed rate insulin as soon as possible; this is 0.1 units/kg/hr
(maximum 15 units/hr)
- 50 units Actrapid in 50ml saline should be used, titrated to weight as above

- Normal long-acting insulin is continued alongside this as it has been shown to accelerate
resolution
Hourly monitoring of glucose, ketones, pH, electrolytes, fluid balance and bicarbonate is essential in
DKA to see progression and determine resolution
- Monitoring is with VBG as ABG is more painful and has higher infection risk. Venous pH is
typically 0.03 units lower than arterial pH
- Consider urinary catheterisation where patients have not passed urine by 60 minutes
Patients are at high risk of DVT/PE and should therefore be given LMWH
The aims of treatment are as follows. If these are not being met, insulin infusion rate can be
increased by 1unit/hr increments hourly
- Blood ketones to fall by at least 0.5mmol/L/hr

- Glucose to fall by at least 3mmol/L/hr
- Bicarbonate to increase by at least 3mmol/L/hr
When DKA is resolved (ketones <0.6 (<0.3 is best), bicarbonate >18, venous pH >7.3, anion gap <10)
the patient can eat and drink normally and should be switched to sliding scale insulin
- If DKA has not resolved by 12 hours seek specialist input

When the patient is feeling well, is eating and drink normally, and is being managed well on the
sliding scale, they can be switched to subcutaneous insulin. Give a dose of background insulin
alongside a dose of rapid acting insulin, give the patient their meal, and 30 minutes later withdraw
the IV infusion
Management in Children
DKA management in children is slightly different
- Treat with oral fluids and subcutaneous insulin if the child is not clinically dehydrated
- Treat with IV fluids and insulin if they are not alert, vomiting, or dehydrated
o Do not give a fluid bolus if pH >7.1, if a bolus is required this should be 10ml/kg
o Maintenance fluids should be 0.9% saline given at a reduced rate to avoid cerebral
oedema. Add 5% glucose when serum glucose <14mmol/L
▪ <10kg give 2ml/kg/hr
▪ 10 – 40kg give 1ml/kg/hr
▪ >40kg give 40ml/hr
o Start IV insulin infusion 2 hours after beginning IV fluid infusion at a rate of 0.05 –
0.1 units/kg/hr
Other management principles and targets are the same as in adults.
Hyperosmolar Hyperglycaemic State
HHS occurs in patients with T2DM, and is typical in elderly patients
- It usually develops due to a combination of illness, dehydration, and a non-compliance with

diabetes medications
As HHS comes on over several days, the dehydration and metabolic disturbances tend to be more
severe than in DKA. This is also in part due to the decreased thirst sensation in elderly patients.
There are no set criteria for diagnosis, however the following is generally accepted
- Hypovolaemia
- Marked hyperglycaemia >30mmol/L
- Absence of ketonaemia
- Osmolality >320mmol/kg
HHS can be caused by many different physiological stresses
- MI, infection, and stroke are common

- Medication that can induce HHS includes diuretics, glucocorticoids, β-blockers, anti-
convulsants, and substances of misuse
- Poor diabetic control and non-compliance is also very common
Patients most at risk of developing HHS are the elderly, particularly those in care homes, with
dementia, or the immunocompromised.
The increased osmolality in HHS puts patients at risk of AKI, thromboembolic events, and circulatory
collapse
Assessment
A to E assessment of these patients is essential, as HHS is a life-threatening condition
- Airway management may be required as some patients will have GCS <8, this is particularly
where plasma osmolality >440
- Assessment of circulation will demonstrate significant dehydration
- Gain IV access and commence fluid replacement
▪ Fluid replacement needs to be cautious in the elderly, so start with 1L/hr
0.9% saline
▪ Consider CVP monitoring where there is a risk of fluid overload
- Take bloods for the following
▪ Plasma glucose and ketones
▪ Serum osmolality (2(Na) + urea + glucose)
▪ U+Es to assess renal function and electrolyte abnormalities
▪ FBC, CRP, and blood cultures to screen for infection
▪ ABG, this is usually normal
▪ Cardiac enzymes or amylase as suspected
Further history and examination should attempt to identify precipitating cause
- Patients will usually present complaining of generalised weakness and lethargy, nausea and
vomiting can occur, and as the condition progresses the patient will become more confused
There should be urinalysis (glucose and MC&S), blood cultures, ECG, and CXR to help determine the
precipitating cause.
Older patients presenting with delirium can often be mistaken as an acute presentation of dementia.
There should be exclusion of acute poisoning/overdose, as well as other causes of metabolic

acidosis.
Management
The goal of initial therapy is fluid replacement; these patients may be up to 20L fluid deplete. After
the initial 1L 0.9% saline given in the first 60 minutes, the following regime should be considered
- 0.9% saline 1L/2hr for 4 hours,

- 0.9% saline 1L/6hr until rehydrated
- Potassium replacement is indicated where potassium is <5.5
- 3.5 – 5.5 (20 mmol) or <3.5 (40 mmol, and seek senior input)
- This should be added to the 0.9% saline
There should be measurement of serum osmolality, glucose, and U&Es hourly to ensure the rate of
fluid replacement is sufficient
- Fluid replacement will unmask hypernatraemia, however 0.9% saline should still be given as
it will be hypotonic to plasma in these patients
Patients should also be given fixed rate insulin at 0.05 units/kg/hr, but this should only be initiated
following fluid resuscitation if glucose levels are not falling sufficiently
- The aim is to reduce glucose levels by around 3mmol/hr, IV fluids alone are usually sufficient
to achieve this
Patients are at high risk of DVT/PE and should therefore be given LMWH as anti-coagulant
prophylaxis
Hyperglycaemia without DKA or HSS
When a patient has a hyperglycaemic BM reading, there are several steps that should be taken to
ensure appropriate management
1. Assess the patient to determine whether they are at risk of DKA or HHS (i.e. are they
clinically dry and unwell, do they have a diagnosis of diabetes)
2. Look at the blood glucose measurements over the last 24 hours, if this is an isolated event it
will not require much further investigation. If BM is persistently high, it will require more
investigation and treatment
3. Is the patient dehydrated
4. Is there any evidence of ketosis, and if so are they acidotic
5. Review the patient’s medication and see if there has been any omission of insulin
6. Is the patient taking anything that could cause hyperglycaemia e.g. steroids, artificial
feeding, food intake in hospital
7. Does the patient have an infection
8. What is the HbA1c? Thus is important to determine how treatment should continue once
the hyperglycaemia is resolved i.e. if they have a high HbA1c one should continue higher
level treatments to lower this
9. If they have an insulin pump is it malfunctioning
Inpatient hyperglycaemia is often best treated with insulin

Hypoglycaemia
Hypoglycaemia is the commonest side effect of insulin and sulfonylurea treatment; it is defined as
blood glucose <3.9mmol/L
- Clinically it is defined by Whipple’s triad: low plasma glucose, symptoms of hypoglycaemia,

and resolution of symptoms with glucose correction
Severe hypoglycaemia is defined as an episode that requires assistance from another person
Risk factors for hypoglycaemia include tight glycaemic control, malabsorption, hot weather, renal
failure, alcohol, long duration of diabetes, and increasing age
- Patients with impaired awareness of hypoglycaemia (hypoglycaemia unawareness) are at

significant risk, this often occurs after recurrent episodes of hypoglycaemia
Emergency Management of Hypoglycaemia
Assessment
Approach patients with hypoglycaemia using an A to E assessment
- When IV access is established, take routine blood tests

o Plasma glucose measurement is more accurate than capillary glucose, and should be
performed
- Ensure to stop any IV insulin infusions
Symptoms of hypoglycaemia can be divided into three groups, summarised below
- Autonomic symptoms will precede neuroglycopenic symptoms occurring at around <3.8 as

opposed to <3
Autonomic Neuroglycopenic General
Sweating Confusion Headache
Palpitations Drowsiness Nausea
Shaking Odd behaviour
Hunger Speech difficulty
Incoordination
In severe cases there may be convulsion, coma or arrhythmia
- Prolongation of QT interval on ECG is a common sign in severe hypoglycaemia

Where a patient is having multiple episodes of hypoglycaemia it is important to ask how frequently
it is occurring, whether there is any pattern, does the patient have symptoms, and what treatment
they are on
Management
Immediately locate, or ask a colleague to collect, the hypo box. There should be a hypo box on every
ward in most trusts.
In adults who are conscious, orientated, and able to swallow, management is with oral glucose
intake
- Initially the patient should be given 15 – 20g of fast acting carbohydrate

- This can be 6 dextrose tablets, 100ml Lucozade, non-diet fizzy drink, 10 jelly beans,
or 200ml fruit juice
- Repeat capillary glucose 15 minutes later
- If capillary glucose is >4, then the patient should eat 15g of long-acting carbohydrate
such as bread or digestive biscuits
- If blood glucose remains <4, repeat step 1 up to three times and if it is still low give
1mg IM glucagon/ IV dextrose
If the patient is conscious and able to swallow but disorientated
- 2 tubes of glucogel or 1mg IM glucagon

- Repeat capillary glucose after 15 minutes and proceed as above
In adults who are unconscious, unable to swallow, or highly confused and disorientated they will
require alternative treatment
- Give IM 1mg glucagon and monitor blood glucose. When blood glucose is >4 and the patient
has recovered give 15g of long-acting carbohydrate
- If IV access is available give 100ml of 20% dextrose over 10 - 15 minutes followed by a large
0.9% saline flush, and repeat until blood glucose >4 (taking BMs every 15 minutes)
Re-check BM every 15 minutes until there are two readings >4. When the hypo has been effectively
treated ensure to give a long acting carbohydrate.
Even when a patient has had a hypoglycaemic episode, insulin should not be stopped. It may be
important to review the insulin dose and adjust medications accordingly, but never stop basal
insulin.
Other Considerations in Hypoglycaemia
Where diabetic patients are experiencing recurrent hypoglycaemic episodes, or a non-diabetic

patient experiences hypoglycaemia; there are other considerations as well as emergency
management
Hypoglycaemia in diabetes can be due to many reasons
- The commonest is iatrogenesis from incorrect insulin or sulfonylurea dosing

- Renal failure (impaired medication excretion)
- Weight loss
- Lipohypertrophy at the injection site
- Malabsorption e.g. gastroparesis, development of coeliac disease
- Decreased endogenous glucose production e.g. alcohol consumption, liver failure
- Increased glucose utilisation e.g. exercise
- Any of the differentials below
Differential diagnosis of hypoglycaemia is more important where the patient is not known to be on
insulin or sulfonylurea therapy
- Addison’s disease/ adrenal crisis

- Hypothyroidism
- Alcoholism
- Insulinoma
- Anxiety disorders
- Mesenchymal tumours (non-islet cell tumour-induced hypoglycaemia) secreting substances
that interfere with glucose metabolism as a paraneoplastic syndrome
- Reactive hypoglycaemia
If a patient is having recurrent episodes of hypoglycaemia, or has hypoglycaemia in the absence of

insulin/SU therapy, there should be further investigation
Blood tests can include
- U&Es
- LFTs
- HbA1c
- Coeliac antibodies
- TFTs
- Short synacthen test
- C-peptide and pro-insulin levels
There can also be investigation into gastric emptying
Insulinoma
Insulinomas are a rare form of benign pancreatic tumours. They present with frequent attacks of
hypoglycaemia when the patient has fasted e.g. overnight or undergone exercise
Investigation will show hypoglycaemia <2.2 when fasted, alongside high serum insulin. Main
differential diagnoses are alcohol abuse and iatrogenesis with insulin or sulfonylureas
- These can be differentiated by measurement of C-peptide, indicating that the insulin is

endogenous
- There should also be measurement of SU metabolites in the urine
Imaging of the pancreas with CT/MRI or endoscopic USS is important, and biopsy should be obtained
for tissue diagnosis.
Treatment is surgical, but while it is being investigated the patient should be advised to reduce
exercise and eat frequently. Diazoxide and ocreotide can also be used to help supress insulin release
- Glucagon should be used with caution in hypoglycaemia due to insulinoma, as it often leads
to a reactive increase in insulin release
Reactive Hypoglycaemia
Reactive hypoglycaemia is the term used to describe people without diabetes that experience
recurrent, symptomatic hypoglycaemia following consumption of a high carbohydrate meal.
Patients with reactive hypoglycaemia should be advised to avoid refined carbohydrates and simple
sugars
- Small, frequent meals are best for these patients

Gastrointestinal Bleeding
Upper GI Bleed
Upper gastrointestinal bleeding (UGIB) is an emergency presentation with a high mortality. There
are three main presenting symptoms of an UGIB
1. Haematemesis is vomiting bright red fresh blood, this is associated with the highest
mortality
2. Coffee-ground vomit is vomiting of black material, this implies that bleeding has ceased
3. Melaena is passage of black tarry stools, this is usually due to acute UGIB but may also be
from a bleed of the right side of the colon
- Differentials of malaena can include iron supplements and bismuth discolouring
stool
There are many potential causes of UGIB
- Peptic ulceration, which may be associated with H.pylori or NSAIDs

- Oesophageal varices
- Erosive oesophagitis/gastritis/duodenitis
- Malignancy
- Mallory-Weiss tear
- Gastric antral vascular ectasia (GAVE). This is a condition in which the vessels of the antrum
are dilated and prone to bleeding; it is commonly associated with systemic sclerosis, portal
hypertension, and collagen disorders
- Small bowel angiodysplasia
- ENT pathology
Assessment
Patients presenting with upper GI bleed should be stabilised using an A to E assessment and kept
NBM
- Optimise airway and breathing as necessary

- Good IV access is essential. Two wide-bore cannulae (ideally grey venflon, at least pink)
should be placed
o Give fluid resuscitation using 250ml 0.9% NaCl boluses
o Consider activation of major haemorrhage protocols where indicated
- Take blood from the cannula
o FBC, with serial measurement of haemoglobin every 6 hours. Assess platelet level
o Group and save, crossmatch 4 – 8 units of blood where necessary
o Coagulation profile
o LFTs and U&Es to detect underlying disease or acute organ injury
- Urine output should be monitored from admission, catheterisation may be required
Where possible try to gather further information from the patient. It is important to try and estimate
the extent of blood loss by asking about duration, volume, and frequency
- In terms of quantifying haematemesis, a kidney dish is around 750ml when full

Also ask about
- Indications of underlying disease e.g. abdominal pain, dyspepsia, weight-loss, vomiting prior
to bleed
- Previous occurrences
- Mediations e.g. NSAIDs, steroids, anti-coagulants, anti-hypertensives (particularly beta-
blockers)
- Alcohol intake
- Previous surgery
On focussed examination it is important to assess signs of the underlying cause
- Stigmata of chronic liver disease

- PR to assess for melaena or fresh rectal bleed
Risk Assessment and Prognostication
The Blatchford score is undertaken on admission to determine patients that may need endoscopy
- Consider discharge for patients with a pre-endoscopy score of 0
The Rockall score is undertaken before and after endoscopy, this enables calculation of mortality risk
Overall Rockall score of <3 indicates a good prognosis, whereas >8 indicates a high risk of death
Further Investigation
Endoscopy is the primary diagnostic investigation in patients with UGIB
- In unstable patients with severe acute UGIB this should be undertaken immediately after
resuscitation
- All other patients should have endoscopy within 24 hours of admission
Imaging can include CXR for oesophageal perforation, CT scan and USS to detect liver disease, and
angiography if endoscopy cannot detect the site of haemorrhage
Where endoscopy detects ulceration there should be testing for H.pylori
Further Management
Continue haemodynamic support with fluids until endoscopy can take place
- Blood transfusion should be considered after loss of >30% of blood volume, or where Hb <10
Where portal varices are suspected, the bleed is immediately high risk and there should be
endoscopy as soon as possible
- Give terlipressin 2mg stat followed by 2mg every 6 hours for 72 hours
- Risk of infection is high, therefore antibiotic prophylaxis with ciprofloxacin is important
- Early endoscopy is essential, with variceal banding ligation or balloon tamponade
Definitive management of upper GI bleed is usually with endoscopy
- Endoscopic therapy should only be delivered to actively bleeding lesions, non-bleeding

visible vessels, and ulcers with adherent blood clots
o Clips or thermal coagulation can be used in combination with adrenaline
- If there is re-bleed or continued bleeding after endoscopic treatment, then interventional
radiology or surgery can be used
For non-variceal bleeding there should be endoscopy as above. Following immediate management,
there should be follow up
- H pylori eradication where indicated

- IV PPI for 72 hours followed by oral PPI for 4 – 8 weeks where indicated
- Repeat endoscopy at 6 – 8 weeks to ensure that the lesion has healed. This is not required
for most aetiologies, but is recommended in peptic ulcer
- Advise on medications to avoid
Melaena continues for up to a few days (~48 hours) following GI bleed
- If the patient complains of melaena following UGIB ensure to check ABCDE to clarify that the
stable and hasn’t had a re-bleed
Lower GI Bleed
PR bleeding presents in two main ways
4. Melaena is passage of black tarry stools, this is usually due to acute UGIB but may also be
from a bleed of the right side of the colon
5. Bright-red rectal bleeding, this can be due to two sources

- The commonest cause is bleeding from the anus, rectum, or colon
- Haematochezia can occur, where a severe upper GI bleed leads to bright red fresh
blood PR
Differentials include
- Anorectal pathology: haemorrhoids, anal fissures, anal prolapse

- Colonic pathology: diverticular disease, colonic angiodysplasia, colitis, colorectal cancer,
gastrointestinal stromal tumour
- Massive UGIB
Assessment
Stabilise the patient using an A to E approach. The following steps should be modified dependent on
the severity of the bleed; typically, lower GI bleeding is less profuse than upper GI bleeding
- Optimise airway and breathing as necessary

- Good IV access is essential in severe bleeds. Two wide-bore cannulae (ideally grey venflon,
at least pink) should be placed
o Give fluid resuscitation using 250ml 0.9% NaCl boluses
o Consider activation of major haemorrhage protocols where indicated
- Take blood from the cannula
o FBC, with serial measurement of haemoglobin every 6 hours. Assess platelet level
o Group and save, crossmatch 4 – 8 units of blood where necessary
o Coagulation profile
o LFTs and U&Es to detect underlying disease or acute organ injury
- Urine output should be monitored from admission, catheterisation may be required
History of lower GI bleed should include
- Quantity and nature of bleeding

- Abdominal pain
- Previous episodes
- Change in bowel habit
- Tenesmus
- Anal symptoms e.g. soreness, itching
Focussed examination should include assessment for signs of anaemia, abdominal examination, and
PR examination
Further investigation into GI bleed differ dependent on the likely cause of bleeding
- Flexible sigmoidoscopy is the investigation of choice for younger patients

- Colonoscopy is used where there is a suspicion of colorectal cancer
Where the source of bleeding is not identified on colonoscopy/sigmoidoscopy, there can be further
assessment
- CT angiogram
- Selective mesenteric angiography
- Isotope labelled red cell scan
- Video capsule enteroscopy
Management
Management of bleeding can usually be with endoscopy, however there may be a need for
interventional radiology or surgery where this fails
Further management should be directed at the underlying cause

Headache and Facial Pain

Headaches can be secondary to another pathological process, or occur as a primary headache
syndrome
Key differential diagnosis of headache include
Primary Headache Migraine, cluster headache, tension-type headache

Altered ICP Space occupying lesion (tumour, haematoma, abscess), idiopathic
intracranial hypertension, low pressure headache (LP, epidural)
Vascular Stroke, SAH, cerebral venous sinus thrombosis
Infection Sinusitis, meningitis, cerebral abscess, encephalitis
Rheumatological Cervical arthritis, TMJ dysfunction, temporal arteritis
Visual Straining from poor visual acuity, acute angle-closure glaucoma
Other CO poisoning, trigeminal neuralgia
Assessment
Where a patient presents complaining of headache, the approach differs dependent on whether the
patient is acutely unwell. It is best to stabilise the patient using an A to E approach initially, before
preceding to focussed examination and history taking
- On exposure in patients with headache, ensure to check thoroughly for evidence of skin rash
that could indicate meningococcal septicaemia
Take history of headache using the SOCRATES framework, and exclude the red flag symptoms below.
Headache red flags include
- Change in pattern of headache

- New headache at >50
- Headache with systemic illness
- Symptoms suggestive of raised ICP, symptoms suggestive of meningism, onset of seizures,
evidence of focal neurological deficit, or personality change
- Acute onset of the worst headache ever
Focussed examination can include full neurological examination where though relevant. However,
the following should always be examined in patients with headache
- Optic fundi
- Blood pressure
- Head and neck (scalp, neck muscles, and temporal arteries)
- Neck stiffness
Investigations
Investigations differ dependent on likely diagnosis
- Take routine bloods to screen for infection and liver/renal failure that could be leading to
encephalopathy or electrolyte imbalance
CT head is indicated where there is a suspicion of intracranial haemorrhage or raised ICP
Migraine
Migraine is a chronic, episodic, primary headache condition. There are three main sub-types of
migraine
- Migraine with aura

- Migraine without aura
- Aura without headache
Presentation
Migraine is characterised by severe unilateral pulsing pain that is disabling, often leading the patient
to have to lie down in a dark room
- Typically, the headaches last between 4 and 72 hours and can be associated with nausea,
vomiting, photophobia, and phonophobia
The headache may be preceded by an aura; this generally develops over 20 minutes. Aura symptoms
can include
- Visual disturbance e.g. fortification spectra, homonymous blurring, and geometric visual
patterns
- Numbness and paraesthesia
- Speech problems
There may also be a prodromal and postdromal phase, where the patient does not feel well in
themselves in the days preceding and following the migraine.
Management
There should always be discussion with the patient about potential trigger factors, which can be
avoided to prevent migraine. These commonly include
- Menstrual cycle (where oestrogen levels are low), stress, relaxation after long periods of
stress, sleep deprivation, anxiety, and certain dietary factors
Drug treatment for acute migraine is in a step-wise process
1. Simple analgesic ± antiemetic, an NSAID ± prokinetic antiemetic (e.g. metoclopramide,

domperidone) is commonest. Opioids should not be used
2. Rectal analgesic ± antiemetic
3. Specific anti-migraine drugs (triptans) e.g. sumatriptan, zolmitriptan. Triptans should be
trialled in turn, however if more than two are ineffective the diagnosis of migraine should be
reviewed
- Triptans can lead to immediate relapse of the migraine within 48 hours
- They are contraindicated in vascular disease, ischaemic heart disease, and
pregnancy due to vasoconstrictive effects
Prophylactic treatments are only used in severe cases, where there are >2 migraines a month that
produce disability lasting >72 hours. The doses of these drugs are built up slowly to avoid side
effects, and then titrated up until symptoms are controlled. There are many examples of
prophylactic drugs
- Beta-adrenergic antagonists, such as propranolol, are first line

- Tricyclic antidepressants and SSRIs, such as amitriptyline can be used, however they have
very sedative effects and are therefore second line
- Anti-epileptic drugs, such as topiramate and sodium valproate
- Acupuncture and botox may also be used
Tension Type Headache (TTH)
TTH is a chronic, non-disabling, primary headache. There are two main sub-types of TTH
- Episodic TTH occurs on fewer than 15 days per month

- Chronic TTH occurs on more than 15 days per month
Presentation
Typically, TTH is described as a generalised/ occipito-frontal pressure or tightness of the head with a
mild-to-moderate pain, not aggravated by physical activity
- When compared to migraine TTH is more gradual in onset, shorter in duration, more
constant in quality, and less severe
o Duration however can range from 30 minutes to 7 days
On examination there may be tension in the neck muscles. There should also be assessment by an
optometrist, as straining for vision can lead to TTH
Management
Non-pharmacological management can include physiotherapy for neck muscle tension, and advising
the patient to carry out more exercise
- The patient should be advised to avoid using too much analgesic medication for a prolonged
period of time, particularly opioid analgesics
Simple analgesia can be used for symptomatic treatment, but should be avoided in chronic TTH.
NSAIDs are first line.
Tricyclic antidepressants are the best treatment for recurring episodic TTH or chronic TTH, with the
best side effect profile seen with nortriptyline
Medication Overuse Headache
Medication overuse headache presents with the same symptoms as TTH, therefore it is important to
ask about the use of analgesics in patients that present in this manner
- This is defined as a headache present on at least 15 days per month alongside regular
overuse for at least 3 months of the following medications
o Triptans, opioids, or ergot derivatives for at least 10 days in a month
o Paracetamol or NSAIDs for at least 15 days in a month
Patients should be advised to stop taking all headache medication for at least 1 month. They should
be advised that rebound worsening of headaches will occur for 2 – 4 weeks, and considerable
willpower will be needed to overcome this
- In some cases, a 3 week course of ibuprofen can break the cycle of medication overuse
headache, but if this is not effective it should not be re-trialled
Cluster Headache
Cluster headaches are a form of terminal autonomic cephalgia
Presentation
Headaches have a rapid onset with pain centred around the eye, temple or forehead. Pain is very
severe, unilateral and lasts for 15 – 180 minutes, occurring multiple times per day. The patient will
be very agitated with the pain, and not be able to stay still
- Headaches generally occur in bouts which last 6 – 12 weeks once or twice a year
- Associated autonomic features of ipsilateral lacrimation, rhinorrhoea, nasal congestion,
sweating, eyelid oedema, or conjunctival injection are important to diagnosis
Consider in all patients ordering an MRI scan to look for skull base or meningeal pathology, or
pituitary enlargement
Management
In an acute attack, 12L/s of 100% oxygen given through a tight-fitting mask alongside 6mg of either
nasal or subcutaneous sumatriptan can reduce symptoms
Prophylaxis against cluster headache is the mainstay of management
- Verapamil 40mg BD is first-line for recurrent clusters of headaches, this can be titrated up to
960mg. Patients will require ECG monitoring for this.
- Prednisolone at 60mg gradually titrated down over 2 - 3 weeks can also be effective at
breaking the cluster of headaches
Headache of Raised ICP
Raised intracranial pressure can be due to many different aetiologies
- Increased arterial blood pressure e.g. malignant hypertension, pre-eclampsia, hypercapnia

- Increased CSF pressure e.g. overproduction (IIH), failure of reabsorption (meningitis),
obstruction to flow (intracerebral mass)
- Increased brain pressure e.g. space occupying lesion (malignancy, abscess, haematoma),
intracranial infection
- Increased venous blood pressure e.g. cerebral venous sinus thrombosis
Presentation
The combination of headache, papilloedema and vomiting is considered indicative of raised ICP
- Headache is worse on lying flat, nocturnal, starting when waking, worse on coughing
(Valsalva) or leaning forward
- Fundoscopy shows papilloedema (blurring of disc margins, loss of venous pulsation, disc
hyperaemia, and haemorrhage)
- Vomiting is intractable
There may be additional focal neurological changes or seizures. Other examination features that
constitute red flag physical signs suggestive of raised intracranial pressure, particularly in paediatrics,
can include
- Visual field defects

- Cranial nerve abnormalities causing diplopia, new-onset squint, or facial nerve palsy
- Abnormal gait
- Torticollis
- Growth failure in children, if the lesion e.g. craniopharyngioma or a hypothalamic lesion
- Cranial bruits e.g. arteriovenous malformation
- Bradycardia
Investigations
CT or MRI to assess for a space-occupying lesion, venous sinus thrombosis or enlargement of the
ventricles. Lumbar puncture (>30mmHg is raised CSF pressure)
Idiopathic Intracranial Hypertension (IIH)
IIH presents with a headache suggestive of raised ICP alongside visual obscurations and VI nerve
palsy in some cases
- There are many precipitating factors to IIH that are largely hormonal. This includes obesity,
OCP, pregnancy, steroid therapies and some antibiotic treatments
Papilloedema, normal head imaging, raised CSF opening pressure but normal CSF biochemical
analysis indicates IIH
Management should be through neuro-opthalmology, closely monitoring visual fields to ensure

vision is not impaired. Any precipitating agents should be removed, and weight loss encouraged
- Acetozolamide and other diuretics can also be useful

- Steroids are used second line where acetazolamide has not been effective
- Surgical therapy includes lumbo-peritoneal shunting or optic nerve sheath re-fenestration to
permanently relieve pressure
Subarachnoid Haemorrhage (SAH)
SAH is usually caused by bleeding from a berry aneurysm in the circle of Willis, some are due to AV
malformation. Non-modifiable risk factors include PKD, EDS, and Marfan’s syndrome.
Presentation
The most characteristic feature of SAH is a thunderclap headache, reaching 10/10 intensity within a
few minutes
- Associated symptoms include nausea and vomiting, depressed consciousness, subhyaloid

haemorrhage (bleeding in the eyeball), neck stiffness, seizures, severe hypertension, and
focal neurological deficit
The Hunt & Hess scale can be used to grade severity based upon initial presentation. This is from
grade 1 – 5 in ascending severity
Investigations
There are many other causes of thunderclap headache (~90% of cases), this includes
- Primary thunderclap headache (crash migraine)

- Acute hypertensive crisis
- Cervical artery dissection
- Primary sexual headache
However, all cases of thunderclap headache should be treated as SAH until proven otherwise.
Therefore, there should be a CT scan at the earliest opportunity followed by a lumbar puncture
- Angiography to determine the site of bleeding should also be performed
Lumbar puncture should occur if CT head is normal but SAH is suspected
- This must be >12 hours after onset, as xanthochromia will not be apparent before this point
Management
In the acute setting there should be occlusion of the aneurysm to prevent further bleeding; this is
with endovascular coiling or surgical clipping of the vessel. The neurosurgical team should be
contacted early
- The risk of cerebral ischaemia from vasospasm should be prevented by giving oral
nimodipine 60mg every 4 hours (calcium channel blocker)
- Mannitol can be given if there is evidence of raised ICP
Cerebral Venous Sinus Thrombosis
Cerebral sinus thrombosis leads to cerebral infarction or haemorrhage through tissue congestion.
There are many risk factors
- Infection
- Hypercoagulable states e.g. pregnancy, OCP, antiphospholipid syndrome
- Rheumatological conditions
Presentation
Cerebral venous sinus thrombosis usually presents with headache alongside focal neurological
deficit ± signs of raised intracranial pressure
- Seizures develop in many patients
Investigations
Routine bloods can give an indication that the patient has experienced thrombosis
- FBC may show elevated Hb or platelets, WCC may be raised in infection

- D-dimer may be elevated
Diagnosis is usually with CT/MRI scanning
Management
Patients should be treated with anticoagulation
- A loading dose of LMWH is given, followed by warfarin titrated to keep INR 2 – 3
Temporal Arteritis
Temporal arteritis is a form of vasculitis that affects the branches of the external carotid arteries
- It is commonly associated with polymyalgia rheumatica
Presentation
Features of temporal arteritis include headache, scalp tenderness, jaw claudication (as there is
decreased perfusion of the masseter and temporalis), fever, weight loss, and proximal muscle
stiffness (polymyalgia rheumatica)
- This generally occurs in individuals over the age of 50
Temporal arteritis can be complicated by blindness, and if the internal carotid arteries are affected
there may be TIA or stroke.
Investigations
- FBC may show anaemia

- ESR will be raised, usually >50mm/hr
- ALP may be raised
Temporal artery USS ± biopsy can also be performed under local anaesthetic, however biopsy has
very poor sensitivity
Management
Treatment will generally take around 2-3 years before symptoms are eradicated; it involves a high
dose (40 - 60mg daily) of prednisolone to give an immediate response, and then the dose is
gradually titrated down
- The dose is reduced by 5mg every two weeks until it is 10mg. After this point it will be
reduced by 1mg per month, until it is finally reduced down to 1mg
If patients have visual symptoms they should be admitted for IV steroids or start with a dose of
80mg PO prednisolone. There should be ophthalmology review of these patients.
Trigeminal Neuralgia
Trigeminal neuralgia is a chronic condition characterised by intense and extreme episodes of pain in
the face
- This results from a neuropathic disorder of CN V
Presentation
TN is a unilateral, stabbing/shooting pain in the distribution of one or more branches of CN V
- The pain is episodic and sudden onset, lasting a few seconds to minutes and stopping
suddenly
- Pain can be provoked by light touch to the face, eating, cold winds, or vibrations
Patients will usually have an MRI scan to exclude extracranial and intracranial masses along the
course of CN V, or intrinsic brain lesions in the trigeminal brainstem pathways
Management
Carbamazepine has the most evidence for efficacy and should be used first-line; dose should be
titrated to achieve adequate pain control
Where medication is not effective, surgery can be considered
- The most effective treatment appears to be glycerol injection or microvascular

decompression of the nerve
CNS Infections
Meningitis
Meningitis is an inflammation of the meninges and CSF; this can be caused by infection with micro-
organisms or by non-infective causes. There are many risk factors for meningitis, particularly
extremities of age
- Diabetes mellitus, immunosuppression and splenectomy, alcoholism, contiguous infection,

defects in the dura mater, IV drug abuse, and malignancy can also increase the likelihood of
developing the condition
Causes
Bacterial meningitis is caused by many different pathogens; however it is most commonly due to
S.pneumoniae (pneumococcus) and N.meningitides (meningococcus)
- If the patient is pregnant or over 60 it is more likely to be L.monocytogenes

- If the patient has recently had surgery the likely cause is S.aureus
- In children, likely cause differs with age
o <3 months: group B strep, E.coli, and listeria monocytogenes
o 1/12 – 6 years: Neisseria meningitides, strep pneumoniae, Hib
o >6 years: Neisseria meningitides, strep pneumoniae
- Other organisms include in adults HIB, gram negatives, group B strep, and TB
Aseptic meningitis can be caused by
- Viral infection e.g. mumps, HSV, HZV, HIV, measles

- Fungal infection
- Parasitic infection e.g. spirochetes, protozoa, helminths
Presentation
Clinical presentation of meningitis may include
- Fever, headache, vomiting

- Stiff neck, back rigidity, photophobia, and (in infants) bulging fontanelle
- Altered mental state, focal neurological deficit, seizure
- Kernig’s sign: pain and resistance on passive knee extension with hips fully flexed
- Brundinski’s sign: forced flexion of the neck causes hip flexion
Invasive meningococcal disease may present with septicaemia, meningitis, or a combination of both.
This may include a generalised petechial (non-blanching) rash, cold and painful extremities, and skin
mottling.
TB meningitis has an insidious onset; however acute presentation can occur if it is complicated by
hydrocephalus or vasculitis
- It will often present with a mild headache, lesions of CN VI, III and IV, papilloedema and
optic nerve damage
Investigations
Investigations must not delay treatment
- Blood tests should include routine bloods as well as blood culture and coagulation screen
- CT scan is indicated where there is impaired conscious level or focal neurological deficit
Lumbar puncture is the key investigation, and should be performed immediately where there are no
signs of raised ICP (in most cases CT scan will precede LP), infection at the site, abnormal clotting, or
cardiorespiratory compromise
- Samples are usually sent for culture, gram stain, Ziehl-Neelsen stain, cytology, virology,
glucose, protein, and rapid antigen screen
- Normal CSF opening pressure is 10 – 20 mmHg, this may be increased in bacterial meningitis
CSF Appearance WBC Protein Glucose

Normal Clear 0 - 5 /mm3 0.15 – 0.4 g/L >50% of blood
Bacterial Turbid Polymorphs Increased Decreased
Meningitis >>5/mm3 (>0.45g/L)
Viral Clear Lymphocytes Normal Normal
Meningitis >5/mm3
TB Meningitis Turbid/Clear/Viscous Lymphocytes Increased Decreased
>5/mm3 (>0.45g/L)
Malignant Clear >5/mm3 Often increased Decreased
Management
Any person presenting with suspected meningitis should be managed as having bacterial meningitis
until proven otherwise. Benzylpenicillin 1.2g IM/IV should be given before transfer to hospital if
meningococcal septicaemia is suspected
TB meningitis is treated with quadruple therapy (rifampicin, isoniazid, pyrazinamide, and

ethambutol) and steroids over two months. Followed by rifampicin and isoniazid for a further 10
months.
Viral meningitis is treated with antipyretics and support until full recovery occurs.
Management of bacterial meningitis is dependent on causative agent; initial blind therapy before
identification of the causative organism should be with IV ceftriaxone
- Meningococcus is treated with IV ceftriaxone or benzylpenicillin; if the patient is allergic to

beta-lactams chloramphenicol can be used. Dexamethasone should also be given
- Pneumococcus is treated with ceftriaxone
- S.aureus is treated with rifampicin/ flucloxacillin
- Group B streptococci are treated with cefotaxime
- H.influenxae is treated with cefotaxime
- L.monocytogenes is treated with amoxicillin
Close contacts of the patient should receive rifampicin prophylaxis
Encephalitis
Encephalitis is inflammation of the brain parenchyma
- Viral encephalitis is most commonly herpes simplex (HSV-1 and HSV-2), but can also be due
to CMV, adenovirus, influenza, polio, and rubella
- Autoimmune encephalitis can be due to a range of autoantibodies leading to a spectrum of
different clinical syndromes
Presentation
Most patients present with a classical triad of fever, headache, and altered mental status
- Other features can include convulsions, focal neurological deficit, raised ICP, and vomiting
Investigations
Routine bloods should be carried out, alongside specific assays for the auto-antibodies below
EEG is useful in the early stages of disease, showing diffuse slowing
- CT scan should be performed to rule out space-occupying lesions, strokes, and raised ICP.
- MRI can provide a more sensitive detection of demyelination, evidencing oedematous
changes in the brain consistent with encephalitis
Lumbar puncture can be diagnostic
- CSF PCR test for HSV, VZV and enteroviruses

- Protein and lymphocyte levels are normally high in encephalitis
Management
Patients should be admitted and treated with a prompt IV infusion of acyclovir
Anti-NMDA Encephalitis
Anti-NMDA receptor antibodies can lead to encephalitis, this leads to the following clinical features
- The condition may be preceded by a prodromal viral-like syndrome

- Psychiatric symptoms e.g. agitation, hallucinations, delusions, catatonia, memory loss
- Seizures
- Movement disorders
Management is typically with IV steroids and IVIg ± plasma exchange
This can be a paraneoplastic syndrome, and there should therefore be a tumour search with whole
body CT scan following treatment
Limbic Encephalitis
Limbic encephalitis can be caused by voltage-gated potassium channel (VGKC) complex antibodies.
The inflammation of the limbic system presents with the following
- Subacute amnesia
- Confusion, behavioural disturbance
- Seizures
- SIADH
Management is as for anti-NMDA encephalitis

Acute Limb Ischaemia

Acute limb ischaemia is either due to thrombotic occlusion of a diseased vessel (commonest) or
embolization from a distant site. It can be defined as a previously stable limb with sudden
deterioration in arterial supply over less than two weeks. This is a limb-threatening event
- Without revascularisation within 4 – 6 hours, there will be necrosis of the limb distal to the
occluded vessel
There are three main causes of acute limb ischaemia, with risk factors relating to these
1. Embolism, most commonly cardiac origin (AF, or mural thrombus post-MI). There can also
be arterial origin due to aortic/femoral/popliteal aneurysm, or venous origin if there is a
patent foramen ovale
2. Trauma causing compression/dissection of an artery or compartment syndrome. This is most
often with supracondylar humerus fracture or posterior knee dislocation
3. Thrombosis, this is less likely to cause acute limb ischaemia as it develops chronically
therefore there are usually collateral vessels present
Presentation
Patients with acute limb ischaemia present with a painful limb with reduced muscle power and
reduced sensation
The signs and symptoms can be summarised as the 6 Ps
- Pale, pulseless, painful, paralysed, paraesthetic, and perishingly cold

- Paraesthesia and paralysis are later features
Key differential diagnoses include DVT, cellulitis, and compartment syndrome
Assessment
Approach these patients using an A to E assessment, keep them NBM and call for senior help as
early as possible
- Give 15L oxygen through a high-flow mask

- Get IV access
o Give crystalloid fluid as needed for haemodynamic status
o Take blood from the cannula
▪ FBC, ischaemia is aggravated by anaemia
▪ Clotting and group & save, these are surgical patients that will likely require
operative intervention
▪ U&Es, there may be associated renal artery stenosis or rhabdomyolysis
▪ LFTs as baseline
▪ Glucose and lipids to establish CVD risk factors
▪ ESR to assess for connective tissue disorder
o Give 5 – 10mg morphine as pain relief
- ABG to assess lactate
- Request a 12 lead ECG to assess for AF
Further history should use the SOCRATES format, but also assess the following features
- Vascular risk factors

- Previous features suggest chronic limb ischaemia
Focussed examination should be of the limb itself, assessing for the temperature, motor function,
sensation, colour and pulses
- All features should be compared to the contralateral limb as changes can be subtle
There should also be cardiovascular examination, and abdominal examination to check for AAA.
Measurement of ABPI can be useful, with <0.5 indicating critical ischaemia
Hand-held Doppler can be used to assess for any residual arterial flow to the limb. Alongside this,
both arterial and venous duplex can be useful for determining the severity of the ischaemia
Pre-operative CT/MRI angiography should be undertaken where time allows, as this can differentiate
embolism from thrombosis and influence treatment options
- Intra-arterial digital subtraction angiography (DSA) is gold standard
There should be further investigation to determine the source of embolization
- Plain CXR
- ECG if not already performed
- Less urgently, there can be the following post-operatively
o Echocardiogram
o Aortic, femoral and popliteal USS
Management
Ensure all patients have adequate analgesia and fluid resuscitation. All patients should receive
anticoagulation with heparin to prevent the clot spreading further
- Give 5000IU unfractionated heparin as a bolus, and start a 1000IU/hr IV infusion, aim for
APTT 2 – 2.5x normal
- LMWH is not used as the half-life is long, therefore the risk of bleeding in theatre is high
Tissue viability assessment should be undertaken by a senior colleague, and guides likely definitive
management Fixed mottling of the skin implies irreversible damage
Description Capillary Paralysis Sensory Arterial Venous

Refill Loss Doppler Doppler
I Viable Not <2 seconds None None Audible Audible
threatened
IIa Salvageable Slow None Partial Inaudible Audible
Threatened if promptly
treated
IIb Salvageable Slow Partial Partial Inaudible Audible

Threatened if
immediately
treated
III Amputation Absent Completely Complete Inaudible Inaudible
Irreversible needed tense
muscles
Limb ischaemia requires urgent surgery; this must be within 4 – 6 hours of symptom onset. Often
there is no time for pre-operative angiography
- The surgical option used is dependent on the patient

o Embolectomy
o Catheter directed localised thrombolysis, angioplasty ± stent, or bypass
o Trauma repair
Amputation may be required as a last resort
Post-operative complications can include compartment syndrome and re-perfusion injury
Peripheral Arterial Disease (Chronic Limb Ischaemia)
Peripheral arterial disease results from atherosclerosis in vessels distal to the aorta (non-cerebral
and non-coronary vessels), resulting in dysfunction of the perfusion of the limbs
- Risk factors for peripheral arterial disease are as for all cardiovascular disease
This generally affects the legs. In order to identify the site of peripheral vascular disease, it is
important to appreciate the anatomy – typically the arteries will bifurcate, with one branch forming
a conduit and the other supplying the surrounding structures
- The common iliac artery is a conduit to the internal and external iliac arteries
- The internal iliac artery supplies the pelvic organs, buttocks, perineum, and
external genitalia (always ask about ED)
- Inflow disease therefore presents with buttock or upper thigh pain
- The external iliac becomes the common femoral artery as it passes below the
inguinal ligament. This is a conduit to the profunda femoris and superficial femoral
arteries
- Outflow disease therefore presents with calf pain
- The superficial femoral becomes the popliteal as it passes through the adductor
canal, formed by adductor magnus. It is a conduit to the anterior tibial, posterior
tibial, and peroneal (fibular) arteries
- Run-off disease therefore presents with foot pain
Presentation
Upper limb disease is relatively rare, but typically affects the subclavian artery and brachiocephalic
trunk
- The patient will have skin changes and claudication pain in the affected arm, and
there will be a difference in blood pressure between the arms
Lower limb disease is far more common, and the presenting complaint is usually intermittent
claudication
- There will be aching, cramping or pain in the buttock, thigh, calf or foot that is
exacerbated by exercise and alleviated by rest
- Always quantify walking distance in these patients
- In severe disease there can be pain at rest and pain at night
- Patients will often say that pain in their foot can be alleviated by hanging the
foot out of the bed
- Tissue loss may occur in very advanced disease e.g. gangrene, ulcers
- Gangrene can be dry or wet. Wet gangrene is dry gangrene with infection
- It is necrotic, cold, and generally has a lack of sensation
Fontaine classification can be used for symptom severity.
On examination, there are several features that can suggest chronic limb ischaemia
- Pallor of the skin, reduced capillary refill, absent/weak peripheral pulses, reduced
temperature
- Trophic changes e.g. hair loss, haemosiderin pigmentation, dry and brittle skin,
onychomycosis
- Arterial ulcers: small, regular (punched-out appearance), deep, painful, and on
pressure points
- Positive Buerger’s test
- Reduced ABPI
- 0.9 – 0.7: Mild ischaemia (claudication pain)
- 0.6 – 0.5: Moderate ischaemia (rest pain)
- <0.5: Critical ischaemia (impending gangrene)
Investigations
All patients with peripheral vascular disease should have a cardiovascular risk assessment
- Bloods including FBC, U&Es, LFTs, lipids, glucose

- ECG
First-line imaging is usually with duplex arterial USS, determining the site and severity of disease
- MRI and CT angiography can also be used, often prior to revascularisation

- Digital subtraction arteriography is gold standard
Management
All patients with peripheral arterial disease should have conservative and medical input to modify
their cardiovascular risk factors
- Smoking cessation, regular exercise, and improvement in diet are important

- Statin
- Anti-hypertensive agents
- Management of diabetes mellitus where relevant
Statin and anti-platelet therapy (with clopidogrel or 75mg aspirin OD) is recommended in all patients
with symptomatic peripheral vascular disease
- Symptomatic patients should also be commenced on an ACE-inhibitor, consider

peripheral vasodilators
Any ulcers or gangrenous areas should be debrided and dressed. Antibiotics should be considered
Surgery is used in critical limb ischaemia, where patients have pain at rest/night or tissue loss. It is
also an option where medical measures have failed to control symptoms
- Endovascular revascularisation is used where possible, TASC classification will

identify suitable patients for this. This is with angioplasty ± stenting
- For more extensive disease, bypass surgery is used. This is either with artificial or
saphenous vein grafts
Amputation is a last resort in patients with chronic limb ischaemia, and is often required where
there is gangrene.
Jaundice
Jaundice is the yellow discolouration of tissues caused by a build-up of bilirubin; this causes a
yellowing of the skin and sclera
- Jaundice is said to become clinically apparent to a physician at 35 µmol/L and to a patient at

50 µmol/L
o NR: 3 – 20µmol/L
Bilirubin is produced from the breakdown of haemoglobin
- Bilirubin is initially unconjugated, circulating in the bloodstream bound to albumin

- The bilirubin-albumin complex is broken down in the liver, conjugated with glucuronic acid,
and excreted into the intestine as a component of bile
- Conjugated bilirubin is converted to urobilinogen in the bowel, colouring the stools brown
- Some urobilinogen is absorbed into the bloodstream to be excreted renally, colouring the
urine yellow
Assessment
Some patients with jaundice will be acutely unwell due to the underlying cause. Ensure to
adequately stabilise the patient using an A to E approach, prior to proceeding with assessment and
investigations
Where possible, take a history from the patient. There are several key aspects to a patient’s history
that can differentiate the different causes of jaundice
- Onset and duration

- Pruritus (specifically occurring in post-hepatic jaundice)
- Pain
o Painful jaundice can indicate gallstones
- Colour of urine and stools
o Dark urine and pale stools indicate obstructive jaundice
- General health over the past days, systemic symptoms
o Flu-like illness could indicate a stressor for Gilbert’s syndrome/G6PD, or could be
symptomatic viral hepatitis
- Ask specifically about the following
o Weight loss
o Travel to any country where hepatitis A is endemic
o Alcohol consumption
o Drug abuse
o Previous blood transfusions (haemolytic transfusion reactions)
o Contact with any other jaundiced patients
Abdominal examination in jaundice is key
- Hepatomegaly, splenomegaly
o The liver can be tender in viral hepatitis
- Signs of chronic liver failure can include spider naevi, palmar erythema, gynaecomastia,
asterixis, splenomegaly, finger clubbing, and ascites
- Pancreatic tumours or enlarged gallbladder may be palpable (Courvoisier's law)
Red flags in jaundice that warrant urgent referral to hospital for investigation/admission include
- Painless
- Palpable mass
- Weight loss
- Signs suggestive of severe hepatic dysfunction e.g. encephalopathy
- Signs suggestive of sepsis
Jaundice can be differentiated into three groups
Pre-Hepatic Intra-Hepatic Post-Hepatic (Cholestatic)

Acquired haemolysis Alcoholic/ Non-alcoholic fatty Intraluminal e.g. gallstones
liver disease
Congenital haemolysis Drug toxicity Transmural e.g. PBC, PSC,
strictures, cholangiocarcinoma
Defective bilirubin conjugation Viral hepatitis Extraluminal e.g. enlarged
e.g. Gilbert’s syndrome, nodes, pancreatic tumours
Crigler-Najjar syndrome
Neonatal jaundice Malignant infiltration
Rare causes e.g. Wilson’s,
haemochromatosis, Budd-
Chiari, autoimmune hepatitis,
α1-antitrypsin deficiency
Certain medications can also lead to jaundice, this includes certain antibiotics (flucloxacillin, co-
amoxiclav), OCP, and anti-depressants
- Always ask jaundiced patients if they are on any new medication

Investigations
Most patients presenting with jaundice will have routine blood tests. This should include FBC, U&Es,
LFTs, clotting, albumin, and inflammatory markers. LFTs are an important factor in differentiating
cause
- Normal LFTs indicate a pre-hepatic jaundice

- Raised ALP (alongside gamma-GT) indicates obstructive jaundice or biliary pathology
- Raised AST and ALT indicate hepatocellular damage
o AST>ALT implies cirrhosis
o ALT>AST implies hepatitis
Urine dipstick and urinalysis are important, dipstick may be positive for blood indicating Hb
fragments in haemolysis, as well as measurement of urinary bilirubin and urobilinogen. This can
further differentiate pre-hepatic from post and intra-hepatic causes
- Raised urinary bilirubin indicates conjugated hyperbilirubinaemia (i.e. Not pre-hepatic)

- Raised urobilinogen indicates hepatocellular failure or increased RBC breakdown
Where there is raised urobilinogen, there should be further investigation into haemolysis
- Full blood count (including MCV), blood film, serum B12 and folate, LDH, reticulocyte count,
haptoglobin level, and iron studies
- Direct Coomb’s test

Where there is derangement of LFTs indicating an intrahepatic picture, full liver screen can help to
determine cause
- Viral serology to identify hepatitis A, B or C

- Autoimmune/vasculitic screen, this includes
- Antinuclear antibody (ANA) – autoimmune hepatitis
- Anti-mitochondrial antibody (AMA) – primary biliary cirrhosis, autoimmune hepatitis
- Anti-smooth muscle antibody (SMA) – autoimmune hepatitis, primary biliary
cirrhosis
- Anti-LKM antibody – autoimmune hepatitis
- Raised IgM – PBC
- Raised IgG – autoimmune hepatitis
- Caeruloplasmin levels and urinary copper can identify Wilson’s disease
- Ferritin and total iron binding capacity (TBIC) can identify hereditary haemochromatosis
- Alpha 1-antitrypsin level
- Alpha-fetoprotein and LDH can indicate HCC
Imaging should be carried out in cases where the cause is likely post-hepatic or intra-hepatic
- Abdominal USS can identify biliary obstruction, venous thrombosis, and can demonstrate
liver texture
- CT is comparable to USS
- ERCP can be used to diagnose and treat obstructive jaundice, MRCP can also be used
diagnostically
Liver biopsy is rarely used, but may be necessary to diagnose and stage disease
Acute Liver Failure
Acute liver disease is liver disease that persists for less than 6 months, after this point it is defined as
chronic. Acute liver disease can lead to acute fulminant liver failure (ALF), which is the onset of
encephalopathy and coagulopathy in a patient without pre-existing liver disease within 6 months of
symptom onset
- Hyper-acute liver failure is encephalopathy within 7 days of the onset of jaundice

- Acute liver failure is encephalopathy 8 to 28 days after the onset of jaundice
- Sub-acute liver failure is encephalopathy 4 to 12 weeks after the onset of jaundice
ALF is characterised by several systemic features
- Acute renal failure (this can be related to type 1 hepatorenal failure, acute tubular necrosis,
or renal vasculitic injury)
- Metabolic derangement, including hypoglycaemia and metabolic acidosis
- Haemodynamic changes, including peripheral vasodilation and increased prothrombin time
- Hepatic encephalopathy is due to cerebral oedema and raised neurotoxins
o Grading is summarised below
Grade 0 Minimal changes in memory, concentration, intellectual function, and coordination
Grade 1 Mild confusion, emotionally labile, disordered sleep pattern
Grade 2 Drowsy, lethargic, personality change, mild disorientation

Grade 3 Somnolent, disorientated, confused, incomprehensible, occasional rage
Grade 4 Coma
Chronic liver failure can lead to acute liver failure; this is known as acute on chronic liver failure or
decompensated chronic liver disease
- This presents with encephalopathy, jaundice, hepatic fever, ascites, and peripheral oedema
on a background of liver disease
Investigations
Initial investigations into ALF should include
- FBC and group and save

- U&Es
- LFTs (aspartate transaminase, alanine transaminase, alkaline phosphatase, gamma-glutamyl
transpeptidase), clotting and albumin
o Direct bilirubin = conjugated, indirect bilirubin = unconjugated
o Cholestatic disease: ALP > 200U/L, γ-GT significantly raised, AST/ALT normal or
slightly raised (< 200U/L)
o Hepatocellular disease: AST/ALT >5x upper limit, ALP normal or slightly increased
▪ ALT/AST levels in the thousands indicate viral, drug, or ischaemic cause
▪ ALT > AST indicates acute liver damage or chronic disease without cirrhosis
▪ AST > ALT indicates established cirrhosis, AST:ALT >2 suggests alcoholic liver
disease
- Glucose
- ABG to measure lactate and pH, metabolic acidosis is a poor prognostic sign
- CXR and blood, urine and sputum cultures are important as ALF commonly leads to infection
Imaging is primarily with ultrasound scanning, although CT/MRI are more accurate if there is massive
ascites
Further investigations can help distinguish differential diagnoses of ALF, this is known as the liver
screen
- Viral serology to identify hepatitis A, B, C

cirrhosis
- Liver-Kidney macrosomal antibody (LKM) - autoimmune hepatitis
- Raised IgM – primary biliary cirrhosis
- Paracetamol level and toxicology screen
- AFP level
Management
Patients with ALF should be managed in an HDU or ITU setting as intubation may be needed
Distributive shock is common in ALF due to haemodynamic vasodilation, it is therefore important to

catheterise and monitor hourly urine output as well as CVP and MAP (aim for MAP >60). Shock can
lead to renal failure in addition to liver failure (stop all nephrotoxic drugs)
- Fluid resuscitation should be with a colloid followed by a crystalloid (using 5% dextrose and
avoiding 0.9% saline)
- Inotropes can be added if the patient does not respond
- Where patients have low albumin, give 20% HUS to maintain intravascular volumes
Vitamin K 10mg/day IV should be given for 3 days to increase PT/INR. It may be indicated to give FFP
or specific clotting factors
Infection should be prevented in ALF by giving prophylactic IV tazocin and fluconazole/ cefuroxime
Ulcer prophylaxis is also important to prevent haemorrhagic gastritis, this is best with IV H2
antagonists but IV/oral PPIs can also be used
Hepatic encephalopathy can be managed with lactulose (reduce nitrogen load from the gut,
neomycin can also be used) and elevation of the head
- In more severe cases IV mannitol and sedation with benzodiazepines or phenytoin to

prevent seizures can be used
- Therapeutic hypothermia can be tried
AKI is common, and should be managed with haemodialysis or continuous arterial haemofiltration
The KCH criteria in non-paracetamol overdose apply in all other causes of ALF to indicate when a
patient is suitable for transplant listing. Cases of ALF that require transplantation may be super-
urgent listed, and will therefore be priority for any available organs
- INR >6.5 with encephalopathy

- Encephalopathy alongside any three of: age >40, jaundice to encephalopathy in <7 days,
bilirubin >300µmol/L, INR >3.5
Paracetamol Overdose
Paracetamol overdose is the commonest cause of ALF in the UK. The therapeutic dose of
paracetamol is 4g/day, however overdose rarely causes damage below 150mg/kg
- Liver damage occurs due to depletion of glutathione, leading to a build-up of damaging

NAPQI
- Single overdose is considered as anything taken in a 1 hour period, and staggered overdose
is taken over >1 hour
Over the first 24 hours following overdose patients are generally well or may have nausea/vomiting
- Hepatorenal failure with jaundice, RUQ pain, hypoglycaemia and encephalopathy generally
follows 48 hours later
- Lactic acidosis occurs later in the course of disease
- Clinically significant toxicity is unlikely if the patient is asymptomatic, with undetectable
plasma paracetamol levels, and normal LFTs/INR >24 hours after the last dose
It is important to measure plasma paracetamol levels in all patients presenting with ALF, these are
accurate >4 hours post-ingestion of the drug
- The paracetamol antidote N-acetylcysteine is given where plasma paracetamol level is above
the threshold indicated on the plasma concentration/time graph
o At 4 hours give parvolex where plasma paracetamol >100mg/kg
o If the patient presents >8 hours after overdose, and it is likely that from the history
that they have ingested >150mg/kg, give parvolex before blood results return
o In staggered overdose measure plasma paracetamol levels, but it is recommended
to commence treatment before results are obtained
- Also measure LFTs, coagulation screen, U&Es, glucose, FBC, and perform an ABG
N-acetylcysteine is most effective if given within 8 hours of overdose, however late presenters
should still be given the drug. It is given as an IV infusion over the course of 21 hours, delivered as 3
bags of fluid, each with a slightly decreased dose
- Bag 1 is 150mg/Kg acetylcysteine in 200ml 5% glucose solution, delivered over one hour
- Bag 2 is 50mg/Kg acetylcysteine in 500ml 5% glucose solution, delivered over four hours
- Bag 3 is 100mg/Kg acetylcysteine in 1000ml 5% glucose solution, delivered over sixteen
hours
If the patient is still in hepatic failure, bag 3 is continued and repeated until improvement is seen
- There is some hypersensitivity associated with the medication and anti-histamine may be
needed
- Patients should be given 10mg single dose of vitamin K
The KCH criteria in paracetamol overdose indicate poor prognosis in ALF, these patients should be
considered for transplantation listing
1. pH <7.25 after 24 hours

2. INR >6.5, creatinine >300µmol/L or anuria, and high grade encephalopathy
Acute Hepatitis Viruses
Hepatitis A only causes acute hepatitis, and typically presents with jaundice and tender
hepatomegaly following a prodromal phase of around 6 weeks. ALF is rare in hepatitis A (<0.1% of
cases)
- Diagnosis is usually confirmed with hepatitis A IgM Ab in the serum. ALT will be markedly
raised
- No specific treatment for acute hepatitis A is available, but high dose steroids can be given if
there is prolonged cholestasis
- If ALF occurs it should be managed as above
Hepatitis B causes ALF in 2% of cases, after which >95% of adults will clear the virus
- Diagnosis is made by the presence of HBsAg, possibly HBeAg, and anti-HBc IgM all indicating
acute ongoing infection. Serum ALT will also be raised
- Lamivudine (antiviral) is used in acute fulminant hepatitis B
Hepatitis E infection is only known to cause ALF in pregnant women, treatment in this circumstance
is supportive with a high rate of liver transplantation.
Hepatitis C can cause symptoms of acute infection in 20% of cases, but acute liver failure is very rare.
CMV and EBV are other causes of acute symptomatic viral hepatitis, but acute liver failure is rare.
Seronegative
Seronegative ALF can be diagnosed after all other causes of liver failure have been excluded
- It may be related to autoimmune, viral, medication (idiosyncratic reaction), or toxin damage

The history in patients with seronegative ALF generally describes a few days prodromal phase with
non-specific symptoms. The patient may be taking multiple medications and there is generally a
history of recent foreign travel.
There is a role for steroids alongside treatments for ALF in this case
Wilson’s Disease
Wilson’s disease is an autosomal recessive inherited disorder of copper excretion. In Wilson’s

disease there is impaired incorporation of copper into caeruloplasmin, meaning that copper builds
up in the tissues as it is not excreted in bile
- In the liver there can be ALF, cirrhosis and portal hypertension, or acute hepatitis
- Neurological changes include parkinsonism, behavioural change, and cognitive impairment
- Coombs negative haemolytic anaemia is a common feature
Diagnosis is made from the presence of Kayser-Fleischer rings, low caeruloplasmin, low serum
copper, positive liver histology, and genetic analysis
Where liver failure is not present patients should avoid foods with high copper content, urinary
copper excretion can be promoted with penicillamine
Budd-Chiari Syndrome (BCS)
BCS occurs where there is obstruction of the main hepatic veins by thrombus formation
- This can be related to thrombophilia, hepatocellular carcinoma, or anomalies of the IVC

Most patients will present with onset of features of portal hypertension over several months (ascites
in BCS will have a high SAAG), however ALF can occur in rare cases
- Diagnosis is usually with Doppler USS or contrast CT scanning

- Venography and venous pressure measurement allow the site of obstruction to be defined
In ALF due to BCS there should be thrombolysis and anticoagulation, but liver transplant may be
required. In chronic BCS TIPSS is effective in most cases at reducing portal hypertension.
Chronic Liver Failure
Chronic liver disease is hepatic injury that persists for >6 months. This consists of a wide range of
disease starting with steatosis, inflammation or iron overload leading to fibrosis and eventually
cirrhosis
- Cirrhosis is diffuse hepatic fibrosis with nodule formation, this can be micronodular
(alcoholic cirrhosis, biliary disease) or macronodular (viral hepatitis)
Complications of cirrhosis include hepatocellular carcinoma and malnutrition
Presentation
Many patients present incidentally due to persistent abnormal LFTs
- The degree of LFT abnormality does not reflect the severity of disease
Patients may present with symptoms related to their underlying disease process
- Pruritus is common in cholestasis e.g. PBC, PSC

Decompensated chronic liver disease may be the first presentation for some patients, this has all of
the features of acute liver failure e.g. jaundice, ascites, encephalopathy, and sepsis
Investigations
Routine bloods should include
- LFTs
- FBC: anaemia (bone marrow toxicity from alcohol, chronic GI blood loss),
thrombocytopaenia (reduced TPO production, splenomegaly), neutrophilia (sepsis)
- Clotting screen: prolonged INR
- Albumin
- U&Es: creatinine (may be low due to muscle wasting, if creatinine is normal/raised there
may be AKI), hyponatraemia (renal dysfunction)
There should be a full liver screen to help identify a potential cause
- Viral serology to identify hepatitis B or C

cirrhosis
- Anti-LKM antibody – autoimmune hepatitis
- Raised IgM – PBC
- Alpha-fetoprotein and LDH can indicate HCC
Abdominal ultrasound is the key imaging investigation and can image the liver, biliary tree, and
vessels
CT/MRI and liver biopsy may be required in select patients
Classification of patients into Child-Pugh category A, B and C can help estimate prognosis in patients
with cirrhosis. This is a combined biochemical and clinical score
- Serum albumin, bilirubin, INR, ascites, encephalopathy

Management
In all patients with cirrhosis there should be routine outpatient follow-up
- Hepatocellular carcinoma screening should be with a 6 monthly abdominal USS and AFP
- Variceal screening should be with gastroscopy every 1 – 3 years
Patients with advanced cirrhosis are usually malnourished, and should therefore be considered for
NG feeding and IV supplementation
Jaundice
Jaundice can occur in chronic liver disease due to many different causes. This can include sepsis
induced cholestasis, acute alcoholic hepatitis, malignancy, or progression of liver disease
Acute alcoholic hepatitis often occurs within 1 – 2 weeks of abstinence and will present with
systemic inflammatory response and deranged liver function
- These patients should be managed with fluids, NG feeding, electrolyte supplementation, and
low threshold to antibiotics
If patients have pruritus associated with jaundice cholestyramine can be given
Portal Hypertension
Portal hypertension is an increase in portal venous pressure (hepatic venous pressure gradient) >5
mmHg. Complications of portal hypertension tend to occur when HVPG >12 mmHg
Causes of portal hypertension can be divided into three groups
- Pre-hepatic includes portal vein thrombosis

- Intra-hepatic includes cirrhosis, schistosomiasis
- Post-hepatic includes Budd-Chiari, cardiac failure
Complications include
- Varices form due to porto-systemic shunting at the oesophagus, rectum, and umbilicus. The
highest risk from varices is haemorrhage from gastro-oesophageal varices
o Grade II or above varices should be treated with long-term beta blocker therapy
(propranolol 40mg or carvedilol)
o Secondary prophylaxis following acute bleeding should be with 2 weekly variceal
banding, or TIPSS if there is re-bleed
- Ascites occurs as splanchnic vasodilation in portal hypertension leads to salt and water
retention
- Renal dysfunction should be managed with cessation of diuretics and other nephrotoxic
drugs, fluid filling with albumin, and terlipressin to increase renal blood flow
Hepatocellular Carcinoma
Hepatocellular carcinoma occurs in cirrhosis due to repeated proliferation of hepatocytes.
Treatment can include
- Transarterial chemoablation or radiofrequency ablation are used in patients that cannot

tolerate surgery
- Surgical resection of amenable tumours
- Hepatic transplantation can occur where there are 3 or fewer small tumours
Hepatitis B (+/- D)
Chronic hepatitis B infection is defined HBsAg positivity for >6 months, this becomes less common
the later the infection occurs in life
- Where ALT is raised in patients with chronic hepatitis B there should be anti-viral therapy
e.g. lamivudine, tenofovir, adefovir, peginterferon alpha
- Patients that do not require antivirals should have ALT and HBV DNA, and surveillance for
HCC (USS and AFP) every 6 months
Hepatitis C
Hepatitis C causes a non-specific acute infection, it can present with deranged LFTs or jaundice.
- 20% of patients will present with symptoms of acute infection, but acute liver failure is
incredibly rare
- Chronic hepatitis C infection (HCV RNA positivity for >6 months) occurs in up to 80% of cases
and is more common the later the virus is contracted in life. Overall risk of progression to
cirrhosis is up to 25%
Management should initially involve exclusion of AIH, as Hep C treatment will exacerbate this
- Genotype 1 Hep-C should be treated with 48 weeks of peg-interferon alpha and ribavirin
o If HCV RNA is still detectable at 12 weeks, this should be swapped to a course of
bovepravir/ telaprevir
- All other genotypes should be managed with 24 weeks of peg-interferon alpha and ribavirin
o Sof-led is second line
Autoimmune Hepatitis (AIH)
AIH is a chronic disease characterised by hepatocellular inflammation and necrosis
- Patients can present with decompensation, or milder symptoms e.g. abdominal discomfort,
nausea, fatigue and pruritus
Diagnosis is from the presence of raised IgG and autoantibodies alongside findings on liver biopsy
- Class I: AMA, IgG, ANA

- Class II: LKM
- Class III: SLA
With treatment, prognosis in AIH is good. Patients can be given prednisolone (starting at 50mg
weening over 2 years) in conjunction with azathioprine 1 mg/kg/day
Primary Biliary Cirrhosis (PBC)
PBC involves destruction of the small interlobular bile ducts progressing to intrahepatic cholestasis
and liver damage. This is commonest in middle-aged women and typically presents with pruritus and
lethargy
- Diagnosis is made by the presence of raised IgM alongside autoantibodies. Liver biopsy can
be used, but the changes in PBC (granuloma formation) are not uniform across the liver
Management of PBC is with ursodeoxycholic acid 15mg/kg/day to reduce the likelihood of
transplantation and death, immunosuppressant drugs can also be used. Pruritus can be eased with
cholestyramine, and fatigue can be managed with modafinil
- PBC can sometimes return in patients post-transplant

Primary Sclerosing Cholangitis (PSC)
PSC is commonly related to IBD and is more common in men, it is inflammation and fibrosis of the
intra- and extra-hepatic ducts. It can present similarly to PBC, but symptoms are usually milder.
- Diagnosis of PSC is with ERCP, there may also be cholestatic LFTs and elevated pANCA
- Liver biopsy can be used to stage the disease, showing fibrosis and stricture formation
Management of PSC is only effective at helping symptoms and will not slow disease progression. This
includes SSRIs for pruritis, nutritional support, ursodeoxycholic acid, and ERCP to dilate some biliary
strictures. Liver transplantation is the most effective therapy
- One major complication of PSC is cholangiocarcinoma, therefore there should be annual USS
screening
- PSC can recur following transplantation
Alcoholic Liver Disease
Alcoholic liver disease progresses through steatosis and alcoholic hepatitis, through to cirrhosis and
liver failure
- Alcoholic steatosis is asymptomatic and develops quickly, this can resolve entirely and
rapidly with alcohol abstinence
- Alcoholic hepatitis presents with malaise, jaundice, and nausea. It should be managed as
acute liver failure
- Alcoholic cirrhosis can be asymptomatic and compensated, or result in liver failure
Alcohol withdrawal progresses over the course of several days, the most dangerous period is around
24-72 hours, due to seizure risk. Management of withdrawal should include
- Wernicke’s encephalopathy is prevented from progressing to Korsakoff’s syndrome by

administration of IV prabinex. Following this, oral thiamine 200-300mg OD and vitamin B
compound strong TDS can be taken
- Withdrawal symptoms are eased with chlordiazepoxide or diazepam, these will help prevent
seizures. The dose prescribed is largely determined by a patient’s CIWA score, and then
gradually reduced
- Maintenance of sobriety can be achieved with psychiatric and social interventions e.g.
alcoholics anonymous. There are also some pharmacological agents available to aid in the
maintenance of abstinence e.g. the ALDH inhibitor disulfiram
Non-Alcoholic Fatty Liver Disease (NAFLD)
NAFLD progresses from steatosis, to steato-hepatitis +/- fibrosis, and eventually will lead to cirrhosis
- Risk factors include obesity and the metabolic syndrome, as well as TPN and starvation
o Visceral fat levels are the key risk for NAFLD development
- Certain medications can cause NAFLD e.g. amiodarone and methotrexate
USS can show fatty liver, but staging of disease should be with liver biopsy or fibroscanning
Management is with control of risk factors and weight loss, this can involve medications
(thiazolidinediones, GLP-1 agonists) or bariatric surgery (gastric banding, roux-en-Y bypass)
Haemochromatosis
Haemochromatosis can be a primary hereditary condition (C28Y mutation of the HFE gene), or
develop secondary to repeated blood transfusion or excess iron. Patients can present with a wide
spectrum of disease
- Hepatomegaly, cirrhosis and HCC

- Cardiomyopathy
- Diabetes mellitus, panhypopituitarism
- Skin pigmentation and hair loss
Diagnosis is with raised serum ferritin and transferrin saturation, liver biopsy is gold standard.
Management is with regular venesection, removing 1 unit of blood every 1 – 3 weeks, aiming for Hb
at the lower end of normal range. Iron chelation with desferrioxamine infusions 3 times weekly can
be used where venesection is not tolerated
Alpha-1 Antitrypsin Deficiency

Alpha-1 antitrypsin is an autosomal recessive condition that leads to liver and lung damage due to a
reduction in the protease inhibitor increasing the levels of neutrophil elastase in the tissues
- Patients present with COPD-like symptoms alongside chronic liver disease

- Diagnosis is from reduced levels of alpha-1 antitrypsin in the serum
Management is with prevention of hepatic and lung insult e.g. no smoking or alcohol. Liver
transplantation is the only treatment for advanced disease
- There should be screening for HCC

Anaemia
Anaemia can be considered either as a reduction in haemoglobin concentration, haematocrit, or RBC
count. The WHO criteria for diagnosis of anaemia differ for males and females
- <130 g/L in males

- <120 g/L in females (<110 g/L if pregnant in the 1st trimester, <105g/L in the 2nd and 3rd, and
<100 g/L postpartum)
Over the first year of life, HbF (2, 2) is gradually replaced by HbA (2, 2) and HbA2 (2, 2). In
children, anaemia ranges therefore differ dependent on the child’s age, but most children will be
asymptomatic until Hb drops below 6 – 7 g/dl
- Neonate <14 g/dl

- 1 – 12 months <10 g/dl (haemoglobin concentration drops over the first year of life, before
increasing again)
- 1 – 12 years <11 g/dl
It is important to note that haemoglobin concentration is related to plasma volume, hence

dehydration may hide anaemia, and high plasma volumes may expose it.
The causes of anaemia can be divided into three main groups
1. Impaired red cell production

o Red cell aplasia e.g. parvovirus B19 infection, Diamond-Blackfan anaemia, transient
erythroblastopaenia of childhood (TEC)
o Ineffective erythropoiesis e.g. iron deficiency, folate deficiency, anaemia of chronic
disease, renal failure
2. Haemolysis
o Red cell membrane disorders e.g. hereditary spherocytosis
o Red cell enzyme disorders e.g. G6PD deficiency
o Haemoglobinopathies e.g. thalassemia, sickle cell
o Immune mediated disorders e.g. Rhesus disease, autoimmune conditions
3. Blood loss
Classification and diagnosis of anaemia is usually determined by MCV into microcytic, macrocytic,
and normocytic forms
Microcytic Normocytic Macrocytic

Iron deficiency Blood loss B12/ folate deficiency
Thalassemia Anaemia of chronic disease Alcohol excess
Sideroblastic anaemia Bone marrow failure Myelodysplasia
Renal failure Hypothyroidism

Haemolysis Haemolysis
Blood transfusion is rarely required in anaemia, but is recommended in the following situations
- Hb <70
- Acute cause
- Severe anaemia with heart failure
Presentation
The signs and symptoms of anaemia depend largely on the degree of anaemia and the rate of its
onset. If anaemia develops gradually over a long period of time, it is often asymptomatic as the body
will compensate for the reduction in haemoglobin in two main ways
1. There will be an increase in the level of 2,3-DPG to right-shift the haemoglobin saturation
curve and promote oxygen release to tissues
2. Heart rate and stroke volume will also increase, to increase the amount of oxygen delivered
to the tissues
Symptoms of anaemia include exertional dyspnoea, fatigue, palpitations, headache and drowsiness,
and angina and intermittent claudication. There may also be volume depletion due to bleeding,
which can cause additional fatigue, muscle cramps, and postural dizziness
- Rarely, there can also be physical signs of anaemia such as conjunctival pallor, koilonychia
and angular stomatitis
Investigations
Key investigations include full blood count (including MCV), blood film, serum B12 and folate,
reticulocyte count, and iron studies
- If reticulocyte count is low, the likely causes are parvovirus B19 or Diamond-Blackfan
anaemia
If reticulocytes are high or normal, iron studies and serum bilirubin can help distinguish the likely
cause
Iron TIBC Ferritin* MCV Bilirubin

Iron Deficiency ↓ ↑ ↓ ↓ Normal
Chronic Disease ↓ ↓ ↑ Normal Normal
Haemolysis ↑ ↓ ↑ Varies ↑
In haemolysis, there will be increased unconjugated bilirubin and increased urinary urobilinogen.
Red cells may have an abnormal appearance on blood film, and there will be increased red cell
precursors in the bone marrow
- If the haemolysis is immune-caused, direct antiglobulin test will be positive
*Serum ferritin is an acute phase protein, and may therefore be increased in inflammation, masking
IDA. Transferrin saturation (where available) is a more reliable test
Haematinic Deficiencies
Iron Deficiency Anaemia (IDA)
Iron deficiency leads to ineffective erythropoiesis, and impaired red cell production. There are three
potential causes of this
- Inadequate intake. This is common in infants, particularly if there is a delay in weening or

weening onto insufficient iron rich roods e.g. cow’s milk
- Malabsorption
- Blood loss
Iron deficiency leads to a microcytic, hypochromic anaemia; where both MCV and MCH are reduced.
-Thalassemia trait should be excluded by measurement of ferritin
- Pencil cells and target cells may also be present

It is important to exclude malabsorption (particularly in children) and chronic blood loss, particularly
where patients are not responding to iron
Treatment should be of the underlying cause, alongside dietary advice and oral iron
supplementation
- In adults, 200mg PO ferrous sulfate TDS is best but associated with significant side effects
- In children, sytron is used
Iron should be continued for 3 months following normalisation of Hb
Vitamin B12 and Folate Deficiency
Deficiencies in B12 or folate will both lead to macrocytic, normochromic anaemias
- There may be neutrophil hypersegmentation on blood film

B12 deficiency is often caused by nutritional lack of B12, this is most common in vegans as B12 is
found only in animal products. Malabsorption is another common cause, as B12 is absorbed from
the terminal ileum in a complex with intrinsic factor
- If there is inflammation of the ileum or absence of intrinsic factor (due to gastrectomy,

pernicious anaemia, or congenital absence of IF) B12 will not be absorbed
o Pernicious anaemia is diagnosed by the presence of intrinsic factor antibody and
parietal cell antibody. These have low sensitivity and specificity
Patients with B12 deficiency may have glossitis, and can develop peripheral neuropathy or subacute
combined degeneration of the spinal cord (dorsal column and corticospinal tract disease)
B12 deficiency can be treated with hydroxocobalamin with folic acid
Folate deficiency is generally dietary, deficiency is assessed by measuring serum folate level and
treated with therapeutic doses of folic acid
Other Microcytic Anaemias
Anaemia of Chronic Disease
Anaemia of chronic disease occurs when there is an inflammatory response to illness. This
upregulates hepcidin, leading to three key factors
1. Poor use of iron in erythropoiesis

2. Cytokine induced shortening of RBC life-span
3. Decreased erythropoietin production

Treatment is of the underlying cause
Sideroblastic Anaemia
Sideroblastic anaemia should be suspected where patients have a microcytic anaemia not
responding to iron
- Blood film will show sideroblasts

Red Cell Aplasia
Red cell aplasia is suggested by a low reticulocyte coun, normal bilirubin, negative Coombs test, and
absent red cell precursors on blood film. There are three main causes
- Diamond Blackfan anaemia (DBA) is a rare condition, usually caused by a sporadic mutation
o Alongside anaemia there are congenital anomalies, including short stature and
abnormal thumbs
o Treatment is PO steroids, and if unresponsive monthly transfusions ± stem cell
transplant
- Transient erythroblastopenia of childhood (TEC)
o This is self-limiting, and usually triggered by viral infection
- Parvovirus B19 can cause aplasia in children with inherited haemolytic anaemias not healthy
children
o Slap-cheek rash may be present
Haemolytic Anaemia
Haemolysis is the premature breakdown of RBC before their 120-day lifespan is complete
- This destruction can occur in the circulation (intravascular) or in the reticuloendothelial

system of the liver, spleen and bone marrow (extravascular)
Haemolysis is suggested by anaemia with a normal/raised MCV, raised LDH, pre-hepatic jaundice
(increased bilirubin with increased urinary urobilinogen), alongside reticulocytes on the peripheral
blood film
- Other features specific to cause may be seen on blood film e.g. sickle cells, schistocytes,
spherocytes, Heinz bodies
Direct Coombs test can also be used in cases of haemolysis. This identifies RBCs coated in antibody
or complement, indicating an immune cause of haemolysis.
Certain features can distinguish intravascular from extravascular haemolysis
- Extravascular haemolysis can lead to splenomegaly

- Intravascular haemolysis can lead to decreased plasma haptoglobin, haemoglobinuria, and
methaemalbuminaemia
Immune Mediated
Coombs positive immune mediated causes include
- Drug induced e.g. penicillin, quinine

- Autoimmune haemolytic anaemia
o Warm haemolytic anaemia can be treated with steroids/ immunosuppressants
o Cold haemolytic anaemia may indicate an underlying connective tissue disease or

haematological malignancy. Treatment is to keep warm and address the underlying
cause
Coombs negative autoimmune haemolytic anaemia is usually due to hepatitis, or as a reaction to
vaccinations/ medications
Hereditary Spherocytosis
Hereditary spherocytosis is an autosomal dominant disease, but the majority of cases are caused by
a novel mutation rather than inherited
- Defects in the red cell membrane alter the cell shape, meaning that there is extravascular
haemolysis in the spleen
Patients usually present with jaundice, splenomegaly, and mild anaemia. There may also be
gallstones due to excess bilirubin excretion
- Aplastic crisis is transient and rare, but can occur if there is parvovirus B19 infection. This can
be managed with blood transfusion
Diagnosis usually follows identification of spherocytes on blood film, and exclusion of autoimmune
haemolytic anaemia.
Most children can be managed with oral folic acid. Where anaemia is more severe, there can be
splenectomy
G6PD Deficiency
Glucose-6-phosphate dehydrogenase is essential for preventing oxidative damage to cells. G6PD

deficiency therefore results in oxidant-induced haemolysis of red blood cells
- This is an X-linked condition, but some heterozygous females may be affected due to a
higher proportion of normal X chromosomes being inactivated
Patients present with neonatal jaundice or acute haemolysis. In acute haemolysis, patients will have
jaundice, fever, malaise, and dark urine
- Acute haemolysis in G6PD deficiency is precipitated by a stressor e.g. infection, broad beans,
medications (antimalarials, sulphonamides, quinolones, aspirin, nitrofurantoin)
Diagnosis is made by measuring G6PD activity in red blood cells. Management is with avoidance of
factors that can precipitate haemolysis
- There may be Heinz bodies (bite cells) on blood film
Sickle Cell Disease
Sickle cell disease is an autosomal recessive condition, caused by mutations in the  globin chain,
result in in production of HbS rather than HbA
- Diagnosis can follow Hb electrophoresis and sickle solubility testing

There are a few clinical variants of the condition
- HbSS is true homozygous sickle cell anaemia, where there is no HbA

- HbSC is a heterozygous state, where they inherit one HbS and one HbC (another  globin
mutation), and therefore there is no HbA
- Sickle -thalassemia is a heterozygous state, where they inherit one HbS and one -
thalassemia gene
- Sickle trait is a heterozygous state with one normal  globin gene and one HbS gene. These
are usually asymptomatic carriers
The presence of HbS in cells results in the formation of rigid, tubular, spiral shaped red blood cells.
These can get trapped in the microcirculation resulting in vaso-occlusion and tissue ischaemia. This
can be precipitated by cold and dehydration
- Vaso-occlusive crisis is painful, and usually occurs in the bones of the limbs and spine, as well
as the hands and feet (presenting with dactylitis)
- More severe consequences of occlusion include mesenteric ischaemia, stroke, leg ulcers,
and priapism
- The most severe manifestation is acute chest syndrome, where there is a need for
mechanical ventilation and emergency transfusion
Other problems can include haemolytic crisis, aplastic crisis (parvovirus infection leading to bone
marrow failure), and sequestration crisis (splenomegaly, anaemia and shock). Childhood stroke is
also a common complication
- Management in crisis is usually analgesia, rehydration, and exchange transfusion
Long term management should include immunisation against encapsulated organisms

(pneumococcus, meningococcus, HIB). Patients with sickle cell are susceptible to such infections as
they have functional asplenia due to chronic microinfarction of the spleen
- Daily oral penicillin and folic acid are recommended

- Hydroxyurea can be given to increase HbF production in children
- Hydoxycarbamide can be given in adults with frequent crisis
- Bone marrow transplant can be curative
-Thalassemia
-Thalassemia is characterised by a severe reduction in the production of -globin and therefore

HbA. There are two forms
- -Thalassemia major is most severe, and there is no HbA production

- -Thalassemia intermedia is milder, and there is production of some HbA (and lots of HbF in
children). This may not require transfusion but there may be splenomegaly
Patients have a transfusion dependent anaemia, alongside jaundice. Extramedullary haematopoiesis

can occur, leading to hepatosplenomegaly and bone marrow expansion (maxillary overgrowth and
skull bossing)
Management is with lifelong monthly blood transfusion, alongside chelation with desferrioxamine to
prevent iron overload
- Where possible, bone marrow transplant is curative

- If patients do not comply with chelation therapy there can be cardiomyopathy, cirrhosis,
diabetes, and hypopituitarism
Seizures
First Seizure
A seizure is an abnormal, synchronous, paroxysmal neuronal discharge in the brain causing abnormal
function.
There are many potential differential diagnoses for a patient presenting with a seizure
- It is important to carefully assess the patient, as the diagnosis of the underlying cause can
have significant consequences on lifestyle
Often, the seizure will have finished by the time the patient presents to A&E. However, it is key to
assess the patient using an A to E approach
- Establish IV access in all patients following seizure, as they may experience a recurrence
- Assessment of disability is key
o Even in patients with normal AVPU, undertake formal assessment of GCS
o Ensure to measure BM
There are many potential causes of seizure
Trauma Haemorrhage, depressed cranial fracture

Toxic Alcohol withdrawal, drug overdose/ withdrawal, sedatives, poisons
Metabolic Particularly hypoglycaemia, hyponatraemia, hypocalcaemia, and
hypomagnesaemia
Also hyperglycaemia, hypernatraemia, hypercalcaemia, hypopituitarism,
hypercapnia, hypoxia, hypothyroidism, liver failure, renal failure
Neurological Epilepsy, raised ICP
Ischaemic CVA, reflex anoxic seizure (cardiac/vasovagal syncope)
Infective Meningitis, encephalitis, septicaemia, cerebral abscess, cerebral malaria
Autoimmune Vasculitis
Other Fever, eclampsia, non-epileptic attack disorder (NEAD)
History
History is key in differentiating the main causes of seizure, particularly in distinguishing between
syncope and seizure
- Where possible, witness accounts and collateral history are very important
History should follow the same format as for all cases of LOC
- Before the collapse

o Pre-syncope symptoms and warning signs e.g. light-headedness, ringing in ears,
blurred vision, flushing
o What was the patient doing at the time?
o Any focal neurological signs or aura
o Any palpitations
- During the collapse
o How long did the episode last?
o Did anyone notice a change in colouring
o Any seizure movement, tongue biting, or incontinence
o Was the patient rigid or floppy?
- After the collapse
o Does the patient recall the incident (did they lose consciousness)?
o How long did it take the patient to recover?
o Any residual symptoms e.g. weakness, confusion
o Any injury
The following table summarises some distinguishing features between differentials of seizure, the
post-ictal phase is the most sensitive for diagnosis
Seizure Cardiac Syncope Vasovagal Syncope NEAD
Trigger Rare e.g. Rare e.g. exertion Common e.g. None

flashing lights prolonged standing
Prodrome Aura None Pre-syncopal ?None

symptoms
Onset Sudden Sudden Gradual Sudden
Duration 1 – 3 minutes Brief <30 seconds Up to an hour
Jerking Common Rare Occasional, brief Prolonged

(waxes and
wanes)
Eyes Open Open Open Closed
Colour Blue Pale Pale Normal
Incontinence Common In recovery Rare Rare
Tongue Bite Lateral Rare Rare Tip
Post-Ictal Phase Prolonged Brief Brief Variable
Fatigued for No fatigue Fatigue for minutes

hours
Other important factors include
- The patient’s health over the previous days, have they had any symptoms suggesting
intracranial infection or metabolic derangement
- Have they experienced seizures before or if they are taking any AEDs
- Alcohol and drug history is key, particularly in withdrawal
- Always ask the patient about driving
Examination
Full cardiovascular and neurological examination are important
Investigations
Regular observations and neuro observations are key in these patients
- FBC
- U&Es, LFTs, calcium and magnesium, glucose, thiamine, blood alcohol, AED level, ?drug
screen
- Clotting
- Prolactin, as elevation >3x suggests epilepsy
ECG and lying-standing blood pressure are important
CT head should not be undertaken in the acute phase, unless the patient suffered a head injury
during the collapse or has focal neurological deficit
- CT/MRI are usually organised as an outpatient during seizure clinic review
EEG is not routinely performed following first seizure. If the patient has a second seizure, there
should be EEG within 48 hours to support diagnosis of epilepsy
Management
If the patient is well, with normal observations and minimal residual symptoms they can be
discharged from A&E
- Follow-up in a neurology outpatient clinic is recommended in all patients with a first seizure
- Follow-up in a cardiology outpatient clinic/ in-patient referral is recommended in the
following circumstances
o ECG abnormality
o Heart failure symptoms/signs
o TLOC during exertion
o Family history of sudden cardiac death
o Breathlessness
o Murmur
Advise all patients following seizure not to drive (notify the DVLA), swim, take showers rather than
baths, and not to operate any machinery until their outpatient appointment
- If there is a second seizure (criteria for epilepsy), it is often close to the first, therefore the
patient should exercise caution
Patients should avoid driving for 6 months following first seizure. If they are diagnosed with epilepsy
they cannot drive for 12 months following seizure.
- For provoked seizures e.g. reflex anoxic seizures, driving is at the discretion of the DVLA
Status Epilepticus
Status epilepticus is defined as a convulsive seizure which continues for a prolonged period (>30
minutes), or when convulsive seizures occur in sequence with no recovery between for >30 minutes
- In the hospital setting, seizures lasting >5 minutes are treated as status
Status epilepticus can be convulsive or non-convulsive, however non-convulsive is rare and

management is less urgent
Precipitating causes are the same as for first seizure, a common additional cause is non-compliance
with AED treatment
Assessment and Management
For patients in status outside of hospital give 10 – 20mg rectal diazepam and repeat after 15
minutes. Ensure rapid transfer to hospital
The initial step in managing status epilepticus is ABC assessment of the patient
- Airway control in an actively seizing patient is difficult, attempt to place the patient in the
recovery position and use suction where possible
- Give 100% oxygen via a non-rebreathe mask
- Ensure that good IV access is secured, ideally with two wide bore cannulas
o Take the following bloods
▪ FBC
▪ U&Es
▪ LFTs
▪ Calcium and magnesium
▪ Glucose
▪ Clotting
▪ AED levels
- Take an ABG to measure lactate and gain rapid information about electrolyte levels
- Check capillary BM, and treat hypoglycaemia if present
o 100ml 20% glucose
- If there is any suggestion of alcohol abuse, give 250mg of thiamine IV/ 500mg pabrinex
5ml of serum and 50ml of urine should be saved for future analysis, particularly toxicology
Following this, there can be administration of medications to stop the seizures
- Administer 5mg IV lorazepam as a slow bolus injection (IV diazepam 10mg can be used
where lorazepam is not available)
- If IV access was not secured, give buccal midazolam 10mg as an alternative
Give a maximum of two doses of first-line treatment, waiting 5 minutes between doses. If this is not
effective, there needs to be phenytoin infusion. Contact ICU at this point
- Give 15mg/kg loading dose of phenytoin at a rate of 50mg/min

o Phenytoin is prepared in normal saline at 10mg/ml, as a general rule use the
following
▪ Dose >1g use 250ml 0.9% NaCl

▪ Dose <1g use 100ml 0.9% NaCl
- Phenytoin has significant side effects, and therefore there should be continuous ECG and BP
monitoring
o IV fosphenytoin is an alternative with a better side effect profile, this should be used
where available
If the patient is in refractory status epilepticus, with seizures continuing after 30 minutes, there
needs to be RSI and tracheal intubation. Options include the following
- Propofol 2 – 10mg/kg/hr
- Midazolam 0.5mg/kg/hr
- Thiopental sodium 3 – 5mg/kg/hr
For non-convulsive status epilepticus treatment is with maintenance of usual AED therapy, or with IV
benzodiazepines under EEG monitoring
Management of Paediatric Patients
General principles are the same, but drug doses differ
- Lorazepam 0.1mg/kg is first line, rectal 0.5mg/kg diazepam or 0.5mg/kg buccal midazolam
are alternatives
o This is repeated only once
- Paraldehyde 0.4ml/kg PR is second line
- Phenytoin 18mg/kg over 20 minutes is third line, if this fails proceed to RSI and intubation
Investigations and Monitoring
When a patient is in status, organise CT and EEG
- CT should only take place when the patient is stable

- EEG monitoring can be continuous in the ICU, or used in the post-ictal phase to assess
response to treatment and confirm diagnosis
ECG monitoring should be carried out where possible. Lumbar puncture may be required in some.
Patients should have regular neuro obs. This includes GCS, pupils, and limb power
Epilepsy
Epilepsy is a tendency towards recurrent seizures (defined as 2 ore more seizures within a year),
with an epileptic seizure as the transient occurrence of symptoms and signs due to abnormal
electrical activity in the brain
- This leads to a disturbance of consciousness, behaviour, emotion, motor function, or

sensation
There are many varied causes of epilepsy, but in the majority of cases the condition is idiopathic.
Epilepsy can be due to:
- Cerebrovascular disease (seizures after stroke are fairly common) and neurodegenerative
conditions
- Following head injury or cranial surgery
- CNS infections and autoimmune conditions
- Brain neoplasms
- Genetic diseases (these usually have onset in childhood generally associated with cognitive
impairment)
- CNS malformations e.g. tuberous sclerosis, hamartomas
Seizure threshold can be lowered by certain drugs, such as alcohol, TCAs and phenothiazines
Classifications of Epilepsy
Focal seizures (partial seizures) originate and are confined to one hemisphere, they may progress
into generalised seizures. There are three sub-classifications
- Simple focal seizures, where there is no loss of consciousness

- Focal dyscognitive seizures, the impairment of consciousness may occur at onset or develop
later into the seizure
- Focal seizure evolving to generalised tonic-clonic convulsions
Generalised seizures are associated with impairment of consciousness, no pre-warning, and

distortion of the electrical activity of the whole or a large part of both hemispheres of the brain
(their site of onset cannot be localised to one hemisphere on EEG). There are many sub-
classifications of generalised seizure
- Absence. These cause someone to completely switch off and become unresponsive for
around 10 seconds with no loss of postural tone, and are most common in children. During
absence there may be eyelid fluttering or automatism
o EEG shows 3Hz spike and wave
- Myoclonic. These result in brief repetitive jerking movements with quick recovery
- Tonic. These typically begin in childhood and cause a sudden generalized increase in tone
- Tonic-clonic. This is characterised by rhythmical jerking following the tonic phase
- Atonic. These lead to a sudden loss in muscle tone (drop attacks)
There are also unclassified epileptic seizures, that do not adequately fit the pattern of other forms of
epilepsy
Presentation
The clinical decision as to whether an epileptic seizure has occurred should be based on the
description of the attack (witness accounts are best) and different symptoms
Generalised seizures cause a disturbance in consciousness, typically passing through tonic, clonic
and post-ictal phases
- Tongue biting (deep and lateral), vocalisation, cyanosis, frothing at the mouth, and
incontinence are suggestive of a seizure
- History of a post-ictal phase is most indicative of seizure, typically consisting of >2 minutes
of confusion, headache, myalgia, and drowsiness
Focal seizures typically have aura, focal motor activity, and automatisms (brief unconscious
behaviours). The features of the seizure differ dependent on the part of the brain where the seizure
discharge occurs from
- Frontal seizures may lead to clonic movements, including Jacksonian march

- Temporal love seizures are commonest, and may present with motor automatisms (lip-
smacking, plucking at clothes and hair, chewing), déjà vu and jamais vu, and strange auras
- Occipital seizures cause distortion of vision
- Parietal seizures cause contralateral dysaesthesias
Investigations
Routine blood tests should be performed to look for any potential metabolic causes of seizure or
identify any significant co-morbidities
- Glucose, as hypoglycaemia can cause seizure

- U&Es as well as calcium. Common metabolic derangements leading to seizure include
hypocalcaemia, hyponatraemia, and uraemia from renal failure
- LFTs as hepatic toxins in liver failure can cause seizure
An EEG should be performed to support a diagnosis of epilepsy, by showing background

abnormalities, but cannot be used alone to make the diagnosis
- Standard EEG should include photic stimulation and hyperventilation, this can determine
seizure type and epilepsy syndrome. This is best within 48 hours of a seizure, but can be
done at any time as it may show inter-ictal activity
- If standard EEG has not contributed to classification or diagnosis, a sleep or sleep-
deprivation EEG should be performed
- Negative inter-ictal EEG does not refute the diagnosis of epilepsy, as the activity may be
deeper in the brain
Neuroimaging (usually MRI) should be used to identify any structural abnormalities that could
potentially be causing epilepsy, this is not routine but used where patients are not responding to
medications
- In children this is indicated in focal seizure or where there is focal inter-ictal neurology
ECG should be carried out in all patients with altered consciousness, as disorders of cardiac rhythm
may stimulate epilepsy e.g. long-QTc
Management
The decision as to whether or not to start anti-epileptic drug therapy is dependent on the relative
risks of recurrent seizures and the commitment to long term medication with potential adverse
effects
Medication should only be started when diagnosis of epilepsy is confirmed (generally following a
second seizure)
- It is best to start with monotherapy, and use a consistent supply from the same
manufacturer
- The dose of each medication should be gradually titrated up to the maximum tolerated dose
Seizure Type First-Line Second-Line Notes

Generalised tonic-clonic Valproate Alternative first-
Lamotrigine line
Carbamezapine Topiramate
Levetiracetam
Tonic/ Atonic Valproate Lamotrigine
Absence Ethosuximide Alternative first- Carbamazepine may
Lamotrigine line exacerbate absence
Valproate seizures
Focal Lamotrigine Alternative first-
Carbamezapine line
Levetiracetam Gabapentin
Valproate
Myoclonic Levetiracetam Alternative first- Lamotrigine may
Valproate line exacerbate myoclonic
Topiramate seizures
Juvenile myoclonic Lamotrigine Alternative first- Carbamazepine may
epilepsy (JME) Levetiracetam line exacerbate JME
Valproate
Topiramate
Anti-epileptic medications have extensive side effect profiles, detailed below. There should be
baseline FBC, U&Es, and LFTs before starting the medications
Medication Side Effects

Carbamazepine Rash, neutropaenia, SIADH, liver enzyme inducing (many interactions e.g.
COC)
Sodium Rash, tremor, weight gain, hair loss, menstrual changes, thrombocytopaenia,
Valproate teratogenicity (neural tube defects)
Lamotrigine Rash, allergic disorders, aplastic anaemia
Topiramate Weight loss, drowsiness, withdrawal, renal calculi
Levetiracetam Weakness, irritability, mood swings
Phenytoin Gum hypertrophy, acne, hirsutism, coarse facies, osteomalacia, teratogenicity,
sedation
Where a patient has been seizure-free for 2 years one can consider medication withdrawal. This
should be carried out slowly, withdrawing one drug at a time. The risk of seizure relapse is highest in
the first year
If seizures are not controlled with medication (as in 30 – 40% of cases) there should be further
assessment for alternative treatments. Drug resistant epilepsy is defined as continuous seizures
despite trials of >2 appropriately selected drugs
- Vagal nerve stimulation is indicated as an adjunctive therapy to reduce frequency of

seizures. This senses pre-ictal tachycardia and increases parasympathetic activity to avert
seizure
- DBS targeted at the epileptiform area is not currently recommended

- Surgical options can be effective in refractory focal epilepsy. This includes focal cortical
resection, anteromedial temporal resection, corpus callosotomy, and functional
hemispherectomy
It is important to tell the patient of their duty to inform the DVLA of their condition, all patients with
epilepsy must not drive within 12 months of their last seizure. Some people may not be able to
continue their job if they are diagnosed with epilepsy e.g. operating machinery
A ketogenic diet (high in fat, low in carbohydrate and protein) may be useful in some cases.
Sudden Unexpected Death in Epilepsy (SUDEP)
SUDEP is a sudden, unexpected, unwitnessed, non-traumatic death of a person with epilepsy
- This does not necessarily occur with a seizure
Generalised tonic-clonic seizure is the highest risk for this, tending to occur during sleep
Juvenile Myoclonic Epilepsy (JME)
JME is a specific form of epilepsy, with myoclonic jerks in the morning alongside mainly
photosensitive tonic-clonic seizures developing in adolescence
- EEG shows generalized spike and wave
For medications used, see above
- In JME medications should never be withdrawn, even if seizures are controlled, as there is a
very high likelihood of relapse when patients stop taking medication
West’s Syndrome
West’s syndrome is characterised by infantile spasms, learning disability, and hypsarrhythmia

(abnormal interictal EEG pattern)
- This typically arises in infants between 3 – 12 months, and carries a poor prognosis with
likely developmental delay and continuing seizures through life
Management is with AEDs (valproate, lamotrigine), steroids, and nitrazepam
Lennox-Gastaut Syndrome
Lennox-Gastaut syndrome is characterised by frequent seizures of different types, often leading to

status epilepticus. This typically affects children from 1 – 7 years’ old
- Interictal EEG shows characteristic 1.0 – 1.5Hz spike with slow waves
It carries a poor prognosis with intractable seizures, and severe developmental and cognitive
difficulties. Surgery is more commonly used in Lennox-Gastaut than other epilepsies, including
corpus callosotomy
Hippocampal Sclerosis
Hippocampal sclerosis is a common cause of complex partial seizures (temporal lobe epilepsy), this
presents with features including
- Automatisms, déjà vu, jamais vu, olfactory auras, unusual behaviour
Patients will typically have experienced childhood febrile seizures
Where these patients do not respond to medication, surgical treatments can be highly successful
Benign Rolandic Epilepsy with Centro-temporal Spikes (BREC)
BREC is an idiopathic epilepsy syndrome that causes simple partial seizures when awake (usually on
awakening), and partial seizures with secondary generalisation when asleep
- EEG shows unilateral or bilateral centro-temporal spikes
This carries a good prognosis, with most patients growing out of the condition. If problematic
however, it can be treated with carbamezapine
Self-Harm
Self-harm and attempted suicide are very common causes of presentation to A&E departments, and
require appropriate assessment and referral
Parasuicide is a term that encompasses deliberate self-harm and attempted suicide
- It is an act with a non-fatal outcome, in which an individual deliberately initiates a non-

habitual behaviour that will cause self-harm
Suicide is the act of killing oneself deliberately, initiated and performed by the person concerned in
full knowledge or expectation of its fatal outcome
Assessment
The approach to the patient should be with A to E assessment
- Secure the patient’s airway, often (in overdose) there is a risk of vomiting, so consider lateral
positioning
- IV access is important as there may be deterioration, or the need for administration of an IV
antidote
- Exposure is important, noting the distribution of self-inflicted injury where present
- Cuts, noting depth and potential need for surgical review
- Burns and scalds
- Insertion of harmful foreign bodies into cavities
- Scratching
Focussed examination should assess for signs of substance misuse/overdose, chronic alcoholism,
and psychiatric disorders (eating disorders, depression, anxiety, psychosis)
- General inspection is most relevant here, but there should also be neurological,
cardiovascular, respiratory and GI assessment
Further History
There are 5 components to suicide risk assessment
1. The history of the current attempt

- What precipitated it, were there any triggers
- Was it planned or impulsive
- What was the intention
- What method did they use; violent methods are more worrying, as they are more
likely to complete
- Presence of plans for others after death e.g. suicide note, updated will. This
indicates motivation and planning
- What steps did they take to avoid discovery?
- Did the patient seek help after the attempt, or were they discovered by someone
else
- How does the patient feel about the attempt now?
2. Assessment of risk factors. The highest risk group for completed suicide is middle-aged men
- Previous suicide attempt or previous deliberate self-harm
- Past psychiatric history, particularly of the following
▪ Affective disorders, particularly depression
▪ Schizophrenia
▪ Alcohol dependence
▪ Borderline personality disorder
- The patient’s current mental state being that of hopelessness, unexplained
symptom improvement, psychotic symptoms (particularly command hallucinations),
or development of insight into their condition
- Past medical history of chronic pain, insomnia, or terminal illness
- Substance misuse
- Financial difficulty
- Relationship problems
- Bereavement
- Discharge from inpatient psychiatric care
3. Assessment of the patient’s current mood e.g. depression, anger. This should include
assessment for symptoms of mental illness
4. What are the protective factors?
5. What are the patient’s current thoughts and plans towards suicide?
Full mental state examination should take place when possible, this is usually not appropriate in the
A&E setting
Often, the patient cannot recall or does not want to disclose the substances they have ingested.
Other toxicology tests are recommended, including
- Plasma paracetamol and salicylate levels

- FBC, U&Es, LFTs, clotting
- ABG/VBG
Urine drugs of misuse screen may be appropriate
ECG is important in all patients with overdose. CXR is indicated where there is risk of aspiration.
Management
All people who have self-harmed should be offered treatment for the physical consequences of self-
harm and a full psychosocial and psychological assessment to determine the need for referral
General treatment for overdose includes
- Activated charcoal
- Access to TOXBASE for further advice on management
General treatment for self-injury includes
- Superficial wound closure

- Referral for wound assessment and exploration in wounds >5cm, deep, or involving deep
structures
Where patients frequently present with self-harm there should be additional advice
- Instruct the patient/ their family on how to manage superficial injuries e.g. compression,
elevation
- Harm minimization techniques can also be discussed, such as using clean blades and cutting
away from major vessels. This is controversial.
Further management of patients following suicide attempt is dependent on risk, and should involve
the patient in the formation of an MDT care plan. This can include the following
- Admission to psychiatric services

- Home with the home treatment team (hospital at home)
- Home with referral to secondary mental health services
- Home with GP follow-up, this is not recommended following attempted suicide
Domestic Violence
Domestic violence is a risk factor for self-harm, and is important for A&E staff to recognise so that
appropriate safe-guarding can be put into place
- Patients are only likely to disclose domestic violence if they are sure that they will receive a
sympathetic and confidential response
The HARKS questions can be useful
- Humiliate: do you ever feel like you’ve done something wrong

- Afraid: do you feel afraid
- Rape: have you ever had sex against your will, or done something that you didn’t want to do
- Kick: have you been hurt or threatened
- Safety: do you feel safe to go home, are there weapons in the home
The Duluth wheels of power and control can be useful to help the patient identify if they are
experiencing abuse
Always ask if there are children in the home, this requires immediate disclosure and safeguarding
referral, ideally with the patient’s consent (but this is not required).
Domestic abuse includes physical, emotional, psychological, sexual and financial abuse. Signs of
domestic violence can include
- There is often an inappropriate delay in seeking medical advice following injury

- History not compatible with the bruise seen
- Inconsistent history
- Contradicting history between partners
- Imprint
- Pathological interaction between partners
- Repeated visits to different EDs
- Unusual patterns of injury and injuries of differing ages e.g. bruising, fractures
Victims of domestic violence should be offered police involvement; if they decline they should be
provided with information and contact details for charitable agencies that may be able to provide
support for them
- Often leaflets with domestic violence advise are placed in the women’s toilets, so that they
can be easily accessed without the abuser being aware
- If the patient decides that the do not want any help, as long as there are no children
involved, their wish must be respected
The most dangerous time for the woman is when she is leaving a violent relationship
Poisoning and Overdose

In poisoning and overdose there are three main priorities, which should be addressed using an A to E
assessment
1. Resuscitate the patient

2. Reduce drug absorption if possible
3. Give a specific antidote if available
Assessment
Rare overdoses should be triaged into majors or resus
Use an A to E approach
- Take U&Es, glucose, LFTs and clotting, and other routine bloods
- Perform an ABG
- Assess and record full GCS, and repeat regularly
If the patient can give a history, try to establish the following. Be mindful that the information in the
history is not always accurate, and the amount/type of substance taken is often unclear. The
acronym MATTERS can be useful here
- Medication or substances ingested (particularly alcohol)

- Amount
- Time (when was the overdose, was the overdose all at once or staggered)
- Toxicology of the drug
- Emesis and presence of pill fragments
- Reasons for taking
- Signs and symptoms
- (How much does the patient weigh, it is important to calculate the overdose in
mg/kg)
Signs of poisoning differ dependent on the drug ingested
Substance Signs
Tricyclic Antidepressants Coma, dilated pupils (mydriasis), divergent squint, tachycardia, UMN
signs
Benzodiazepines Coma, hypotension, respiratory depression, hypotonia
Opioids Coma, respiratory depression, pinpoint pupils (miosis)
Salicylates Tinnitus, deafness, hyperventilation, sweating, tachycardia
Amphetamines/Cocaine/ Agitation, tremor, tachycardia, mydriasis, hyperthermia, hypertension
SSRIs
Plasma toxicology is very useful alongside the routine blood tests above
- Paracetamol and salicylate levels (ensure to record the time that the sample was
taken in the notes)
- Comprehensive drug screening is rarely needed
Save a sample of urine for toxicological analysis
Record an ECG in all patients, and monitor as per instructions on toxbase. CXR may be indicated if
there has been vomiting in the unconscious patient
Management
Always consult the national poisons unit or TOXBASE for appropriate management options
Measures to reduce drug absorption include
- Gastric lavage or aspiration, effective if used <1 hour after overdose

o This is not recommended unless there specialist advise and severe poisoning
- 50g activated charcoal, effective if used <1 hour after overdose. 4 hourly doses can
also increase elimination
o Check that it is recommended in the specific overdose, as some drugs do not
bind to charcoal e.g. lithium, iron, ethylene glycol
- Bowel lavage with Klean-Prep 2L/hr is rarely needed
In most cases of poisoning, there is no specific antidote available. Appropriate supportive care and
observation periods are suggested on toxbase, but common actions to take are summarised below
- Protect the airway, ET intubation is recommended in patients GCS<8

- Closely monitor breathing, and ventilate where necessary
- Manage hypotension with fluid boluses, and escalate to ITU where appropriate
- Cardiac arrhythmias generally require input from a poisons expert
o Correct any hypoxia, respiratory depression, metabolic acidosis, and
electrolyte abnormalities
o Common causative agents include TCAs, beta-blockers, digoxin, potassium,
bronchodilators, verapamil, and amphetamines
- Manage convulsions with AEDs only if they are repeated or prolonged
- Hyperthermia should be addressed with cooled IV fluids and sponging. Use
chlorpromazine or dantrolene if needed (only with senior input)
Overdoses with specific antidotes are summarised below
Drug Antidote
Benzodiazepines Flumazenil
Beta-blockers Atropine, glucagon
Carbon monoxide Hyperbaric oxygen therapy
Digoxin Digibind (digoxin antibodies)
Ethylene glycol Ethanol, fomepizole
Iron Desferrioxamine
Methanol Ethanol, fomepizole
Opiates Naloxone
Paracetamol N-acetylcystiene
TCAs Sodium bicarbonate
Warfarin Vitamin K, beriplex
Most patients who take overdoses suffer no serious ill effects, and can be adequately treated in ED
- Some will require referral to medical wards or ICU

- For those physically well, but having taken deliberate overdose, it is usually advisable
to admit for psychiatry review
Drug Overdose
Benzodiazepines
The effects of overdosing on benzodiazepines, unless combined with other sedatives, are usually
mild
- Drowsiness, slurred speech, nystagmus, mild hypotension, ataxia

- When combined with other sedatives e.g. alcohol there is a more severe
presentation with respiratory depression, coma, and cardiac arrest
Flumazenil is given as 0.2mg boluses up to a maximum of 3mg
- The use of flumazenil is controversial and should not be given in mixed overdose or
in patients dependent on benzodiazepines (due to adverse psychological effects)
Amphetamines and Cocaine
Patients with amphetamine/cocaine overdose with have sympathetic hyperactivity
- Dilated pupils, hypertension, tachycardia, skin pallor

In overdose there can be intracranial haemorrhage (SAH), vasospasm, heat-stroke, rhabdomyolysis,
AKI, and acute liver failure
- The vasoconstrictive effects of cocaine can cause myocardial ischaemia even in

individuals with normal coronary vessels. Therefore, ECG should be monitored
continuously for evidence of ischaemia, infarction or arrhythmia
Management is with sedation (where necessary) using 5 – 10mg diazepam
- Seizures should be controlled with 10mg stat diazepam

- Significant hypertension can be controlled with nitrates e.g. GTN 1 – 2mg
- Hyperpyrexia can be managed with tepid sponging or cooled IV fluids, aim to keep
core temperature <38.5
- Narrow complex tachycardias can be treated with diazepam or verapamil.
Ventricular arrhythmias should be treated with sodium bicarbonate
Tricyclic Antidepressants
TCA overdose presents with anti-cholinergic features (tachycardia, dry mouth, dilated pupils (can be
unreactive), urinary retention, ataxia, and jerky limb movements
- There may be coma, often with a divergent squint

ECG changes are key in diagnosis, including prolonged PR interval and QRS duration leading to VT.
Arrhythmias are best treated by correcting hypoxia and acidosis with oxygen and sodium
bicarbonate.
Ethylene Glycol
Ethylene glycol is ingested as an ethanol substitute, and is present in antifreeze. It causes

inebriation, but metabolic acidosis develops soon afterwards
- Stage 1: intoxication, N&V, haematemesis, coma and convulsions. There may be

nystagmus, opthlamoplegia, hypotonia, and myoclonic jerks
- Stage 2: tachypnoea, tachycardia, hypertension, congestive cardiac failure
- Stage 3: flank pain, renal tenderness and ATN leading to AKI (crystal nephropathy)
Management is with gastric lavage and ethanol/fomepizole (will compete for breakdown by alcohol
dehydrogenase and prevent development of toxic metabolites)
- Monitoring with ABG is essential

- Dialysis may be required
Lithium
Lithium overdose can be deliberate or accidental; this can occur when patients are dehydrated,
hyponatraemic, or have ingested NSAIDs/diuretics
Thirst, polyuria, diarrhoea, vomiting, and coarse tremor are common initial symptoms
- Ataxia, dysarthria, seizure, and coma can follow this

It is essential to check lithium level, which is usually >1.5 in overdose. Activated charcoal is
ineffective in lithium overdose, but gastric lavage can be used if the patient presents <1 hour post-
overdose
- Give IV fluids and consider dialysis

Paracetamol
Paracetamol overdose is the commonest cause of ALF in the UK. The therapeutic dose of
paracetamol is 4g/day, however overdose rarely causes damage below 150mg/kg
- Liver damage occurs due to depletion of glutathione, leading to a build-up of

damaging NAPQI
- Single overdose is considered as anything taken in a 1 hour period, and staggered
overdose is taken over >1 hour
Over the first 24 hours following overdose patients are generally well or may have nausea/vomiting
- Hepatorenal failure with jaundice, RUQ pain, hypoglycaemia and encephalopathy

generally follows 48 hours later
- Lactic acidosis occurs later in the course of disease
- Clinically significant toxicity is unlikely if the patient is asymptomatic, with
undetectable plasma paracetamol levels, and normal LFTs/INR >24 hours after the
last dose
It is important to measure plasma paracetamol levels in all patients presenting with ALF, these are
accurate >4 hours post-ingestion of the drug
- The paracetamol antidote N-acetylcysteine is given where plasma paracetamol level

is above the threshold indicated on the plasma concentration/time graph
o At 4 hours give parvolex where plasma paracetamol >100mg/kg
o If the patient presents >8 hours after overdose, and it is likely that from the
history that they have ingested >150mg/kg, give parvolex before blood
results return
o In staggered overdose measure plasma paracetamol levels, but it is
recommended to commence treatment before results are obtained
- Also measure LFTs, coagulation screen, U&Es, glucose, FBC, and perform an ABG
N-acetylcysteine is most effective if given within 8 hours of overdose, however late presenters
should still be given the drug. It is given as an IV infusion over the course of 21 hours, delivered as 3
bags of fluid, each with a slightly decreased dose
- Bag 1 is 150mg/Kg acetylcysteine in 200ml 5% glucose solution, delivered over one

hour
- Bag 2 is 50mg/Kg acetylcysteine in 500ml 5% glucose solution, delivered over four
hours
- Bag 3 is 100mg/Kg acetylcysteine in 1000ml 5% glucose solution, delivered over
sixteen hours
If the patient is still in hepatic failure, bag 3 is continued and repeated until improvement is seen
- There is some hypersensitivity associated with the medication and anti-histamine

may be needed
- Patients should be given 10mg single dose of vitamin K
The KCH criteria in paracetamol overdose indicate poor prognosis in ALF, these patients should be
considered for transplantation listing
3. pH <7.25 after 24 hours

4. INR >6.5, creatinine >300µmol/L or anuria, and high grade encephalopathy
Opiates
Opiate overdose can occur in prescribed or illicit use. Where patients have previously been addicted
to illicit opiates and begin re-using, they are at highest risk of overdose as they over-estimate their
tolerance
- There is no single dose of opiate that constitutes overdose, reaction is entirely

dependent on the patient’s tolerance
Signs of opiate overdose include
- Pinpoint pupils, respiratory depression, myoclonic jerks, coma, hypotonia

Give naloxone IV 400mcg initially, continue 400mcg boluses every 2 – 3 minutes until the patient is
rousable. If 2mg total does not reverse coma, consider alternate diagnosis
- As naloxone is a competitive antagonist, the dose may have to increase to up to 4mg

in severe overdose
- The half-life of naloxone is shorter than opiates, the effects should be apparent
within 30 seconds or so. Due to the half-life, naloxone will wear off rapidly, therefore
an IV infusion should be set up following the IV boluses
o Give 2/3 of the dose required to initially rouse the patient per hour diluted in
500ml normal saline
- IM naloxone can be given where IV access cannot be secured
Be mindful that naloxone can precipitate a severe withdrawal reaction, and therefore where the
patient is highly opioid dependent use half-doses
Salicylate Poisoning
Salicylate poisoning tends to occur at >150mg/kg and is severe at >500mg/kg
- Common symptoms include tinnitus, deafness, hyperventilation, sweating,

tachycardia
- Metabolic acidosis is a key feature, and hypokalaemia may also occur
Treat patients with IV fluids and sodium bicarbonate. The bicarbonate alkalinises the urine and
promotes excretion of the drug. Dialysis may be required.
Digoxin
Digoxin poisoning leads to nausea, vomiting, delirium, xanthopsia, and adverse cardiac effects
- Bradycardia and ECG changes such as PR and QRS prolongation, down-sloping ST

depression (reverse tick), and VT/VF
Measure digoxin concentration at least 6 hours post-ingestion, severe effects tend to occur at
>4mcg/L (anything >2mcg/L is overdose)
- Give digibind in any patient with severe bradyarrhythmias or hyperkalaemia

Iron
It is important to establish what preparation of iron was used in overdose, as different forms have
different elemental iron content
- Serious toxicity is unlikely unless >60mg elemental iron/kg has been taken. Try to
measure serum iron concentration within 6 hours
Symptoms include
- GI upset is common
- Metabolic acidosis, cardiotoxicity, falling GCS, shock, convulsions, and GI bleed are
severe features
There may be haemolysis as a result of the iron overdose, therefore haemolysed blood results
should not be assumed to be spurious.
Give IV desferrioxamine infusion where there are severe features or where iron concentration
>5mg/L, this chelates iron and the complex is excreted n.b. urine will be discoloured red
Carbon Monoxide Poisoning
Carbon monoxide poisoning usually occurs from smoke inhalation, poorly maintained gas
appliances, or deliberate inhalation of car exhaust fumes
- CO leads to hypoxia by outcompeting oxygen for haemoglobin binding and

interrupting electron transport in mitochondria
Presentation
Patients present with hypoxia (falsely normal SpO2) without cyanosis, cherry-red skin and mucosal
surfaces, and symptoms such as headache and dizziness
- Where there are high levels of carboxy-haemoglobin there can be syncope,

tachypnoea, tachycardia, arrhythmias, dizziness, ataxia, and seizure
- Hypoxia leads to reduced CNS function, AKI, myocardial ischaemia, rhabdomyolysis,
and skin blistering
Some symptoms will occur several weeks after initial recovery; this includes disorientation, apathy,
irritability, difficulty concentrating, and Parkinsonism
Where patients have chronic CO poisoning there can be headache, flu-like symptoms, alteration in
consciousness, and subjective weakness
- CO poisoning should be suspected if more than one person in a household has these
symptoms, and there does not appear to be viral infection
Investigations
ABG with measurement of carboxyhaemoglobin concentration is essential
- Use a tight-fitting high flow oxygen mask in conscious patients, intubate and
ventilate comatose patients
- Check 12 lead ECG and take venous bloods for FBC, U&Es, CPK and cardiac enzymes
- Place the patient on continuous heart monitoring
- Control seizures with IV 10mg diazepam
Management
Keep patients on 100% oxygen and correct complications as they arise using continuous A to E re-
assessment
Where available, hyperbaric oxygen should be used as this accelerates the wash-out of
carboxyhaemoglobin
- This should be used where patients have been unconscious, COHb >30%, significant
symptoms, or metabolic acidosis
Sepsis
Sepsis can be defined as life-threatening organ dysfunction due to a dysregulated host
response to infection. Derangement in physiology in sepsis can include
- Abnormal coagulation
- Poor glycaemic control
- Cell apoptosis
- Increased circulating cytokines, proteases, lipid mediators, gaseous substances, and
vasoactive peptides
NICE criteria for sepsis involve identification by suspected infection (due to symptoms, fever
etc.) and the presence of ≥1 red criteria or ≥2 yellow criteria
Red Yellow
Mental State Objective altered mental state History of altered behaviour
RR >25 (or increased oxygen >20
requirement)
HR >130 >100
SBP <90 (or >40 below normal) <100
UO <0.5ml/kg/hr, or no output for <1ml/kg/hr, or no output for
>18 hours >12 hours
History Deterioration in function
Rigors
Immunosuppression
Recent surgery
The international guidelines suggest that sepsis should be identified using the sequential
organ failure assessment (SOFA) score. In patients with suspected sepsis, the presence of
two or more of the qSOFA criteria indicates likely sepsis
- Hypotension: SBP <100mmHg
- Altered mental status: GCS <15
- Tachypnoea: RR >22
Where patients have a qSOFA >2, there should be calculation of a full SOFA score. An
increase in baseline of 2 or more points on the total SOFA score indicates organ dysfunction.
In patients where the baseline SOFA score was not known prior to infection, assume a
baseline of 0
- SOFA score includes PaO2, platelet count, bilirubin, MAP, GCS, creatinine, and urine
output
Septic shock is a subset of sepsis, defined as sepsis alongside the following (despite
adequate volume resuscitation)
- Persistent hypotension requiring vasopressors to maintain MAP >65mmHg
- Lactate >2
The previous definition of sepsis was SIRS alongside infection, this should still be used as a
guide to indicate when a patient potentially has sepsis. SIRS was defined as two or more of
the following
- Temperature >38 or <36
- Heart rate >90

- Respiratory rate >20, or PaCO2 <4.3 kPa
- WCC >12 or <4
- Blood glucose >7.7 in a non-diabetic patient
- New confusion/ drowsiness
Severe sepsis was defined as sepsis alongside organ dysfunction, which can be evidenced by
any of the following
- SBP <90 or MAP <65, and/or lactate >2
- INR >1.5
- Bilirubin >34
- Urine output <0.5ml/kg/hr for 2 hours (or other AKI criteria)
- Creatinine >177
- Platelets <100
- SpO2 <90% on room air
Presentation
Early recognition of sepsis is essential to improve patient outcomes. Often, patients will
have presented a few days earlier with a focus of infection and continued to deteriorate
despite adequate oral antibiotics
- Non-specific symptoms are common e.g. lethargy, nausea and vomiting, abdominal
pain, and diarrhoea
Often, risk factors for sepsis will be present
- Extremes of age
- Immunosuppression e.g. chemotherapy, splenectomy, steroids, immunosuppressant
medications, pregnancy
- Recent trauma, invasive procedure, or surgery in the past 6 weeks
- IV drug users
- People with indwelling lines, drains, or catheters
Assessment
Approach patients with suspected sepsis using an A to E assessment

- Airway is usually patent, however some patients will have a reduced conscious level
and therefore be unable to protect their airway
- Breathing is usually tachypnoeic and SpO2 may be low
o Administer oxygen to achieve target saturations
- Septic patients are usually hypotensive
o Establish IV access, and take the following bloods from the cannula
▪ FBC
▪ U&Es and creatinine
▪ LFTs
▪ CRP
▪ Clotting screen
▪ Venous blood gas, including lactate and glucose measurement
o Give 500ml crystalloid fluid boluses to increase SBP

▪ Escalate to ITU as necessary, some patients will require vasopressors
and CVP monitoring
o Take blood cultures
o Take an ABG
▪ An ABG (or VBG) is essential to determine lactate level. Lactate is a
strong predictor of mortality, with lactate >4 giving a high risk of
death from sepsis
o Consider catheterisation
- Decreased conscious level indicates severe sepsis
Where a patient has suspected sepsis, there should be initiation of the sepsis 6. This should
be identified and undertaken during A to E assessment, and all should be applied within the
first hour following assessment as early treatment improves outcomes
1. Give oxygen, this may need to be through a non-rebreathe mask

2. Give IV fluid boluses to maintain SBP
3. Give IV broad spectrum antibiotics, as per local guidelines – usually co-amoxiclav or
tazocin
4. Take ABG for lactate measurement
5. Either catheterise the patient or commence hourly urine output monitoring
6. Take blood cultures, and consider an infective source
Focussed examination should take place to assess for a source of infection. This should
include cardiovascular, respiratory, and abdominal assessment. Common causes of sepsis
include
- Pneumonia
- Cellulitis
- Intra-abdominal infection e.g. perforation, post-op leaking anastomosis, biliary tract
infection
- UTI, pyelonephritis
- Wound infections
- Septic arthritis
- PID
- Endocarditis
- CNS infections e.g. meningitis, cerebral abscess
Further to the investigations carried out during A to E assessment, there should be the
following
Septic screen
- Urine dipstick and urinalysis for MC&S
- Erect CXR
- At least two sets of blood cultures, ideally prior to antibiotics

o Do not delay antibiotics for the culture result
o Give antibiotics prior to culture if the patient’s clinical picture indicates that
they should be given without delay
- Further investigations for source as appropriate e.g. abdominal USS, CT scan, lumbar
puncture, echocardiogram, bronchoscopy, laparoscopy, sputum culture, skin/wound
swabs, joint aspirate
Carry out an ECG to look for any abnormalities that may have occurred due to systemic
upset
Further Management
Antibiotics should be prescribed according to MC&S, the following antibiotics may be

appropriate
Mild Severe
CAP 500mg Amoxicillin PO TDS and 1.2g Co-Amoxiclav IV TDS and
500mg Clarithromycin PO BD 500mg Clarithromycin IV BD
HAP 625mg Co-Amoxiclav PO TDS 4.5g Tazocin IV TDS
COPD exacerbation 500mg Amoxicillin PO TDS 1g Amoxicillin IV TDS
UTI 200mg Trimethoprim PO BD 1.2g Co-Amoxiclav IV TDS and
5mg/kg Gentamycin IV
Skin/ soft tissue/ 1g Flucloxacillin IV/PO QDS 2g Flucloxacillin IV QDS
bone/ joint
Intra-abdominal 625mg Co-Amoxiclav PO TDS 1g Amoxicillin IV TDS and 5mg/kg
Gentamycin IV and 500mg
Metronidazole IV TDS
Endocarditis (Native 2g Amoxicillin IV 4 hourly with As before
Valve) 1mg/kg Gentamycin BD
Meningitis 2 – 4g Ceftriaxone OD
Surgical intervention at the source of infection/ removal of infected devices should be

carried out where required.
Potential complications of sepsis are summarised in the table below

Complication Evidence
Hypovolaemia/ shock SBP <90
ARDS Increased oxygen requirement to maintain sats
AKI Urine output <0.5ml/kg/hr
Creatinine >75
Hyperbilirubinaemia Bilirubin >35
DIC Platelets <100
INR >1.5
Encephalopathy New confusion/ decreased GCS
Where patients have septic shock requiring vasopressors (or lactate >4, or a potential need
for intubation), there should be management in an ITU setting
- First-line vasopressor in sepsis is noradrenaline ± vasopressin
- When a second-line vasopressor has been added, adrenaline should also be

added/substituted for noradrenaline
Where hypoperfusion is on-going despite adequate MAP, inotropic therapy with
dobutamine (beta agonist) should be added to the vasopressors
ARDS may develop
- NIV with PEEP should be used initially
- Sedation and intubation may be required if NIV is not meeting oxygen requirements
Thromboprophylaxis and ulcer prophylaxis should be considered in all ITU patients. There
should be regular monitoring of glucose, and management with insulin infusion where
required
Neutropaenic Sepsis
Cancer causes immunocompromise in two main ways

- Malnutrition and debilitation of patients
- Damage to the immune system, from either the cancer itself (e.g. leukaemias) or
from the cancer treatment (e.g. myelosuppression from chemotherapy)
Neutropaenia is a common after-effect of myelotoxocity from chemotherapy. Typically

patients will present having measured a high temperature or feeling symptoms of severe
infection
Diagnosis of neutropaenic sepsis comes where a patient has a neutrophil count <0.5x109/L
and either
- Temperature >38°C
- Signs consistent with sepsis e.g. temperature <36°C, respiratory rate >20 min -1 or
PaCO2 <32 mmHg (4.3 kPa), heart rate >90, confusion
Suspected neutropaenic sepsis should be treated as a medical emergency, and the patient
should be given empiric IV antibiotics without delay
- This is typically tazocin (or meropenem), but differs dependent on trust policy
Investigation and management should be as for all causes of sepsis, and ideally the patient
should be barrier nursed in a side-room
To reduce the risk of neutropaenic sepsis there should be infection control procedures,
prophylactic antibiotics (levofloxacin) where appropriate, and use of growth factors such as
G-CSF
Common infections include

- Candida albicans, potentially leading to candidaemia
- Aspergillus species are ubiquitous, but can lead to respiratory infection. This can be
seen as a crescent sign on CXR
- Pneumocystis jiroveci leads to pneumonia, causing a ground glass appearance to the
CXR
- Listeria monocytogenes causes meningitis, and is commonly treated with amoxicillin
Shortness of Breath
Acute shortness of breath is a common and distressing symptom for patients presenting to
emergency medical care
- Breathlessness is the sensation that the body’s demand for breathing outweighs the ability
of the respiratory system to satisfy it
Patients that are acutely breathless should be assessed using an A to E approach
- Ensure that the airway is patent, or that the breathlessness is not due to impending airway
compromise e.g. anaphylaxis
- The main focus of resuscitation is usually correction of hypoxia, this is best initially assessed
with SpO2
o Unless there is known COPD, give all breathless patients high flow oxygen
o Other management steps during assessment of breathing can include nebulised
salbutamol or re-positioning the patient so that they are sat upright
Bloods to request when IV access is established should include the following as a minimum
- FBC, inflammatory markers, U&Es, LFTs, clotting

All acutely breathless patients should have an ABG, ECG and CXR as soon as possible
History
History should include
- Duration of breathlessness and speed of onset

- Precipitating events
- Severity, this can be assessed as to whether the patient can speak in full sentences
- Associated symptoms to ask about specifically include
o Cough, and if productive the nature of sputum (frothy, purulent, haemoptysis)
o Fever
o Palpitations
o Syncope
o Wheezing
o Chest pain, and nature as cardiac or pleuritic
o Ankle swelling
- Clarify whether there is any change in breathlessness with position
When assessing past medical history and social history, consider the following factors
- Risk factors for CVD, COPD or PE

Certain medications can precipitate dyspnoea e.g. beta-blockers/NSAIDs in asthma
Examination
Respiratory and cardiovascular examination are key in breathlessness
Inspection
- Evidence of acute respiratory distress: dyspnoea, accessory muscle use, nasal flaring,
cyanosis
- Raised JVP could indicate tension pneumothorax or fluid overload
- Facial oedema could indicate anaphylaxis
- Tachycardia, irregular pulse, bounding pulse, or pulsus paradoxicus may be present

Palpation
- Tracheal deviation could indicate tension pneumothorax

- Uneven chest expansion indicates underlying pathology of the under-expanded lung
- Displaced or akinetic apex beat
Percussion
- Dullness can indicate consolidation, collapse (foreign body, tumour) or fluid

- Resonance can indicate pneumothorax
Auscultation
- Added heart sounds e.g. gallop rhythm can indicate heart failure
- Crepitations may indicate pulmonary oedema, infection
- Wheeze
Acute breathlessness can be caused by the following conditions
Cardiac Pulmonary Other
Acute pulmonary oedema Pneumonia Pain
MI Pneumothorax Metabolic acidosis e.g. sepsis,

DKA
Arrhythmia PE Drug overdose
Pericarditis Asthma Trauma
Pericardial effusion Exacerbated COPD Anxiety
ARDS Altitude sickness
Airway obstruction e.g.

anaphylaxis, foreign body, lung
cancer
Pleural effusion (usually

chronic)
Investigations
Peak flow is a useful bedside test in suspected asthma exacerbation
Further blood tests should be carried out dependent on likely cause
- Troponins
- D-dimer
- BNP
Further imaging can include echocardiogram, CTPA, high resolution CT scanning of the chest
Lung function tests may also be useful dependent on the ability of the patient to undertake them
Asthma
Asthma is due to paroxysmal and reversible airway obstruction due to
- Bronchospasm and smooth muscle hypertrophy

- Excessive production of secretions narrowing airways
Presentation
Asthma should be suspected where there is cough, wheeze, breathlessness and chest tightness
- Typically symptoms are worse at night and early in the morning, and present in response to
exercise/cold air/allergens
Other factors that make asthma more likely are personal/family history of atopy, widespread
wheeze and prolonged expiratory phase on auscultation
- Children may have Harrison sulci

Asthma is less likely if there is chronic productive cough without wheeze, normal chest examination
when symptomatic, voice disturbance, significant smoking history, cardiac disease, and normal PEFR
Investigations
Where a patient has a high likelihood of asthma, commence treatment with 6/52 of inhaled steroid
- Assess response to treatment with PEFR; patients should be asked to record a peak flow
diary for a couple of weeks to see treatment response
o Initial diurnal variation >20%, with improvement on treatment indicates asthma
- An alternative is to assess using spirometry at baseline and 6 weeks, with >12%
improvement
If there is an intermediate likelihood of asthma, diagnosis should follow spirometry
- FEV1/FVC <0.7 confirms airway obstruction. There should then be assessment for
reversibility to either short-acting bronchodilator (400mg salbutamol, wait 15 minutes) or a
trial of asthma treatment for 2-3 months
o Change of >400ml (>12%) in FEV1 when treated with a short acting bronchodilator is
diagnostic
- Normal spirometry obtained where the person is asymptomatic does not exclude a diagnosis
- Spirometry and PEFR results are dependent on sex, age, and height. This is what is used to
calculate predicted values
There may also be tests for atopy e.g. FBC (eosinophilia), skin-prick test, IgE
Management
Patients with asthma are reviewed at least annually. Three questions are always asked
1. Have you had any difficulty sleeping because of your asthma symptoms, including cough?
2. Have you had your usual asthma symptoms during the day (cough, wheeze, chest tightness
of breathlessness)?
3. Has your asthma interfered with your usual activities (housework, work, school, etc)?
There will also be a check of inhaler technique, PEFR diaries, lung function testing (PEFR), and review
of any exacerbations.
Lifestyle advice should be given on smoking cessation, avoiding triggers, recognising poor asthma
control (symptoms or worsening PEFR)
Medical management of asthma is a step-wise progression
Step 1 – Minimal Intermittent Asthma (infrequent short-lived wheeze)
- In step 1, short-acting selective β2 agonists such as salbutamol and terbutaline are used.
- These are given when PRN by inhaler, causing a rapid bronchodilation to give quick relief
- The individual’s inhaler technique is important in delivering the drug correctly. If they are
struggling, it can also be given by nebuliser, intravenously, or orally
- There is no specific contraindication to their use and side effects are minimal,
however high doses can cause tremor, tachycardia and hypokalaemia
Step 2 – Regular Preventer Therapy
- In step 2, inhaled corticosteroids such as beclometasone, fluticasone, or budesonide, are

used. These drugs are taken by inhaler usually twice a day at the lowest dose appropriate to
the severity of the asthma in question (usually 800µg or 200 in children)
- Inhaled corticosteroids are only used where patients have had an exacerbation in the last 2
years, they have symptoms requiring short-acting β2 agonist use over three times a week,
and/or they have symptoms at least one night a week
- Adverse effects include osteoporosis at high doses in adults, growth suppression in
children, sore throat, and oral thrush
Step 3 – Initial Add-On Therapy
- In step 3 a long-acting selective β2 agonists, such as salmeterol or formoterol, are used.

These have a long duration of action of around 12 hours, giving relief of reversible airway
obstruction
- They should always be used alongside a corticosteroid, and can sometimes be given as a
combination inhaler e.g. seretide (salmeterol and fluticasone)
- Where the LABA is partially effective, but control is still not optimum, increase the
steroid dose
Step 4 – Persistent Poor Control (refer at this point)
- In step 4 there are two main therapeutic options that can be used, both are oral
preparations
- Leukotriene receptor antagonist, such as monteleukast or zafirlukast
- Xanthine derivative, such as modified-release theophylline
Stepping down treatment should only occur where the patient feels that their asthma is well
controlled
- Reduce the dose of inhaled corticosteroids slowly, 50% every 3 months. When that is
reduced to the lowest dose possible, remove add on therapies
Acute Exacerbation (Status Asthmaticus)
Risk factors for asthma exacerbation include taking >3 classes of asthma medication, heavy use of β2
agonists, and brittle asthma (wide variation in PEFR, or sudden severe attacks on a background of
good control)
Triggers for asthma exacerbation include
- Environmental allergens
- Infections
- Exercise
- Medications e.g. beta blockers, NSAIDs
- Emotional factors
In acute severe asthma there is airway collapse in expiration, leading to air trapping and increased
self-PEEP. This means that inspiration is more difficult as higher pressures need to be overcome to
intake breath, tiring the patient
- Classification of acute asthma exacerbation is summarised below
Moderate exacerbation does not require referral to hospital, and can be managed with short
courses of prednisolone (40mg OD for 5 days) and increased use of salbutamol (10 puffs every four
hours)
For patients with acute severe asthma, there should be management following A to E assessment
and stabilisation
- Ensure airway is patent and give 100% oxygen through a non-rebreathe mask
- Careful assessment of breathing is important as asthma exacerbation can be complicated by
tension pneumothorax
- Continuous oxygen saturation monitoring, pulse rate, and respiratory rate should be
established
- Measure PEFR where possible
- Gain IV access and take routine bloods to establish baseline/ potential trigger. Perform an
ABG where saturations are reduced
Ensure to carry out CXR and ECG as soon as possible to exclude arrhythmia, consolidation or
pneumothorax
Initial treatment should be established during the breathing assessment in A to E where signs of
asthma are elicited
- High flow oxygen through a non-rebreathe mask (aiming for 94 - 98% saturation)
- High dose β2 agonist (2.5 – 5mg salbutamol), best given via 6L oxygen driven nebuliser and
repeated back to back, this is usually after 15 – 30 minutes
- If there acute severe or life threatening asthma, or if there is poor response to the β2
agonist, ipratropium bromide 0.5mg should be given alongside salbutamol for up to three
back-to-back nebulisers, and then four hourly PRN
- Oral/IV steroids (either prednisolone 40 – 50mg or hydrocortisone 100mg) should be given
as soon as possible and continued for 5 days
- IV magnesium sulphate (2g over 20 minutes) or aminophylline can also be given if response
is not adequate and the condition is life threatening
- These should only be given following consultation with senior medical staff
Contact ITU for any patient with life-threatening asthma or near fatal asthma
- There may need to be intubation and ventilation

Thromboprophylaxis is recommended, and peak flow should be monitored QDS. ABG should be
repeated.
Discharge should only occur where PEFR is >75% predicted, ensure the patient completes a 5-day
course of oral steroids.
Paediatric Asthma
Diagnosing asthma in pre-school children is difficult, as many children wheeze in early life. There are
two main patterns of wheeze
- Transient early wheezing (viral induced wheeze), this occurs with or without viral infection.
This will usually resolve by age 5
- Persistent and recurrent wheezing is usually due to atopic asthma. It can also be caused by
recurrent aspiration of food, cystic fibrosis, and congenital airway abnormalities
It may be indicated in children to perform skin prick testing to assess for triggers, or CXR to rule out
alternative causes (may show hyper-inflation or mucosal plugging (segmental collapse))
- Peak flow is difficult in children <7, therefore spirometry is used as an alternative. Normal
values are based upon weight
Management in >5s is as in adults, but there are some slight differences if the child is <5
- Step One: short acting beta-agonist

- Step Two: leukotriene receptor antagonist
- Step Three: leukotriene receptor antagonist and inhaled steroid (200mcg)
- Step Four: increase dose of inhaled corticosteroid (400mcg), consider theophylline
- Refer children <2 not responding to regular preventer therapy, and children <5 with
persistent poor control
It is important to deliver medications in a form that the child can access, this is usually a spacer
Acute Exacerbation in Children
Children require admission to hospital if they have acute severe, or life threatening asthma
Acute Severe Life Threatening

SpO2 <92% SpO2 <92%
PEFR 33 – 50% predicted PEFR <33% predicted
Cannot talk in full sentences, too breathless to Silent chest, fatigue, agitation, drowsiness
feed
HR >125 (if >5) or >140 (if 1 – 5) Cyanosis

RR >30 (if >5) or >50 (if 1 – 5) Poor respiratory effort
- Parents of asthmatic children should be advised to seek urgent medical attention if the child
does not respond to up to 10 puffs of salbutamol over 5 minutes
Management is equivalent to adults, but with half-doses.
Pneumonia
Pneumonia is inflammation of the lung parenchyma caused by bacterial or viral infection, leading to
accumulation of purulent material (polymorphoneucleaer leucocytes) within the alveoli
- Respiratory compromise occurs due to shunting and hypoxaemia, alongside reduction in

local pulmonary blood flow and restriction in chest movement
There are two main subdivisions of pneumonia
- Community acquired pneumonia (CAP)

- Hospital acquired pneumonia (HAP)
Presentation
Pneumonia typically presents with symptoms of lower respiratory tract infection
- Productive cough, tachypnoea, pleuritic chest pain and signs of systemic illness (pyrexia,
tachycardia, malaise, rigors)
- There may also be cognitive disturbance with confusion and drowsiness
In the community setting, any patient with a CRB-65 score (without urea) of >1 or SpO2 <94% should
warrant hospital admission
Assessment
Patients should initially be resuscitated using an A to E approach
- Titrate oxygen according to SpO2

- Gain IV access (some patients will require fluid resuscitation) and take the following bloods
from the cannula
o FBC may show raised WCC
o U&Es and LFTs as baseline for antibiotic treatment, and as part of CURB-65. LFTs can
be deranged in legionella pneumonia
o ESR/CRP may be elevated
- There should be ABG in any patient with SpO2 <94%
Initiate sepsis bundles where the patient fulfils criteria
Focussed examination may reveal new focal signs
- Reduced expansion, dull percussion, reduced breath sounds, bronchial breathing,

crepitations, wheeze and increased vocal resonance/whispered pectoriloquy
- There may be cyanosis, but carbon dioxide retention does not usually occur
Further Investigation
Microbiological assessment is not routinely recommended in the community, but is common in the
hospital setting where the pneumonia is moderate or severe
- Blood and sputum cultures

- Pneumococcal and legionella urine antigen test

Undertake ECG to help exclude differentials
Ensure that there is CXR, this will show consolidation in the affected lobe(s) and may show air
bronchograms
To assess the severity of pneumonia, CURB 65 is used
- Confusion of new onset

- Urea >7mmol/l
- Respiratory rate of >30 breaths per minute
- Blood pressure <90 systolic or <60 diastolic
- Age 65 or over
A score of 2 indicates moderate pneumonia, a score >3 indicates severe pneumonia (>4 may require
ITU management)
CAP
The commonest causative pathogen in CAP is streptococcus pneumonia, followed by haemophilus

influenza
- Atypical causes of CAP include legionella pneumonia (mostly travel related, common),
mycoplasma pneumoniae, and chlamydophila pneumoniae
- Aspiration pneumonia is more commonly caused by anaerobes and gram negatives
Supportive management in CAP should include the following, there should also be VTE prophylaxis
- Intravenous fluids
- Supplementary oxygen
- Analgesia and antipyretic agents
Definitive treatment is with antibiotics, when cultures return there should be adjustment of
antibiotics to match sensitivity
- In the community (mild pneumonia) amoxicillin 500mg TDS for five days (or
clarithromycin/doxycycline if pen allergic)
- If moderate the CAP should be treated with oral dual antibiotic therapy with 500mg
amoxicillin TDS and 500mg clarithromycin BD for 7 – 10 days
- If severe it will be treated with an IV β-lactam and macrolide e.g. 1.2g TDS of IV co-
amoxiclav and 500mg BD of IV clarithromycin, moving on to oral when there is
improvement. A total therapy of 7 – 10 days is recommended
Symptoms should steadily improve on therapy with chest pain and sputum production reduced by 4
weeks. Cough and SOB should have gone by 3 months, but the patient may still be fatigued up to 6
months
- If symptoms persist there should be follow-up CXR

HAP
HAP is defined as pneumonia that develops >48 hours after hospital admission
- A subset of HAP is ventilator acquired pneumonia (VAP), developing following endotracheal

intubation
The commonest causative pathogens in VAP include pseudomonas aeruginosa, staphylococcus
aureus, and enterobacteriaceae.
For HAP there should be the equivalent supportive management to CAP, however antibiotic
guidelines differ
- If patients develop pneumonia within 48 hours of admission it should be treated as CAP

- For true HAP there should be prolonged IV treatment with 1.2g co-amoxiclav, ceftriaxone or
4.2g piperacillin-tazobactam
Acute Heart Failure
Acute heart failure is often used to describe patients with specific clinical manifestations
- Acute-onset dyspnoea and pulmonary oedema

- Cardiogenic shock
In acute heart failure compensatory mechanisms have not yet become operative, therefore the
impact of the heart failure is more severe
There are several potential causes of acute heart failure
- ACS
- Acute mechanical disruption
o Acute valve regurgitation
o Rupture of the ventricular septum
- Arrhythmia
- Acute cardiac outflow obstruction
o Massive PE
o Tension pneumothorax
o Tamponade
Pulmonary Oedema
There are two main types of pulmonary oedema
- Cardiogenic pulmonary oedema

- Non-cardiogenic pulmonary oedema
o ARDS
o Neurogenic pulmonary oedema
o Iatrogenic fluid overload
o Hypoalbuminaemia
o Lymphangitis carcinomatosis
o Smoke inhalation
o Near drowning incidents
Initial Assessment and Management
Patients that acutely develop pulmonary oedema present characteristically
- Acute breathlessness, sweating, nausea, anxiety

- Cough productive of frothy pink sputum
- PND and orthopnoea
Signs include raised JVP, widespread crackles, decreased oxygen saturations, and gallop rhythm
Assess and stabilise the patient using an A to E approach
- Sit the patient up in bed and give oxygen by non-rebreathe mask

- Take an ABG
- Ensure the patient is attached to cardiac, blood pressure and SpO2 monitoring
- Establish IV access
o Give 20 – 40mg furosemide by slow IV injection
o Diamorphine 2.5–5 mg IV and metoclopramide 10 mg IV
- If SBP >90 give GTN spray
If the patient is hypotensive they will require inotropic support, therefore urgently contact ITU. If
there is any haemodynamically unstable arrhythmia, follow ALS protocol
Further Investigation and Management
Blood tests
- U&Es, troponins, INR, BNP

12 lead ECG
- There is commonly sinus tachycardia but there may be cardiac arrhythmia or evidence of
acute ST change
CXR is used to confirm the diagnosis of acute pulmonary oedema
Echocardiography
Fluid restrict the patient to 1.5L per day until the pulmonary oedema is well controlled
Cardiogenic Shock
The causes of cardiogenic shock can be broadly divided into two groups
- Pump failure: MI, arrhythmia, myocarditis, acute valve failure, aortic dissection
- Obstruction: PE, tamponade, tension pneumothorax
Management of cardiogenic shock should again follow an A to E approach, attempting to identify the
underlying cause
- Perform careful assessment of fluid balance, but if the patient is hypotensive it is best to
give fluid and correct later unless pulmonary oedema is present
Treat any reversible causes
Arrhythmias
Palpitations and Syncope
Palpitations are an increased or abnormal awareness of the heartbeat, which may be rapid, irregular
or forceful. Syncope is a transient loss of consciousness due to a disorder of the circulation
- These symptoms can be due to cardiac or non-cardiac causes, including arrythmia

The most important investigation in terms of identifying a cardiac cause is an ECG trace, which can
capture the potential arrhythmia in many different settings
- An ECG when the patient is asymptomatic should be carried out in all

- Where patients have daily symptoms an ambulatory holter ECG for 24/72 hours
- An internal loop recorder (inserted subcutaneously via injection) is used where patients
have symptoms relatively frequently. This records 10 minutes of trace continuously, erasing
as it records. The patient can press a button when they experience symptoms (including
after waking from syncope) that stores the last 10 minutes of trace, keeping the
symptomatic episode for review
- If patients have very infrequent prolonged symptoms, they should be told to visit A+E/GP to
have an ECG when symptomatic
- Event recorders are used where patients have very infrequent short symptoms. This is an
external device held against the chest when symptomatic to record a trace
Other investigations from a cardiac perspective can include
- Bloods to detect underlying metabolic disease: U&Es, FBC, TFTs

- Echocardiography where there is suspected structural heart disease or cardiomyopathy
- Head-up tilt testing where reflex syncope is suspected
Haemodynamic Compromise
Arrhythmias can lead to haemodynamic compromise, this is cardiovascular collapse
- Hypotension (MAP <65mmHg)

- Systolic BP <90
- Tachycardia or bradycardia
- Increased capillary refill time, decreased peripheral temperature, oliguria can also be seen
Haemodynamic instability is best managed with an A to E approach, with a view to cardioversion
- Ensure airway is patent

- If SOB or SpO2 <94% give high flow oxygen through a non-rebreathe mask
- Monitor BP, HR, and CRT
o Lie the patient flat and elevate their legs
o Establish wide-bore IV access and request bloods
▪ FBC, U&Es, LFTs, coagulation profile, TFTs, bone profile, cardiac markers, D-
dimer
o Request a 12-lead ECG
With a tachyarrhythmia
- Synchronised DC cardioversion up to 3 shocks

- Amiodarone 300mg IV over 20 minutes, repeat shock
- Amiodarone 900mg IV over 24 hours
With a bradyarrythmia
- Atropine 500mcg IV (repeat up to 3mg maximum) ± adrenaline

- Seek expert help to arrange transcutaneous/transvenous pacing
Atrial Fibrillation (AF)
AF is the commonest sustained cardiac arrhythmia; it is due to disorganised electrical activity within
the atria preventing coordinated contraction. It can be classified into three main groups
- Paroxysmal AF is self-terminating within 7 days, this can be recurrent

- Persistent AF lasts >7 days and is not self-terminating, termination can be with cardioversion
to sinus rhythm. This can degenerate into permanent AF
- Permanent AF lasts >1 year and has not been terminated by cardioversion
AF is commonly caused by hypertension, diabetes mellitus, left ventricular failure, coronary artery
disease, infiltrative disease, mitral or tricuspid valvular disease, HOCM, PE and thyrotoxicosis
- The triggers to AF can include short bursts of focal atrial ectopy from inside the pulmonary
veins or due to abnormal atrial anatomy
Presentation
Only just over half of patients with AF are symptomatic
- Palpitations, dyspnoea, fatigue, presyncope/syncope, and angina-type chest pain

- Stroke or TIA may be the first presentation of AF as blood pools in the atrial appendages due
to abnormally turbulent blood flow leading to thrombus formation and embolization. There
are additional superadded changes in coagulation
Hospital admission is recommended in patients that are symptomatic, haemodynamically unstable,
fast AF with rate >150, presenting with complications, or if the patient presents within 48 hours of
onset
Physical signs are an irregular pulse (faster at the apex than the wrist)
Investigations
ECG is the most important investigation, and is diagnostic except between attacks of paroxysmal AF.
With paroxysmal AF there can be 24 hour ambulatory ECG or use of an event recorder
- Irregular ventricular rhythm, absence of p waves, wandering/undulating baseline

- Ventricular rate is variable
- TFTs, FBC (anaemia can precipitate CCF), U&Es (potassium derangement can lead to
arrhythmia), LFTs and coagulation screen (pre-warfarin)
Imaging can include
- CXR can indicate structural causes of AF

- Echocardiogram can be used where there is suspicion of underlying structural/functional
heart disease and where cardioversion is being considered
Management
Emergency management is indicated if the patient is haemodynamically compromised (as above)
In stable patients, rate control is the first-line strategy in AF. Heart rate in AF is generally 150 –
160bpm, this is slowed by targeting AV node conduction. Target HR is 60 – 80, review after one week
to ensure HR is decreased
- First line medications used for rate control are cardioselective β-blockers (bisoprolol,
atenolol)
- Calcium channel blockers (verapamil or diltiazem) can also be used
o If the patient is sedentary digoxin can be used, this is only effective at rest
Rhythm control should be considered in patients with continuing symptoms after rate control
- Electrical cardioversion
o TOE prior to this to ensure there is no thrombus in the heart, anticoagulate prior to
cardioversion if there is thrombus
- If cardioversion fails, there are other strategies
o Flecainide and sotalol can be used. Amiodarone use is limited by side effects
o Catheter ablation, this is targeted at pulmonary vein ectopics
o Pace and ablate, this involves AVN ablation (iatrogenic complete heart block)
following DDD pacemaker insertion
Anticoagulation is indicated in certain patients, aiming for an INR 2 – 3 with warfarin. Novel oral
anticoagulants such as dabigatran, rivaroxaban or apixaban can also be used
- CHA2DS2-VASc is used to assess stroke risk, if >1 in men or >2 in women there should be
anticoagulation
o Congestive heart failure (1)
o Hypertension (1)
o Age 65 – 74 (1)
o Diabetes (1)
o Stroke/TIA history (2)
o Vascular disease (1)
o Age >75 (1) i.e. patients over 75 score 2 points
o Sex category (female = 1)
The need for anticoagulation may be offset by bleeding risk, this is calculated by HAS-BLED. Risk
factors include alcohol use, liver and renal disease, and uncontrolled hypertension.
If the AF is acute, presenting within 48 hours of onset, there can be electrical/medical cardioversion.
Atrial Flutter
Atrial flutter has many aspects similar to AF, but differs in terms of mechanism and management. It
can co-exist with AF
- Electrical activity rotates around the right atrium, generally leading to ventricular
contraction every second/ third atrial contraction. Ventricular rate is generally around
150bpm
Presentation
Flutter is generally more symptomatic than AF
- The commonest symptom is palpitations. There can also be dyspnoea, fatigue,

presyncope/syncope, and chest pain
- Stroke or TIA may occur
Pulse is regular but rapid
Investigations
ECG is commonly diagnostic
- ‘Saw-tooth’ appearance to the ECG, with p waves occurring frequently. QRS complexes are
regular, and will follow a certain number of p waves
Further investigations are as for AF
Management
Management goals are similar to that of AF
- Catheter ablation is first-line in patients with flutter, if this is contraindicated there can be
ventricular rate control with beta blockers or calcium channel blockers
- Electrical and medical cardioversion can be used, but there must be anticoagulation if the
flutter has persisted for >48 hours
- Anticoagulant therapy has the same indications as for AF
Supraventricular Tachycardias (SVT)
SVT includes atrioventricular nodal re-entry tachycardia (AVNRT - commonest), atrioventricular re-
entry tachycardia (AVRT), and atrial tachycardia
- SVTs are fast, regular heart beats with a ventricular rate of 150 – 250bpm
- QRS complexes are usually narrow and the p wave may be difficult to visualise
- These are usually paroxysmal with infrequent episodes
The different forms of SVT can be recognised by different features on ECG
- Atrial tachycardias are due to ectopics in the atria, these lead to abnormal p wave
morphology and axis on ECG
- The p wave may be negative in I, II, AvL and AvF and positive in AvR
- AVNRT are due to an atrial ectopic taking an abnormal circuit in the AV node, this enables
cycling of electrical signals within the AV node leading to fast ventricular contraction until
termination
- AVRT are due to accessory pathways that conduct electrical signals from the atria into the
ventricles bypassing the AV node. This causes a pre-excitation where the ventricle begins
contracting before AV delay, but continues to full contraction when stimulated by the
normal pathway
Presentation
SVT symptoms differ dependent on ventricular rate and SVT duration
- Syncope, palpitations and dizziness are commonest

During an attack, tachycardia may be the only finding
- There can be signs of resulting heart failure

Acute Investigation and Management
Use an A to E approach to stabilise the patient, ensure early IV access and take the above bloods
- Request an ECG
- This will show a narrow QRS tachycardia. No visible p waves indicate AVNRT and
there may be a short PR interval in AVRT
- If the patient is haemodynamically unstable, manage as above

If the patient is haemodynamically stable it is still important to terminate the SVT to prevent high-
output cardiac failure
- Vagal manoeuvres should be used first line to try and terminate the SVT. This includes
carotid sinus massage, valsalva manoeuvre, and blowing into a pressurised syringe
- Adenosine 6mg IV is the medication of choice when manoeuvres fail
- Adenosine has a very short half-life, and should be injected into wide bore cannula
in the ACF. Warn the patient that it will be unpleasant
- Verapamil is an alternative (often used in asthmatics), but is contraindicated in
patients taking beta-blockers
Long-Term Management
Identification of any possible precipitating factors is important e.g. caffeine, exercise, recreational
drugs
Long term preventative treatment is not required in all people, and depends on the frequency and
severity of SVT
- Medications include beta blockers, calcium channel blockers, and digoxin

- Radiofrequency catheter ablation can be used first-line or where the SVT does not respond
to medication
Wolff-Parkinson-White
WPW is a form of SVT in which the accessory pathway conducts electrical activity from the atria to
the ventricles
- This is an antegrade AVRT and needs urgent treatment due to the risk of degeneration into
VF if AF develops (as all atrial activity will be conducted by bypassing the AV node)
It presents as for any other SVT, most commonly in the teenage years
ECG is characteristic in WPW
- Short PR interval and broad QRS showing a delta wave pattern – slurred upstroke into QRS.
There can also be right or left bundle branch block
Management is with radiofrequency catheter ablation. Digoxin in contraindicated in these patients.
Ventricular Tachycardia
Presentation
Patients present either with
- Haemodynamic compromise
- Symptoms include chest pain, palpitations, dyspnoea, dizziness, and syncope
- Cardiopulmonary arrest as pulseless VT
Investigations
ECG is diagnostic of VT
- Fast rate >120bpm, regular rhythm, no p waves, broad QRS (>120ms)

- The QRS complexes may vary in amplitude (Toursades-de-Pointe) where the cardiac axis
twists around the iso-electric line
Routine blood tests should include serum electrolytes as calcium, potassium, magnesium and
phosphate abnormalities can all degrade into VT
Management
Pulseless VT is treated as for VF by following the ALS protocol.
VT with a pulse is managed as for any tachyarrhythmia causing haemodynamic compromise, as

above
In the long term ICDs should be considered for patients with sustained VT causing syncope, previous
cardiac arrest due to VT or VF, and where VT has developed as a complication of MI
Ventricular Fibrillation
Presentation
VF is more common in patients with a history of coronary artery disease due to formation of fast-
conducting infarction scars
- It is commonly a terminal event and presents as cardiopulmonary arrest

Investigations
ECG is diagnostic of VF
- Very fast rate, irregular rhythm, no p waves, broad QRS with abnormal morphology
Management
There should be defibrillation following ALS protocol. If the patient is successfully resuscitated, long-
term management can include ICD insertion and CABG if indicated
Heart Block
Heart block (AV node block) is due to a delay or complete block in conduction from the atria through
to the ventricles at the AVN
Most commonly this is due to fibrous tissue formation at the AV node, usually following ischaemia or
infarction. It can also be due to
- Lyme disease, myocarditis or endocarditis, SLE

Presentation
Heart block causes bradycardia, this may be asymptomatic but can present in several ways
- Syncope, fatigue, and dizziness are commonest. In some cases, there may be heart failure or
cardiovascular collapse and sudden death
Investigations
ECG is the main investigation into heart block, and can distinguish the three main forms
- First degree heart block is where there is a prolongation of the PR interval, this should
usually be no more than 0.2 seconds (5 small squares)
- Second degree heart block is in two types; Mobitz 1 and 2 (intermittent failure of
conduction)
- Mobitz type 1 (Wenckebach) heart block occurs where the PR interval elongates
each time until there is a dropped beat
- Mobitz type 2 heart block occurs where there is a fixed PR interval with a fixed heart
block (example below shows 2:1 block). This is due to a conduction block below the
AV node
- Third degree heart block occurs where there is no conduction at the AVN, therefore the
ventricles and atria contract independently. The QRS is broad.
There should be investigation into ischaemic heart disease, or the other differential causes, if
suspected
Management
Where patients are haemodynamically unstable manage as for bradyarrhythmia above
Where patients are stable, treatment is indicated if there are significant symptoms
- First-line is to stop all AV nodal blocking medications e.g. beta blockers, calcium channel
blockers, and digitalis
- If this is ineffective, there should be permanent pacemaker insertion, and ICD placement
should be considered where LVEF <35%
Pacemakers and Other Implanted Devices
On CXR, several aspects of any device should be described
1. The size of the device, small implies pacemaker and large implies ICD
2. The path of the leads through the venous system
3. The number of leads
4. The location of lead tips (chamber(s) paced)
5. Any coils on the leads, these are the defibrillators of an ICD
Permanent pacemakers play a central role in the management of arrhythmias, predominantly for
bradycardia. There is a three letter identification code for pacemakers e.g. AAIR, VVIR (rare), or DDD
- The first letter is the chamber paced: A = atria, V = ventricle, D = dual

- The second letter is the chamber sensed: as above
- The third letter is the response of the pacemaker to native electrical activity: I = inhibits, T =
triggers, D = dual function
- Inhibition means that the pacemaker does not fire when it senses a native QRS, this
prevents tachycardia
- Trigger means that the pacemaker fires in response to native activity e.g. sensing a p
wave and triggering a QRS
- There can be an R added at the end, this is rate modulation. Rate response works in similar
way to a pedometer, increasing heart rate in response to increased activity
Implanted cardioveter defibrillators, which can be dual or single chamber (one or two leads). They
have three functions
1. Pacing bradyarrhythmias
2. Overdrive pace to bring patients out of VT without shocking
3. Shocking when VF is detected
Cardiac resynchronisation therapy is used where patients have LBBB and heart failure, this
coordinates contraction of the ventricles and reduces symptoms. This is also a pacing device known
as CRTP and can have additional ICD function (CRTD)
- There are three leads, one into each ventricle and one into the right atrium
- The lead to the left ventricle is placed via the right atrium into the coronary sinus
Complications of device insertion include
- Early: haematoma, infection, pericardial effusion

- Late: lead displacement/fracture, box erosion to the skin surface, and device failure
If a pacemaker is malfunctioning a magnet should be applied to the chest wall; this resets the
pacemaker to A00/V00/D00 i.e. solely pacing function at a rate of 60bpm
- This prevents the pacemaker from being influenced by any external electrical interference
Chronic Obstructive Pulmonary Disease (COPD)
COPD is characterised by fixed airflow obstruction that is not fully reversible with bronchodilators
and is minimally variable from day-to-day
COPD is characterised by two clinically distinct but overlapping conditions
- Chronic bronchitis is diagnosed clinically, defined as a chronic productive cough for three
months of the year over the last two years
- Emphysema is diagnosed morphologically, defined as permanent enlargement of air spaces
distal to the terminal bronchioles
The condition is almost exclusively seen in smokers, particularly with >20 pack years
Presentation
A diagnosis of COPD should be considered in patients over the age of 35 with a risk factor (usually
smoking) and symptoms including
-Exertional dyspnoea, chronic cough, regular sputum production, frequent chest infections,
and wheeze
- There should be exclusion of red flag symptoms such as weight loss, haemoptysis, ankle
swelling, and PND
MRC dyspnoea scale
1 Not troubled by breathlessness except on strenuous exercise

2 Short of breath when hurrying or walking up a slight incline
3 Walk slowly on flat because of breathlessness
4 Stops for breath after a few minutes/100m on flat
5 Too breathless to leave the house/ breathless on dressing and undressing
Signs indicative of COPD include
- Cachexia, hyper-inflated chest, pursed lip breathing, use of accessory muscles, paradoxical
movement of lower ribs, reduced cricosternal distance
- Wheeze, prolonged expiratory phase
- Signs of emphysema e.g. quiet breath sounds, reduced cardiac dullness
Investigations
Spirometry should be performed in all patients where COPD is suspected
- An obstructive pattern will be seen with FEV1/FVC ratio <0.7, FEV1 <80% predicted, and a
characteristic ‘scooped out’ flow-volume loop
o FEV1 can be used in staging with mild >80%, moderate 50% – 79% severe 30% –
49%, and very severe <30%
- There will be little or very mild reversibility to bronchodilators
If there is diagnostic doubt as to whether the patient has COPD or asthma, it can be useful to record
a peak flow diary over the course of several weeks
All patients should have the following additional investigations
- CXR this can show a flattened diaphragm (distance between costphrenic and cardiophrenic
angle <1”) and hyper inflated lungs
- FBC to identify anaemia or polycythemia
- Calculation of BMI
Calculation of BODE index (BMI, airflow Obstruction, Dyspnoea, Exercise capacity) is a good
prognostic tool
Other investigations can be carried out as indicated
- Alpha-1-antitrypsin should be measured if there is early onset or family history

- Gas transfer if symptoms are disproportionate to spirometry
- ECG to look for cor pulmonale as pulmonary hypertension is near universal in later stages of
COPD
- Pulse oximetry to assess the need for oxygen therapy
- Sputum culture
Management
Conservative management strategies in COPD include
- Smoking cessation
- Immunisation
- Education, particularly in recognising the early signs of exacerbation
- Pulmonary rehabilitation is indicated in patients with an MRC score of >3
Medical management is in a stepwise fashion, aiming to relieve symptoms and reduce exacerbations
- Short acting β2 agonists for symptom relief

- If patients remain symptomatic a LABA or long-acting muscarinic agent (LAMA e.g.
tiotropium) should be added
- All patients with FEV1 <50% should be prescribed inhaled steroids alongside the above
- Oral agents such as theophylline can be added if the patient is still symptomatic
- Mucolytics such as carbocysteine are useful to aid sputum clearance
Oxygen therapy can be ambulatory/SBOT for symptomatic relief, or as LTOT in patients with long
term PaO2 <7.3 kPa or SpO2 <92%
Prophylactic antibiotics are indicated in those with very frequent exacerbations, this is usually with
azithromycin
There are some surgical options for COPD patients
- If the patient is breathless and has a single large bulla on CT scan with FEV1 <50% there can
be bullectomy
- Bronchoscopic or open lung volume reduction surgery can be used in some cases of
advanced emphysema
- Lung transplantation can be considered
Acute Exacerbation
Exacerbation of COPD is defined as an acute event characterised by worsening of the patient’s

respiratory symptoms and leads to a change in medication
- The commonest trigger for exacerbation is viral or bacterial infection

- Other triggers include air pollution and interruption of normal maintenance therapy
Typical presentation of exacerbated COPD includes the following symptoms. The patient may not
have a prior diagnosis of COPD, therefore it should be suspected in all smokers >35 that present
similarly
- Increased dyspnoea, increased cough, increased sputum volume and/or purulence,

increased wheeze, chest tightness, reduced exercise tolerance, fatigue, and confusion
Initial assessment and investigation should follow an A to E approach
- Measure pulse oximetry and use controlled oxygen to achieve SpO2 88 – 92%
o Use clinical judgement on the route of oxygen administration, if the patient has life-
threatening hypoxia use non-rebreathe. In all other situations titrate using venturi
o Perform a baseline ABG and repeat at 30 minutes when giving oxygen to monitor for
hypercapnic acidosis. Use PaCO2 to guide oxygen therapy
- Gain IV access and take bloods including
o FBC looking for raised WCC
o U&Es, LFTs, and CRP
o Blood cultures if indicated
Further investigation should include ECG, CXR, and sputum MC&S
Treatment is with
- Nebulised salbutamol (2.5 – 5mg) ± ipratropium (0.5mg) via air, use nasal specs alongside
the nebuliser if needed to keep SpO2 at 88 – 92%
- If there is inadequate response to this, IV aminophylline can be considered but only
with senior medical input
- Systemic corticosteroids, usually 40mg prednisolone for 7 days
- Broad spectrum antibiotics, either IV or oral dependent on severity
If the patient has failed to respond to conventional therapy, and type 2 respiratory failure persists,
there should be consideration of NIV, usually in the form of BiPAP (IPAP + EPAP)
- IPAP (inspiratory pressure) augments respiratory effort, increases tidal volume, and
decreases the work of breathing
- EPAP (expiratory pressure) prevents collapse of small airways, increases tidal volume, and
improves the work of breathing
If pH <7.26 there should be NIV in an ITU setting, with a low threshold to intubation
Interstitial Lung Disease
Interstitial lung disease (pulmonary fibrosis) is a chronic condition leading to loss of lung elasticity
- There is thickening and fibrosis of the alveolar walls (between the alveolar epithelium and
capillary endothelium) and septal/bronchovascular tissues
- Frequently there is additional involvement of the airways, vasculature, and alveolar
airspaces
The commonest cause of pulmonary fibrosis is idiopathic disease (IIP), however there are several key
known causes
- Replacement fibrosis secondary to lung damage

- Pneumoconiosis e.g. coal worker’s pneumoconiosis, silicosis, asbestosis, berylliosis
- Hypersensitivity pneumonitis (EAA) e.g. farmer’s lung, bird fancier’s lung
o Acute EAA follows a short period of exposure to high concentration of antigen,
usually reversible
o Chronic EAA follows long exposure to low antigen doses, less reversible
- Granulomatous diseases e.g. sarcoidosis
- Iatrogenesis e.g. amiodarone, nitrofurantoin, methotrexate, gold, penicillamine, radiation
exposure
- Connective tissue diseases e.g. systemic sclerosis, SLE, RA
- Inherited diseases
There are many different classifications of idiopathic interstitial pneumonias (IIPs) summarised in the
table below
Presentation HRCT Findings Prognosis Management Additional

Features
Idiopathic Onset over Fibrosis and Poor Acetylcysteine Commonest
pulmonary months to honeycombing and pirfenidone form
fibrosis (IPF) years (subpleural can be used to
and basal). slow course of
Usual disease
interstitial
pneumonia
(UIP) pattern
Non-specific Onset over Ground-glass, Variable Corticosteroids
interstitial months to minimal
pneumonia years honeycombing
(NSIP)
Cryptogenic Onset over Consolidation Generally Corticosteroids. If

organising months good no response -
pneumonia cyclophosphamide
(COP)
Acute Onset over Diffuse Poor Biopsy is required Often

interstitial days, ground-glass, (mortality to diagnose preceded
pneumonia presents patchy >50%) Treat infection, with viral
(AIP) similarly to consolidation high dose IV illness
ARDS steroids
Respiratory Onset over Nodules, Good Smoking cessation Occurs in
bronchiolitis- years ground-glass Corticosteroids smokers
associated
interstitial
lung disease
(RB-ILD)
Desquamative Onset over Ground-glass Good Smoking cessation Very rare,
interstitial weeks to Corticosteroids only in
pneumonia months smokers
(DIP)
Lymphoid Onset over Ground-glass Variable Corticosteroids Very rare

interstitial years
pneumonia
(LIP)
Presentation
The presentation of interstitial lung disease is variable, and related to the underlying disease
process. It usually presents with gradual onset of dyspnoea, chronic non-productive cough (there
may be haemoptysis), wheeze, and chest pain. Low-grade fever and myalgia are also common
- There can be acute presentation with a fulminant, progressive, remitting, or resolving course
It is essential to discuss occupational history and exposure to animal proteins
On examination there are several non-specific features
- Central cyanosis
- Tachycardia
- Fine end-inspiratory crackles
- Finger clubbing
- Signs of pulmonary hypertension and right heart failure occur late in the disease course
Investigations
Routine blood tests are important
- FBC may show mild anaemia, ESR and/or CRP may be raised dependent on cause
- Autoantibody screen may be indicated: RhF, anti-CCP, ANA, anti-dsDNA
- Serum IgG precipitin to different allergen epitopes can identify EAA
ABG may show oxygen desaturation, this is particularly on exertion as VQ mismatch increases
Lung function tests are essential in both aiding diagnosis as well as tracking disease progress
- A restrictive pattern will be seen (FEV1/FVC >0.8, FVC<0.7) with reduced total lung capacity,
reduced residual capacity, reduced residual volume, and reduced gas transfer
- Peak flow is increased due to traction bronchiectasis
Imaging studies should include
- CXR, this can show no abnormality but disease may still be present. Specific findings include
o IIP may show reticular/nodular opacities. Honeycombing can be seen in severe
disease
o Pneumoconiosis can show nodular shadowing in the upper and middle zones
o Sarcoidosis can show bilateral hilar lymphadenopathy and calcification
o EAA can show upper/mid zone reticulation. In acute disease there can be ground-
glass change with apical sparing
- High resolution CT scanning (HRCT) can be diagnostic dependent on features seen
o There can be beading of the fissures, pathognomonic of fibrosis
Lung biopsy may be used if CT scan findings are not conclusive, this is usually with VATS or
thoracotomy
- Histological features need to be interpreted in the context of clinical and radiological

features
Management
General supportive measures should include smoking cessation, avoidance of any triggering causes,
and seasonal vaccinations
- Some patients may also benefit from LTOT/ ambulatory oxygen and pulmonary
rehabilitation
Specific management is dependent on cause
- IIP is managed as above

- Hypersensitivity pneumonitis is managed with antigen avoidance and corticosteroids
- Pneumoconiosis can be managed with minimising dust exposure
- Sarcoidosis and berylliosis are both managed with corticosteroids
Lung transplantation may be an option in some cases
Lung Cancer
Lung cancer is the commonest cause of cancer death in the UK
- The vast majority of cases are smoking related

- Five year survival is as low as 5% in some cases
Aetiology
There are several fixed risk factors for lung cancer
- Age
Modifiable risk factors include
- Smoking, both active and passive

- COPD
- Occupational exposure particularly to asbestos, radon gas, and iron oxides
Pathophysiology
Almost all primary lung tumours are bronchial carcinomas, and can be divided into non-small cell
and small cell groups
Non-small cell lung cancer includes various different forms of cancer, which are less aggressive and
have later metastases
- Squamous cell carcinomas are generally more central and obstructive and commonly have
local spread, these show keratin formation
- Adenocarcinomas are more peripheral, common in non-smokers and typically invade the
pleura and mediastinal nodes
- Large cell carcinomas are undifferentiated and metastasis typically occur earlier
- Carcinoid tumours
- Bronchoalveolar cell tumours
Staging of NSCLC is with TNM
T1 Any tumour <3cm in maximum dimension confined within the lung and not involving the
main bronchus
T2 1. >3cm but <7cm in maximum dimension
2. In the main bronchus but >2cm from the carina
3. Invading the visceral pleura
4. Causing collapse or obstructive pneumonitis extending into the hilum
T3 1. Invading into the chest wall, diaphragm, mediastinal pleura, or parietal
pericardium
2. In the main bronchus <2cm from the carina
3. Collapse or obstructive pneumonitis of the whole lung
4. Separate tumour nodules within the same lung lobe
T4 1. Invades the mediastinum, heart, great vessels, trachea, oesophagus, vertebra, or
carina
2. Has separate tumour nodules within different lobes of the same lung
- N1 is involvement of nodes within or close to the affected lung, N2 is involvement of

mediastinal or subcarinal nodes, and N3 is more distant spread
- Metastasis is common to the contralateral lung, liver, brain, bone, adrenal glands, and
kidney
Stage grouping in NSCLC is important in determining prognosis
- Stage I = T1-2 N0
- Stage II = T1-2 N1; or T3 N0
- Stage IIIa = T1-2 N2; T3 N1-2
- Stage IIIb = T4 any N
- Stage IV = M1
Small cell (oat-cell) carcinomas are derived from APUD endocrine cells leading to undifferentiated,
highly malignant, tumours composed of small primitive neuroendocrine cells
- It has often spread widely by the time of diagnosis and prognosis is poor
- PTHrp and ADH secretion is common from these tumours leading to hypercalcaemia and
hyponatraemia. There can also be Lambert-Eaton myasthenia syndrome and ACTH secretion
Staging of small cell lung cancer is into limited or extensive disease. Prognostic factors such as
performance status, gender, LDH, ALP, and serum Na are all involved in defining subgroups.
- Limited-stage disease is confined to one hemithorax, only involving ipsilateral nodes

- Extensive-stage disease has contralateral lung and distant metastases
Pleural malignancy includes mesothelioma, this usually results from asbestos exposure. This can also
occur at the peritoneum, pericardium and testes
Examination
Patients presenting with lung cancer typically have characteristic symptoms, these are persistent (>3
weeks) or unexplained
- Haemoptysis
- Persistent cough, for more than 3 weeks
- Recurrent chest infection
- Hoarseness of the voice
- Dyspnoea
- Weight loss
- Chest and shoulder pain, this suggests chest wall or pleural involvement
On examination patients may have finger clubbing, cervical or supraclavicular lymphadenopathy,
Horner’s syndrome, and may have signs suggestive of SVC obstruction (dilated chest veins, pounding
headaches, rubor of the face, arm swelling)
- Auscultation of the chest may be suggestive of collapse or pleural effusion

Investigations
Any patient with red flag symptoms of lung cancer should receive an urgent referral for chest x-ray.
If chest x-ray is suggestive of malignancy, further scans are essential
- CT thorax with IV contrast will give a detailed view of the lung fields, demonstrating the
presence of any tumours and suggesting any metastatic spread
- CT abdomen/ pelvis or PET scanning are also used in staging the disease
Tissue diagnosis is essential, therefore there must be biopsy obtained by the least invasive route
possible
- FNA cytology can be used in palpable disease

- Biopsy of easily accessible metastases
- For central tumours there can be bronchoscopy with direct biopsy or brushing/washing for
cytology
- For peripheral tumours there can be CT guided percutaneous transthoracic biopsy
- Pleural aspirate cytology if there is effusion, this is common in mesothelioma
- Pleural biopsy is common in mesothelioma
- Endobronchial ultrasound guided transbronchial needle aspiration (EBUS TBNA) can also be
used
- Biopsy of mediastinal or hilar metastasis with mediastinoscopy can be used where less
invasive techniques have not been successful
- Surgical biopsy may be the only option in some cases
If biopsy has not been possible, PET scanning is used
In NSCLCs where radical treatment is being considered there should be investigations for metastasis.
This includes staging whole body PET-CT, contrast enhanced head CT, bone scanning with
technetium 99, and liver ultrasound.
In SCLCs where intensive treatment is being considered there should again be investigations for
metastasis. This should be with contrast enhanced CT of the chest and abdomen.
There should always be assessment of performance status (0 to 4), lung function tests, FBC, and
biochemical profile.
Where there are symptoms suggestive of metastasis, there should be bone scanning and head CT.
There are many different types of lesion that can cause the appearance of a circumscribed shadow
in the lung field on CXR
- Metastasis from another primary

- Bronchial adenoma
- Abscesses, granulomas, and cysts
Treatment
Surgery in lung cancer is typically lobectomy, but can be more extensive to obtain tumour-free
margins. Extensive surgery includes pneumonectomy, bilolobectomy, and bronco-angioplastic
surgery
- Surgery can only be carried out where FEV1 is >1.5 for lobectomy and >2 for
pneumonectomy
- All patients undergoing surgery for lung cancer should have hilar and mediastinal lymph
node sampling for accurate staging
Radiotherapy is used in radical and palliative settings, with radical radiotherapy requiring good
baseline lung function
- In NSCLC the standard dose is 60 Gy over 30 fractions in 6 weeks

Different chemotherapy agents are used in the treatment of lung cancers
- In NSCLC double therapy with a platinum agent and one of

gemcitabine/vinorelbine/paclitaxel/docetaxel is recommended
- In SCLC etoposide plus cisplatin or carboplatin is recommended. Second-line chemotherapy
is usually taxanes
- In mesothelioma pemetrexed is most commonly used
There are some biological agents commonly used in the treatment of non-small cell lung cancers
that express mutated EGFR
- Iressa (gefitinib) and tarceva (erlotinib) are the two most frequently used
- EGFR mutation is more common in adenocarcinomas, never smokers, females, and people
of Asian descent
Management
Management of lung cancer differs considerably between small cell and non-small cell types. In both
cases, the patient should be counselled on smoking cessation as this will prolong life.
For non-small cell lung cancer, treatment has a more positive outlook and can be curative in some
cases
- Every patient with non-metastatic NSCLC should be considered for surgery, however it is
often not possible due to co-morbidity, therefore the most operable phase of the cancer is
stage I or II
- Radical radiotherapy can also be used where surgery is not possible in stage I/II disease, or in
stage IIIa/IIIb disease where the tumour volume and pulmonary function are adequate.
Again this is in early stage (I – III) disease. Radical radiotherapy has less success in curing
patients than surgery
- Chemotherapy can be used neo-adjuvantly or adjuvantly in stage I/II, or as palliation in stage
III or IV disease
Small cell lung cancer is more difficult to treat definitively, and is usually palliation
- There can be surgery if there is no evidence of metastasis

- Patients with limited stage disease should be offered 4 – 6 cycles of chemotherapy alongside
thoracic irradiation. Cranial irradiation as prophylaxis can also be offered if response to
chemotherapy is good
- In extensive disease there should be chemotherapy to a maximum of 6 cycles
Palliative therapies in lung cancer are essential to alleviate symptoms. This can include drainage of
pleural effusion, opiates to supress cough, steroids for brain metastases, and ENT involvement to
reduce hoarseness
- Radiotherapy is a common treatment for distressing symptoms by reducing tumour bulk

- Pleurectomy and decortication can be used as surgical palliation in mesothelioma
Small cell lung cancers can be hormone releasing, particularly causing high ADH secretion, PTH
secretion, and thyroid hormone secretion
- Management of these complications is important

Local and regional disease recurrence in lung cancer is indicated by the return of original presenting
symptoms. Whereas distant disease recurrence can be suspected where there is bony pain,
abdominal pain, jaundice, dizziness, paraesthesia, or vomiting
- Where lung cancer is recurrent treatment is typically chemotherapy and radiation as

palliative treatments
Trauma
Major trauma should be suspected in the following groups of patients
- High speed road collisions, particularly where there has been death of another individual in
the same collision
- Pedestrians thrown up or run over by a vehicle
- Falls of >2m
- Crush injuries
The kinetics of the accident can help to predict the patterns of trauma that the patient presents with
e.g. vehicle hitting something, patient hitting inside of vehicle, internal organs hitting skeletal frame
Where there is multiple trauma, patients should be triaged. T1 (immediate), T2 (urgent), T3

(delayed), or dead.
Management of these patients should be in accordance with advanced trauma life support (ATLS),
passing through the following four phases
1. Primary survey with <C>AcBCDE assessment

o This is catastrophic haemorrhage, airway and cervical spine stabilisation, breathing,
circulation, disability, exposure
o It is generally recommended to manage <C>AB in the field, and CDE en route to
hosptial
2. Resuscitation phase, in which treatment continues for problems identified during primary
survey
3. Secondary survey is with focussed head-to-toe examination, relevant imaging, and other
investigations. A to E assessment should be repeated
4. Definitive care phase, in which there is management of injuries e.g. fracture stabilisation/
operative intervention
General Pre-Hospital Measures
Approaching a trauma scene should involve adequate protective equipment and safe scene
approach (blue light or green light use where appropriate, noting acceptable road traffic
exemptions)
On approach ensure safety in four dimensions
- Left and right, up and down, front and back, time (scene evolving)
Exclude or control catastrophic haemorrhage
- Control catastrophic haemorrhage by applying at CAT tourniquet at a single bone proximal

(but as close as possible) to the wound
Ensure adequate airway control and provide high flow oxygen to all trauma patients
- Patients who are apnoeic or hypoventilating may require bag-valve-mask ventilation prior to
tracheal intubation
Cervical spine protection is essential in any patient with a possible spinal injury; this can be
suggested by the mechanism of injury, neck pain, or neurological deficit
- Immediate manual cervical immobilisation can be achieved by placing one hand on each side
of the patient’s head and holding it steady (without traction) in line with the remainder of
the spine
o Whilst maintaining manual immobilisation, ask a colleague to apply an appropriately
sized had cervical collar
o Sizing of the collar is estimated by the number of finger breadths between the
patient’s jaw (chin) and shoulder (bulk of trapezius), this should equate to the
number of finger breadths from the black stud to the bottom of the yellow plastic
- After the collar is in place, manual immobilisation must also be maintained, or simulated
with placement of blocks/rolled towels either side of the collar
Management of breathing is expected; however, it may be useful to perform a trauma chest

assessment using the RV FLAPS WET mnemonic
- Rate and Volume of breathing

- Feel
- Look
- Armpits and auscultate
- Press and percuss
- Search the back, shoulders and sides of the chest
- Wounds around the neck
- Emphysema around the neck
- Tracheal deviation
IV access should be established using two large-bore cannulae in the forearm or ACF veins, and
administer appropriate fluid resuscitation titrated to radial pulse
- 1g tranexamic acid IV/IO over 10 minutes should be given within 1 hour if there is major
haemorrhage
Analgesia is essential in all trauma patients experiencing pain, usually IV morphine titrated to
response
If possible, try to establish a history of the incident as well as a brief AMPLE history
Handover to colleagues following trauma can use SBAR, or AT MIST to prepare ED for the arrival of
the patient
- Age
- Time of incident and estimated time of arrival to ED
- Mechanism of injury
- Injuries found or suspected
- Signs and symptoms
- Treatments given
In-Hospital Assessment
Repeat the <C>AcBCDE assessment
- Reassess airway, and intubate where required

- Circulation should include ensuring BP, ECG, and urinary catheterisation
o ABG in all major trauma patients
o Bloods to include: FBC, U&Es, clotting, LFTs, group and save/crossmatch
o Consider the need for activation of major haemorrhage protocols
Resuscitate as appropriate, and commence secondary survey
Antibiotic and tetanus prophylaxis should also be considered, particularly where there are
compound (open) fractures or penetrating wounds
Investigations in Secondary Survey
Urinalysis should be carried out in all patients with abdominal injury, as microscopic haematuria is a
useful marker of intra-abdominal damage
FAST scanning can be performed in the ED, and takes only 2 – 3 minutes. It looks for free fluid in the
hepatorenal recess, splenorenal recess, pelvis, thorax, and pericardium
- Disadvantages include operator dependence, and the fact that it cannot identify the source
of bleeding just the presence of free fluid
o Visible free fluid indicates a minimum volume of 500ml
- Focussed assessment with sonography for trauma (FAST) scan, as above

- Multiple X-rays may be required
o CXR and pelvis should be obtained as a minimum
- CT traumagram, this can only be used where patients are haemodynamically stable
Diagnostic peritoneal lavage (DPL) is only used in situations where CT and USS are unavailable. It
involves making an incision in the peritoneum and aspirating free fluid for analysis
- Positive DPL is an indication for a laparotomy
Immediate Life-Threatening Injuries in Trauma
Chest injuries
- Tension pneumothorax
- Flail chest
- Massive haemothorax
- Cardiac tamponade
- Open pneumothorax
Abdominal injuries
- Splenic rupture
- Open book pelvic fracture
Penetrating Trauma
In the UK, penetrating trauma is most commonly stab wounds but can also include gun-shot injuries
- The external wound has no correlation with the potential for internal injury
- Always check for spinal cord injury, particularly in gun-shot wounds
Gunshot wounds are associated with high-energy transfer, and therefore can be bone/ bullet
fragments that inflict other injuries alongside the trajectory of the bullet. Stab wounds are typically
more predictable
Penetrating Chest Trauma
Where patients are stable, the following investigations and initial management steps are
recommended
- Perform a FAST scan to assess for haemothorax or cardiac tamponade

- Obtain CXR and ECG
If the patient is unstable consider the life-threatening chest injuries above, particularly tamponade
Penetrating Abdominal Trauma
Where patients are stable, the following investigations and initial management steps are
recommended
- Urinalysis for blood

- Perform a FAST scan to assess for intra-abdominal fluid that may require a laparotomy
- Obtain erect CXR and supine AXR
Pregnant Trauma Patients
Involve a senior obstetrician and gynaecologist early
- USS to assess for foetal viability and uterine rupture
Check rhesus status
Head Injury
Head injuries can be classified according to many different factors
- Mechanism e.g. blunt, penetrating

- Morphology of skull fractures e.g. base or vault (sub-classified as linear/stellate,
depressed/non-depressed, open/closed)
- Type of intracranial lesion e.g. focal (epidural, subdural, intracerebral) or diffuse
(concussion, ischaemic injury, shearing)
Classification can also be by severity, this is measured by several different scales
Mild Moderate Severe

Duration of Post- <1hr 1hr – 24hr >24hr

Traumatic amnesia
(PTA)
Duration of LOC <20m 20m – 6hr >6hr
GCS >12 9 – 12 <9
Assessment
Patients with head injury should be managed using A to E assessment and stabilisation
- Assessment of disability should be repeated, as serial AVPU readings are more informative in
the context of head injury to determine response to treatment
- If at any time there is deterioration in neurological status, A to E should be repeated.
Decreasing conscious level may not necessarily be due to the head injury and could be due
to e.g. airway adjunct moving out of position
Focussed examination should include assessment of the scalp for lacerations or obvious skull
fracture, signs of skull fracture, re-assessment of pupils, ad examination of the limbs for lateralised
weakness
Where patients can provide a history, try to ascertain the following
- Mechanism of injury
- Time of injury
- LOC
- Subsequent symptoms including: amnesia, headache, nausea and vomiting, limb weakness,
paraesthesia, diplopia, rhinorrhoea, otorrhoea
Admission
Many patients present to A&E with head injuries, but few require admission or CT scanning.
Indications for a CT scan within one hour are indicated in the table below
Adult Children
GCS <13 on assessment in ED GCS <14 on assessment in ED
GCS <15 2 hours after injury (as assessed in ED) GCS <15 2 hours after injury (as assessed in ED)
Suspected open/depressed skull fracture Suspected non-accidental injury
Signs of basal skull fracture* Post-traumatic seizure
Post-traumatic seizure Suspected open/depressed skull fracture, or
tense fontanelle
Focal neurological deficit Focal neurological deficit
>1 episode of vomiting Presence of bruise, swelling, or laceration >5cm
*Signs of basal skull fracture include haemotympanum, bruising around the eyes, CSF leak from ears
or nose, subconjuctival haematoma, and Battle’s sign (bruising behind the ear). Pneumocranium on
imaging also indicates skull fracture
- It is important to admit these patients as due to the risk of meningitis there should be
antibiotic prophylaxis
Indications for CT scan within 8 hours (often requiring admission for monitoring until the scan takes
place in the morning) are summarised below for adults
- Any patient on warfarin or NOAC

- LOC or amnesia alongside any of
o >65 years old
o Dangerous mechanism of injury
o History of bleeding or clotting disorder
o Retrograde amnesia >30 minutes from time of injury
In children, there are further guidelines to indicate that the patient may require in-hospital
observation for >4 hours post-injury
- Witnessed LOC >5 minutes

- Abnormal drowsiness
- Dangerous mechanism of injury
- >3 discrete episodes of vomiting
Management
Traumatic brain injury occurs in two phases. The general aims of management are to prevent
secondary brain insults
- Primary brain injury is the structural and functional damage sustained at the time of injury
o Mass lesions e.g. haematomas, intracerebral contusions
- Secondary insults are subsequent events to which the injured brain is acutely susceptible
o Hypoxia/ hypoperfusion and ischaemia, hyperthermia, cerebral oedema, raised
intracranial pressure, metabolic derangements, infection
Management of head injury is therefore focussed at preventing secondary insult. All patients should
have frequent neuro-obs
Cerebral Perfusion
There needs to be regular assessment of cerebral perfusion pressure (CPP = MAP – ICP). CPP is
usually 70 – 85mmHg, CP 5 – 15mmHg, and MAP 80 – 90mmHg
- ICP can increase due to oedema of the brain substance, space occupying lesion, obstructed
CSF flow, increased cerebral blood volume due to hypercapnic vasodilation
- MAP can decrease due to cardiogenic shock, hypovolaemia, peripheral vasodilation, or
decreased venous return to the heart
Raised ICP leads to the Cushing response as there is hypertension to increase MAP as compensation,
but this leads to reflex bradycardia
To maintain CPP in the face of decreased MAP and/or raised ICP, the following measures should be
attempted
- Elevate the head of the bed

- Close management of arterial CO 2 and O2 with mechanical ventilation where required,
avoidance of hypercapnia is important
o Therapeutic hyperventilation can be used to cause vasoconstriction from
hypocapnia where required
- Avoidance of pyrexia
- Avoid hypotension, keep SBP>90
- Where ICP remains increased despite the above measures, the following can be considered
o Mannitol and other osmotic diuretics
o Intraventricular CSF drains
o Decompressive craniectomy
Seizure Control
Seizures in the acute phase following traumatic brain injury are not uncommon therefore
levetiracetam or phenytoin can be given as prophylaxis for one week
- Post-traumatic epilepsy is a late complication of brain trauma (particularly where bone

fragments remain in the skull), and should be managed according to the type of seizure that
the patient experiences
Metabolic Homeostasis
Metabolic complications include hyponatraemia and malnutrition
- Hyponatraemia may be due to SIADH or cerebral salt wasting, and should be corrected with
saline
- Malnutrition can be avoided by insertion of PEG feeding tubes early in the course of coma
Complications
Concussion
Concussion (minor traumatic brain injury) is brief neurological deficit following a blow to the head
- Symptoms include loss of consciousness, headache, amnesia, visual disturbance, and

confusion that quickly resolve
o Initially the patient is usually irritable and repeating questions
- There may be a post-concussion syndrome (PCS) where symptoms can last for several weeks
or months
When serious injury has been ruled out, the patient can be discharged but should be advised to be
vigilant for increasing drowsiness, worsening headache, or development of neurological deficit
- Someone should stay with the patient for 48 hours following injury
The patient should rest until they feel well enough to carry on with every day activities, take simple
analgesics PRN, and avoid alcohol for several days
Second impact syndrome occurs where there is a second head injury following a recent concussion
- This secondary injury can lead to severe brain swelling

Prevention of second impact syndrome is essential by advising patients to avoid any risk of loss of
consciousness for at least 3 weeks following concussion
Contusion
Coup and contrecoup contusions are common where there is focal head trauma
- Deceleration injury tends to impact the frontal and temporal lobes; this can lead to
hydrocephalus from local compression of the third ventricle
These are best seen on CT scan, and management is supportive as above.
Diffuse Axonal Injury
Diffuse axonal injury results from shearing of axons within brain matter in a closed brain injury
(acceleration/deceleration injury). This leads to immediate loss of consciousness and persistent
coma
- MRI is more sensitive than CT scanning at detecting this, seen as multiple hyper-intense
lesions at the grey-white matter interface
Management is supportive as above. Prognosis is poor, and the patient may remain in a persistent
vegetative state.
Subdural Haemorrhage
Subdural haemorrhage is due to a tear in the bridging veins that traverse the subdural space
between the dura and arachnoid mater
- Acute subdural haemorrhage leads to immediate loss of consciousness and progressive

decline in GCS
- Chronic subdural haemorrhage leads to gradual evolution of headache, cognitive decline,
ataxia, hemiparesis, and impaired conscious level. The patient usually presents several
weeks following the injury
CT scanning will show a crescentic hyper-dense mass, this may cross sutures and extend into the
interhemispheric fissure
Severe subdural haemorrhages will require emergency craniotomy and haematoma evacuation
- In less severe cases there can be burr hole drilling followed by insertion of a subdural drain
Extradural Haemorrhage
Extradural haemorrhage is commonly due to a tear in the middle meningeal artery under a temporal
bone (usually pterion) fracture, this results in a collection of arterial blood between the dura and the
bone
Classically, extradural haemorrhage presents with a traumatic head injury leading to loss of
consciousness followed by a lucid period over which the patient deteriorates
- Signs can include alteration in GCS and focal neurological deficit

The investigation of choice should be CT imaging of the head
- This may show a biconvex (lenticular) high-density extra-axial mass

Extradural haemorrhage is a neurosurgical emergency, requiring burr hole drilling followed by
craniotomy and evacuation of the haematoma. This should occur alongside full trauma assessment
for associated injuries
Spasticity
There should be vigilance for the development of spasticity in all neurotrauma patients, as if
untreated it can lead to fixed flexion deformity
- Treatment can be with splinting and stretching, antispasmodics (baclofen, dantrolene), and
botulinum toxin
Dysautonoma/PSH
Dysautonomia (sympathetic storms, paroxysmal sympathetic hyper-reactivity (PSH)) leads to

tachycardia, tachypnoea, hypertension, diaphoresis, hyper-pyrexia, and rigidity. This occurs due to
disrupted brainstem output
- Treatment can be with beta-blockers, clonazepam, clonidine, morphine, and dopamine

agonists
Chest Trauma
For patients with simple chest wall trauma e.g. following a sporting injury or minor fall, it is
appropriate to assess via history and examination
- Important factors to consider in the history include the mechanism and timing of injury,
associated symptoms (pain, breathlessness), and any past medical history of respiratory
disease
On examination assess for any signs of musculoskeletal injury, and ensure to observe chest wall
movement for a short while to identify any potential flail segment
- Palpation for subcutaneous emphysema can indicate underlying pneumothorax

- Ensure to examine the abdomen, due to the risk of splenic/liver injury by the lower ribs
Patients that have suffered major chest wall trauma, or appear acutely unwell, should be assessed
using an A to E approach
Chest Wall Fractures
Rib Fractures
Rib fractures are suggested by a history of trauma with subsequent musculoskeletal pain
- Diagnosis is clinical, with localised chest wall tenderness
It is essential to check for features suggestive of pneumothorax, secondary pneumonia, or flail

segment
Where multiple rib fractures are suspected there should be measurement of SpO2, ABG, and CXR
Uncomplicated cases should be managed with oral analgesia (co-codamol ± NSAID), and advise the
patient that the area may remain tender for >3 weeks
- Advise the patient that it is important to take deep breaths every so often, and cough when
they feel the need, to avoid LRTI
Where there is rib fracture in a child, this is should be a major red flag for NAI as it is very rarely
accidental
Flail Chest and Pulmonary Contusion
Fractures of >2 ribs in 2 places allows a part of the chest wall to move independently. This usually
indicates significant underlying lung injury, particularly pulmonary contusions
- Pulmonary contusion is an injury to lung parenchyma, leading to oedema and blood

collecting in the alveolar spaces
The flail segment causes pain and moves paradoxically compared with the rest of the chest wall
- This limits the effectiveness of respiration and is usually associated with respiratory distress
(cyanosis, tachypnoea)
Pulmonary contusions are more likely to lead to respiratory compromise than flail chest alone due to
increased V/Q mismatch and risk of ARDS. Crackles on examination suggest pulmonary contusion.
Diagnosis is clinical, but there should be assessment of the extent of respiratory compromise
- SpO2, ABG, CXR

o CXR can demonstrate fractures as well as associated injuries e.g. pneumothorax,
haemothorax, pulmonary contusions (patchy opacification)
o Pulmonary contusion usually becomes more obvious on later CXRs (24 – 48 hours
after injury)
- CT is very sensitive for identifying pulmonary contusion
Manage any immediate life-threatening complications and contact ITU. Patients with pulmonary
contusion may require RSI for tracheal intubation and IPPV
Sternal Fractures
Sternal fracture is suggested by anterior chest pain with localised tenderness over the sternum.
Further investigation is important as there may be associated myocardial contusion, great vessel
injury, or spinal injury
- Place the patient on a cardiac monitor and obtain a 12 lead ECG

- Check troponins
- CXR and lateral sternal XR
Where patients have a normal ECG, no associated injuries, and normal pre-existing cardiopulmonary
function there can be discharge with analgesia and GP follow-up
Haemothorax
Haemothorax is a collection of blood in the pleural space, usually as a result of rib fractures leading
to venous injury/ lung parenchyma injury
- Massive haemothorax is defined as a haemothorax sufficient to cause haemodynamic

instability and hypovolaemic shock. This is usually associated with arterial bleed
Most small haemothoraces are not detectable on examination, but will be identified on CXR, FAST or
CT scan. A large haemothorax will be clinically identical to a pleural effusion alongside features of
shock
- There will be evidence of chest trauma e.g. external bruising, lacerations, or palpable
crepitus
Management should be with IV fluids (or blood products where indicated), followed by insertion of a
wide-bore chest drain
- If the chest drain yields >1500ml of blood initially, or >200ml/hr for 2 hours there should be
urgent referral to a thoracic surgeon for thoracotomy
Abdominal and Pelvic Trauma

Assessment of patients with blunt abdominal trauma should follow the same format as other trauma
cases. However, there are some key features to assess for on examination
- Look for abdominal bruising, ensure to log roll to check for loin tenderness/bruising/injury
- Feel for tenderness and evidence of peritonism
- Check femoral pulses
- Examine the perineum and perform a PR
o This can assess for neurological function, but also for urethral/ rectal injury
All patients should have urinalysis (including pregnancy test), and other investigations as for trauma.
Further investigation can include
- Plain erect CXR, supine AXR if bony injury or bowel perforation are suspected
- FAST scan
- Abdominal CT
Further evaluation and treatment is dependent on clinical situation
- If the patient is haemodynamically unstable refer to a senior surgeon for laparotomy early,
this is known as ‘damage control’ surgery
- If the patient has clinical peritonism, perform primary survey and resuscitation and refer
urgently for laparotomy. Give IV antibiotics
- If the patient is haemodynamically stable with no signs of peritonism, perform primary
survey/resuscitation and investigate using FAST ± CT scanning. Refer to a surgeon for further
investigation and observation
Splenic Rupture
Splenic rupture is a common complication of blunt abdominal trauma, due to the vulnerable position
of the spleen, deep to the inferior ribs
There can be significant blood loss from splenic injury, therefore it should be suspected in patients
with abdominal trauma and signs of shock
- Tenderness and peritonism in the left upper quadrant is indicative
FAST scanning is an important first-line investigation, and if patients are stable enough, CT scanning
is important.
- CT scanning enables grading of injury from I to V dependent on the size, depth and vessel
involvement with the splenic laceration
Non-operative, conservative management is becoming more common in splenic injury, this is for
young stable patients with grade I/II injury
- Interventional radiology with angioembolisation can be used in some cases

- Surgical therapy is usually reserved for patients with haemodynamic instability or on-going
bleeding. This is usually with emergency laparotomy with splenic repair or removal
Pelvic Fractures
Pelvic fracture range in severity from low-energy injuries to life-threatening unstable fractures
- The pelvic bones surround vital structures including major blood vessels, nerves, and
digestive and reproductive organs
- The walls of the pelvis are lined with an extensive network of delicate veins, which are liable
to damage in pelvic fracture
Pelvic fractures should be suspected in all cases of major trauma. Signs and symptoms can include
- Tenderness, bruising, swelling and crepitus of the pelvic bones

- Haematuria or PR bleeding (±PV bleeding)
- Perineal and/or loin bruising
High-impact, unstable pelvic fracture will likely present with shock, and there may rarely be obvious
pelvic deformity
Tile Classification and Management
Approach these patients using a <C>AcBCDE approach. In type B and C fractures resuscitation is
generally required as below, whereas type A fractures are usually stable. Alongside fluid
resuscitation, the initial aim is reduction of blood loss by reducing pelvic volume, stabilising clot
formation, and reducing ongoing tissue damage
- This is best achieved with a pelvic binder

o Unroll the binder under the patient’s pelvis, and secure the Velcro straps over the
pubic symphysis with the wings over the greater trochanters. Ensure the binder is
tight enough to not slip down, but not so tight as to cause tissue under-perfusion
o The SAM pelvic sling and T-POD devices are the pelvic binders with best evidence for
use
- Avoid log-rolling patients with unstable pelvic fractures
- Where pelvic binders are not available, a sheet can be used
Where the pelvic binder stabilises the patient’s haemodynamics, there should be ICU referral and
imaging prior to definitive fixation with surgery
- Pelvic x-rays should be obtained in all patients with multisystem injury

- Examine the pubis, iliac bones, hips and sacrum for tenderness, bruising, swelling or crepitus
Where the patient remains haemodynamically unstable following application of the pelvic binder
there needs to be urgent damage control surgery or endovascular embolization.
Type A fractures are stable injuries e.g. avulsion fractures, fractures of the pubic ramis/ iliac wing
- These will generally not require surgery, and can be treated with bed rest for 3 – 6 weeks
and pain relief. Avoidance of weight-bearing for several months is advised
Type B fractures are rotationally unstable but vertically stable. There are three main forms
1. Open book pelvic fracture: this is an anteroposterior compression fracture, causing

compression of the symphysis and widening of the sacroiliac joints
2. Ipsilateral compression causing the pubic bones to fracture and override
3. Contralateral compression causing compression injury to the sacro-iliac joint on one side and
pubic ramus fracture on the other side
Type C fractures are rotationally and vertically unstable. This is where the pelvic ring is completely
disrupted or displaced at >2 points. There is often significant blood loss
1. Unilateral
2. Bilateral
3. Also involving acetabular fracture
Spinal Injury and Stabilisation
Spinal injury should be considered while managing every trauma patient, and spinal immobilisation
should be provided in patients with
- Major trauma
- Minor trauma with spinal pain and/or neurological symptoms (paralysis, focal deficit,
paraesthesia)
- Altered conscious level after injury
- High risk mechanism of injury
o Fall from a height, axial load to the head, high speed motor collision,
rollover/ejection motor accident, bicycle collision
- Pre-existing spinal disease
- Patients aged >65
In patients that may not need to be immobilised (absent/delayed neck pain, ambulatory, low risk
injury), check that they can actively rotate their neck to the left and right without significant pain/
neurological symptoms
- If in doubt, immobilise
It is important to note that cervical and full-spinal immobilisation is not without risks, this can
include
- Aspiration from vomiting

- Respiratory compromise
- Raised ICP
- Decubitus ulceration
However, it is generally accepted that the risks of the above are outweighed by the benefits of
preventing CNS injury
Assessment
Patients should be approached using a <C>AcBCDE approach

Cervical spine protection and airway management occur together, but management of the airway,
breathing and circulation should take priority over potential concerns about spinal injury
- Immediate manual cervical immobilisation can be achieved by placing one hand on each side
of the patient’s head and holding it steady (without traction) in line with the remainder of
the spine
o Open the airway using a jaw thrust ± suction, and maintain with simple adjuncts
o Whilst maintaining manual immobilisation, ask a colleague to apply an appropriately
sized had cervical collar
o Sizing of the collar is estimated by the number of finger breadths between the
patient’s jaw and shoulder
- After the collar is in place, manual immobilisation must also be maintained, or simulated
with placement of blocks/rolled towels either side of the collar
Breathing assessment can indicate spinal cord damage

- Damage to the thoracic spine can impair ventilation by eliminating intercostal muscle
activity below the injury level, this will be seen as diaphragmatic breathing
- Injury to C3 – C5 can result in diaphragmatic paralysis and respiratory arrest, requiring
urgent ventilatory support
Circulation assessment can indicate neurogenic shock
- Hypotension, bradycardia, warm peripheries

- Always exclude hypovolaemia as the cause of shock in these patients
Immobilisation of the thoracic, lumbar and sacral spine is by placement of the patient on a spinal
board. Again, this should never delay assessment of airway, breathing, and circulation
- Transfer the patient from the spinal board to a vacuum matress (using an orthopaedic scoop
stretcher) when the patient arrives in hospital
- The spine should remain immobilised until injury is excluded
Imaging
C-spine x-ray should be performed in accordance with Ottowa guidelines
- >65
- Dangerous mechanism
- Neurological symptoms
- Midline tenderness of c-spine
- If able to safely assess range of motion (e.g. sitting up, walking around): unable to actively
rotate neck 45 degrees
With C-spine x-ray there should be AP, lateral, and open-mouth odontoid peg views. If indicated,
perform additional AP and lateral views of the thoracolumbar spine
CT and MRI are used in cases where there is clinical suspicion of injury, but normal X-rays
Spinal Cord Injury
Like brain injury, spinal cord injury occurs in two phases

- Secondary spinal cord injury can be caused by hypoxia (particularly due to airway
obstruction or inadequate ventilation, but also by hypovolaemia)
- Further primary injury can occur with inappropriate handling leading to pressure from
unstable bone fragments/ dislocations
Recognition of spinal cord injury should be with recognition of potential mechanisms of injury that
may cause spinal damage. Cord injury itself can present with the following symptoms/signs
- Pain at the site of spinal injury

- Loss of sensation/function below the painful level
- In unconscious patients: diaphragmatic breathing, flaccid limbs, no pain response,
neurogenic shock
Where spinal cord injury is suspected ensure to perform and record an accurate neurological
examination to assess progression.
Patterns of incomplete spinal cord injury include
- Anterior cord syndrome: loss of pain and power below the injury, with preservation of touch
and proprioception
- Posterior cord syndrome: loss of sensation but preservation of power
- Brown-Sequard syndrome: hemisection of the cord producing ipsilateral paralysis and
touch/proprioception loss, and contralateral loss of pain and temperature
Fractures and Dislocations

Fractures
There are many factors that should be included when describing a fracture to a colleague
- Age of the patient, and how the injury occurred

- Name the bone, specifying whether right or left
- Position of the fracture
- Type of fracture
o Simple (oblique or transverse): single fracture line with two bone fragments
o Spiral: twisting injury with two bone fragments
o Comminuted: complex fracture with >2 fragments
o Crush: loss of bone volume due to compression
o Avulsion: bony attachment of ligament/muscle is pulled off
o Hairline: barely visible with no displacement
o Greenstick: incomplete fracture of immature bone
o Stress: repeated sub-clinical injury results in fracture. Patients present with pain and
radiological fracture without history of trauma
- Describe any associated deformity in terms of displacement, angulation or rotation. Usually
one describes the position of the distal fragment relative to the proximal
- State the grade of classification of the fracture where appropriate
- State presence of any complications e.g. pulse absent, paraesthesia, tissue loss
Long bones consist of a diaphysis (shaft) with an epiphysis at each end, the metaphysis is the
transitional zone between the two
Fractures and Pre-Hospital/Trauma Care
In some patients, there is a risk of crush syndrome. This is a condition caused by skeletal muscle
injury
- Removal of the compressive force leading to sudden release of electrolytes and sudden fluid
shift
- Re-perfusion of the limb risking pulmonary embolus or fat embolus
Give high flow oxygen and fluids prior to release of the compressive force to help offset renal failure
and hypovolaemic shock
Splinting limbs in the pre-hospital setting can help to reduce pain and haemorrhage, and decrease
risk of fat embolus
- Assess colour, sensation, and movement before and after splinting to ensure that
neurovascular status remains intact
Always splint the joint above and below the fracture. Splint types include vacuum splints, short box
splints, and traction splints (only for femur fracture in the absence of pelvic fracture).
Compound Fracture
A compound fracture is where a fracture is open to the air through a skin wound, risking infection.
This should be treated as an orthopaedic emergency. Classification is by Gustilo classification
- Type I: wound <1cm, clean

- Type II: wound >1cm, but no associated significant damage
- Type III: extensive soft tissue loss and/or exposed bone and/or vascular injury needing repair
Compound fracture wounds should be addressed with an A to E approach, followed by irrigation

with saline and covered with a sterile, moist dressing. Give IV antibiotics and splint the limb. Refer
urgently to T&O
- Some type III (particularly with vascular injury) may require amputation
- Operative repair should ideally occur within 6 hours to reduce the risk of osteomyelitis
Complications
Early complications of fracture include
- Neurovascular damage
- Compartment syndrome. This is suggested by increasing pain, sensory deficit, swelling, and
features of ischaemia. Treatment is with prompt decompression, this may require open
fasciotomy
- Fat embolism. This is suggested by breathlessness and chest pain ~24 hours after injury,
features of SIRS occur alongside this
- Fracture blisters
Late complications include

- Non-union in which the fracture does not heal. This is suggested by pain at the fracture site
persisting for months, movement around the fracture site, and a palpable gap at the
fracture site
o This can be managed with bone grafting
- Malunion, where the fracture does not heal in alignment
Casting
Fracture fixation is carried out to restore anatomy, stabilise the fracture, preserve blood supply, and
ensure early and safe immobilisation
- Other indications include ligament injuries, reduced dislocations, musculoskeletal infection,

deformity correction, severe soft tissue injuries, and post-operatively
Plaster of Paris is the most common material used for casting as it can be moulded to the shape of
the limb
- It is applied to the limb over a layer of stocking and wool. Padding should be applied over
bony prominences
- Plaster of Paris sets using an exothermic reaction, so it is important to warn the patient that
the process will feel warm
X-rays should be carried out after the application of the cast, to ensure that the fracture is
immobilised in a functional position.
There are certain complications to all casts, an additional complication to plaster of Paris is the risk
of disintegration if the material gets damp
- Circulatory compromise from a tight cast. This presents with the 5Ps of an acutely ischaemic
limb
o Elevate the limb and completely cut off the cast
- If a cast is too loose there is a risk of fracture slippage, therefore loose casts should be
replaced
- Local discomfort is common over pressure points, and may be an indication of pressure
ulcers. Cut a window in the cast to allow inspection of the underlying skin
- Allergic dermatitis is a common complication
Dislocations
A dislocation involves a complete loss of congruity between articular surfaces, whereas subluxation
is movement of the bones of the joint with some articular contact
Dislocations should ideally be reduced as soon as possible to prevent neurovascular complications,

decrease risk of recurrence, and decrease pain
- In general, it is advisable to x-ray prior to reduction
Certain dislocations should be reduced immediately, prior to any investigation
- Dislocations associated with neurovascular compromise

- Uncomplicated patellar or mandibular dislocations

- Patients with recurrent dislocations without significant trauma e.g. EDS
Soft Tissue Injuries
Soft tissue injuries are a very common presentation to accident and emergency departments and GP
surgeries, this includes damage to ligaments, tendons, muscles and other supporting
musculoskeletal structures
On assessment of patients with isolated soft tissue injuries, a non-emergency approach is

appropriate
Assessment
There are several key features to elicit during the history
- Mechanism and timing of injury

- Timing and presence of pain, swelling and/or bruising
- Instability of the joint, and loss of joint function (e.g. movement, weight bearing)
- Weakness or paraesthesia
Assess the impact of the injury on the patient’s social circumstances
On examination check for tenderness over bony points to assess for likelihood of fracture, ensure
there is no neurovascular compromise, and assess the range of joint movement/ weight bearing
Tendonitis
Tendonitis typically occurs as an overuse injury. The main symptoms are a gradual onset of pain,
tenderness, stiffness and swelling of the affected part of the tendon. Common examples include
- De Quervain’s tenosynovitis presents with pain over the base of the thumb
- Trigger finger, preventing the patient from straightening their finger fully
- Tennis elbow (lateral epicondylitis), where there is pain on the lateral aspect of the elbow
- Golfer’s elbow (medial epicondylitis), where there is pain on the medial aspect of the elbow
- Achilles tendonitis, where there is pain at the Achilles tendon worsened with walking
- Rotator cuff tendonitis
Ultrasound or MRI may be necessary to differentiate tendonitis from partial tendon rupture, but
generally history and examination are sufficient for diagnosis
Management is with abstinence from activities that aggravate the tendon, sometimes a splint or
brace can be used to aid this
- Ice packs can alleviate pain, as well as oral/topical NSAIDs

- Steroid injections can be considered
- Surgical release of a tendon can be used in resistant cases
Bursitis
Bursitis presents with pain, tenderness, swelling and erythema over the affected bursa as well as
reduced joint movement
- This can be precipitated by trauma, recurrent minor injury, infection, or co-existing

inflammatory disease
It is important to differentiate between septic and non-septic bursitis, therefore there should be
fluid aspiration from the bursa where septic bursitis is suspected
- The aspirate should be cultured and assessed for white cells and glucose, crystals, and gram
stained
- Septic bursitis is managed with aspiration and antibiotics. Incision and drainage may be
required where there is no response to therapy
Imaging is not usually required, but USS can be useful in diagnosis
Non-septic bursitis is managed with rest, ice, NSAIDs PRN, and physiotherapy
- Aspiration of the bursa with corticosteroid injection can be used where symptoms are
resistant
- Surgical bursectomy can be indicated where medical therapy has failed
Sprain
A sprain is caused when a joint is forced beyond its normal range of motion, resulting in
overstretching and tearing of ligaments supporting it
There are three grades of sprain depending on severity
1. The ligament is stretched with microscopic tearing. Swelling is mild, with little or no
functional loss and no joint instability. Partial weight bearing is possible
2. The ligament is stretched with partial tearing. Swelling is moderate-to-severe, with
ecchymosis. There is moderate functional loss and mild-to-moderate instability. Patients
have difficulty weight bearing
3. The ligament is completely ruptured. Swelling is immediate and severe, with ecchymosis.
The patient cannot weight bear and the joint is unstable
Fractures and sprains can present similarly. Fracture is suggested by obvious deformity, swelling,
bruising, inability to weight-bear, and bony tenderness
- X-ray should only be performed where there is a suspicion of fracture, this can distinguish
fracture from sprain
- CT or MRI are sometimes needed to identify fracture and assess ligamentous injuries
Prolonged immobilisation of sprains seems to be detrimental to recovery, therefore management

should follow the general principles below alongside progressive mobilisation as soon as symptoms
allow
- Management of severe sprains is with a short period of immobilisation using a cast or

pneumatic brace. There may be a requirement for surgery if there is gross joint instability
Muscle Injuries
Muscle strains are suggested by pain on palpation over the site of injury also being re-created by
passive movement/ active contraction of the affected muscle unit
Direct muscle injuries are from a direct impact to muscle; leading to pain, bruising and soft tissue
swelling
Most muscle injuries can be treated with the general measures below. However, if there is a severe
injury e.g. complete rupture, crush injury, large haematoma additional measures may be required
- Specialist review for surgical repair or surgical drainage of haematoma

- Assessment and management of rhabdomyolysis
- Assessment of haemodynamic stability, coagulation screen, and need for blood transfusion
Myositis ossificans can occur as a complication of muscle injury, due to calcification within a
haematoma. This presents with restriction of movement and loss of function following injury
- The limb should be immobilised for several weeks followed by delayed excision of the
calcified structures
Investigations
In the ED, investigation depends on likelihood of differential diagnosis and severity of injury
- X-ray can be used to rule out fracture, but can also show soft tissue swelling
- Joint aspiration may be required to exclude crystal arthritis or septic arthritis
- USS, CT scanning or MRI may also be used
Management
General management of soft tissue injuries is with (P)RICE
- Protection e.g. use of crutches

- Rest, usually advising 24 – 48 hours of rest following injury. Gradual controlled exercise
should follow injury as soon as symptoms allow
- Ice can be used to decreased swelling and pain, apply for 10 – 15 minutes repeating every
few hours as needed
- Compression is usually with tubigrip
- Elevation
Where possible, refer selected patients to physiotherapists within the ED. This enables the patient to
be given education and advise on exercise following injury
Acute Weakness
Acute onset weakness is a distressing symptom, and can have many potential causes. Rapid and
thorough assessment is essential for many key reasons
- Assessment of the need for intubation and respiratory support

- So that time-dependent treatment can be administered where relevant
- The consequences of progression can be treated
Patients complaining of acute weakness should be approached with an A to E assessment, breathing

is particularly important due to the risk of diaphragmatic involvement with the disease process
- Ensure the airway is patent

- Assess breathing
o Often in neuromuscular respiratory failure the patient doesn’t show obvious
respiratory distress
▪ Orthopnoea occurs as the diaphragm is paralysed, therefore abdominal
contents move towards the thorax when the patient lies flat
▪ Abdominal (paradoxical) breathing
▪ Tachycardia
▪ Weak cough
▪ Rapid, shallow breathing
▪ Speech interrupted by breathlessness
o ABG is important where these signs are present, as type II failure will occur in late
stages
▪ Maintain target saturations of 88 – 92% in these patients to ensure hypoxic
drive
- Establish IV access and take routine blood tests
o Ensure to treat any neurogenic shock
o FBC, U&Es, LFTs, glucose, and clotting
- Thorough assessment of disability
o Full GCS rather than AVPU
History
Where patients are well enough, take a history including the following aspects
- Speed of onset
- Progression
- Severity
- Muscle groups affected
o Upper limb and/or lower limb (proximal or distal), trunk, facial
o Trouble with speech or swallowing
o Sphincter disturbance
o Symmetry of the groups affected
- Associated sensory symptoms
- Associated pain in the neck or back
- Headache
- Visual loss
- Involuntary movements
- LOC
- Fits/funny turns
- Associated systemic symptoms e.g. recent illness, fever, sweats, malaise, weight loss
Examination
Full upper limb, lower limb, and cranial nerve examination is important. Specific patterns of
weakness should be assessed, distinguishing between UMN and LMN lesions
- UMN monoplegia and hemiplegia tend to indicate a problem with the contralateral cortex or
internal capsule
- Quadriparesis and diparesis tends to indicate a spinal lesion
- Proximal weakness of all four limbs tends to indicate myopathy
- Distal limb weakness tends to indicate neuropathy
- Fatigability indicates NMJ disorders
Weakness should be graded using the MRC scale
Assess objectively for loss of sensation and the distribution of this
- Brown-Sequard syndrome indicates cord hemisection; with loss of ipsilateral

vibration/proprioception/light touch and contralateral pain/temperature sensation
- Glove and stocking indicates peripheral nerve
- Hemisensory loss indicates cerebral cortex
Assess for autonomic involvement by measuring blood pressure, ECG, and bladder scan to assess for
urinary retention
The most urgent conditions to consider include the following
- Ischaemic stroke
- Intracranial haemorrhage
- Spinal cord compression
- Myasthenic crisis
- Guillain-Barre syndrome
- Compartment syndrome
The level of dysfunction can be cerebral, spinal, peripheral nerve, neuromuscular junction, or
muscle. The most likely site of the lesion is then determined by history and examination findings,
with many potential causes for each
Cerebral Spinal Peripheral NMJ Muscle

Vascular Stroke Stroke
TIA
SAH
Trauma Haemorrhage Acute cord Compartment
Focal/ diffuse compression syndrome
lesion Cord
transection
Infection Encephalitis Abscess HIV Botulinium

Abscess Polio toxin
Meningitis
Autoimmune MS MS AIDP MG Myositis
Sarcoid Dermatomyositis
Vasculitis
Metabolic Encephalopathy Diabetes Hypothyroid
Renal failure Cushing’s
Hypothyroid Rhabdomyolysis
B12/B1 ICUAW
ICUAW Drug/toxin
Toxins
Neoplastic SOL Acute cord Paraneoplasia LEMS Paraneoplasia
compression
Other Todd’s paresis Syringomyelia MND
Hemiplegic Transverse
migraine myelitis*
Sleep paralysis
* Causes of transverse myelitis is an acute spinal demyelination. Causes include infections (lyme
disease, HSV, VZV, HIV), MS, and paraneoplastic syndromes
Assess FVC ± ABG in all patients at risk of neuromuscular respiratory failure, and repeat this
assessment regularly
- If FVC <15ml/kg or decreases by >20% this is an indication to ventilate the patient, either
invasively or with NIV
- Consider the need for additional respiratory support at 30ml/kg due to impaired clearance
of secretions
More specific blood tests can be undertaken
- ESR and/or CRP looking for evidence of inflammation. This could indicate myositis, infection,
or other autoimmune processes
- Bone profile, PSA and myeloma screen
- B12, folate and B1 levels
- TFTs
- Syphilis serology
- Muscle enzymes: CK, LDH, AST, ALT, serum myoglobin
Imaging may be indicated depending on likely cause, this can include cerebral and/or spinal CT and
MRI
- The urgency with which imaging is required depends on the likely diagnosis
CSF analysis can also be indicated in many presentations of weakness. Lumbar puncture should only
be undertaken prior to CT scan if there is no sign of raised ICP, seizure or immunocompromise.
Electrophysiological tests can also be useful

- Visual evoked potentials

- Electromyography
- Nerve conduction studies
Specific other tests may be indicated
- Tensilon test
- Muscle biopsy
Cranial Nerve Lesions
There are some differentials for multiple cranial nerve lesions in the same patient
- Chronic meningitis e.g. TB, malignant

- Brainstem strokes
- MS
- Mononeuritis multiplex e.g. vasculitis, diabetes mellitus
- AIDP
- SOL e.g. tumour, aneurysm, haematoma
o Cerebellopontine angle tumour (VII, VIII, V, IX)
o Cavernous sinus thrombosis, orbital pathology (III, IV, VI)
Differentials for isolated cranial nerve lesions obviously differ dependent on the nerve, but can
include any differential for peripheral neuropathy alongside compression (SOL, aneurysm), MS, and
trauma
Metabolic Diabetes, renal failure, hypothyroidism

Inflammatory GBS, CIDP, sarcoid, vasculitis
Neoplastic Paraneoplastic changes
Infectious HIV, Lyme disease, leprosy, polio
Nutritional B12 deficiency, B1 deficiency
Inherited CMT, porphyria
Drugs/Toxins Lead, isoniazid, chemotherapy, phenytoin
It is also important to always consider myopathy as an alternative explanation
- Inherited disorders include muscular dystrophy, myotonic dystrophy, and metabolic/

mitochondrial/ channelopathy disorders
- Acquired myopathies may be inflammatory, endocrine, or drug-induced
For CN II, III, IV, and VI do not forget simple intrinsic eye and orbit lesions
Stroke
A stroke (cerebrovascular event) is a clinical syndrome caused by disruption of blood supply to the
brain leading to sudden onset of focal or global neurological disturbance persisting for >24 hours
There are two main forms of stroke

- Cerebral infarction is the commonest (a potential cause of this is carotid or vertebral artery
dissection, therefore be mindful of this where this is a history of trauma or neck
manipulation)
- Intracerebral haemorrhage
Presentation
Signs and symptoms of stroke differ dependent on the area of brain without blood supply (stroke
territory), this can be summarised by Bamford’s classification
Aetiology Presentation
Total anterior circulation Occlusion of the internal Hemiparesis and hemisensory loss
stroke (TACS) carotid or proximal middle Homonymous hemianopia
cerebral artery Cortical dysfunction e.g. dysphasia
Partial anterior Occlusion of the anterior or 2/3 of the above or cortical
circulation stroke (PACS) middle cerebral artery dysfunction alone
Lacunar stroke (LACS) Occlusion of small perforation Hemiparesis OR
lacunar arteries Hemisensory loss OR
Hemi-sensorimotor loss OR
Ataxia
NO CORTICAL DYSFUNCTION
Posterior circulation Occlusion of vertebral, basilar, Cerebellar/ brainstem syndromes
stroke (POCS) or posterior cerebral artery Isolated homonymous hemianopia
LOC
Approach A to E. Several factors in the history can distinguish different forms of stroke (the ROSIER
score can indicate likelihood of stroke given history)
- Headache or drowsiness makes haemorrhage more likely

- Recent fall or head trauma points more towards subarachnoid haemorrhage
Examination should include several factors
- NIH stroke scale (NIHSS) is a clinical evaluation that can assess severity of stroke and aid in
decisions regarding thrombolysis
o Grades consciousness, orientation, gaze, visual fields, facial weakness, motor
function, ataxia, sensation, language, dysarthria, and inattention
- Neurological examination should include upper limb, lower limb, and cranial nerve
o In the limbs there may be acutely diminished tone (will increase later), weakness,
and initially absent reflexes
o Cranial nerve examination can reveal visual inattention or visual field defect
- Assess speech
- General inspection for any signs of trauma and cardiovascular signs (AF, carotid bruit) is
important
Investigations
Routine blood tests should be performed, including
- FBC to see if the patient is anaemic or polycythaemic, if there is an elevated WCC indicating
infection, or any derangement in platelet count
- U&Es for evidence of dehydration or rhabdomyolysis
- LFTs as baseline
- ESR/CRP to check for infection or inflammation (e.g. GCA, vasculitis)
- Creatine kinase may be raised if the patient has been lying on the floor for a long time
- Glucose (hypos can mimic stroke) and lipid profile as vascular risk factors
ECG to assess for signs of AF, ischaemic heart disease or hypertension is important
CT head is indicated in all patients within 24 hours for all strokes. Urgent CT should be performed if
the patient is a likely candidate for thrombolysis, is taking anticoagulant treatment, GCS <13,
progressive symptoms, features of meningism, or severe headache
- CT is very sensitive at diagnosing haemorrhagic stroke, but will be normal for <6 hours in
ischaemic stroke
Carotid Doppler can also be used to assess for stenosis
Management
In acute stroke the initial management should involve maintenance of homeostasis
- Supplemental oxygen should be given if SpO2 <95%

- Blood sugar should be between 4 – 11 mmol/L. This can be treated with IV insulin or glucose
- Blood pressure reduction should be considered where BP >185/110 in thrombolysis
candidates
300mg aspirin should be given as soon as primary haemorrhage is excluded, and continued for 2
weeks
- Clopidogrel 75mg daily can then be substituted and continued indefinitely

The window of opportunity for effective thrombolysis is 4.5 hours from the onset of ischaemic
stroke
- Contraindications to thrombolysis include: seizure, intracerebral or subarachnoid

haemorrhage, INR >1.7, uncontrolled hypertension, GCS <8, abnormal BM, head injury, or
rapidly improving signs
- Thrombolysis is with IV rTPA (usually alteplase) as a 10% bolus, and then the remaining 90%
of the dose infused over the following hour
Consider neurosurgical input for haemorrhagic stroke, or where there is evidence of raised ICP.
Swallow assessment should be carried out early by speech and language therapists
1. Sit patient upright and listen to chest to establish baseline

2. Ask the patient to cough, assess strength and effectiveness
3. Give the patient a teaspoon of water and hold it in their mouth, look for leakage of water
from the closed mouth
4. Ask the patient to swallow and watch for signs of aspiration
5. If no problems, try half a glass of water
Nutrition screen should assess BMI and percentage unintentional weight loss, the MUST screening
tool can be used for this purpose
- Nutritional support should be indicated for stroke patients at risk of malnutrition, this can
include oral supplements, specialist dietary advice and/or tube feeding
Patients should be encouraged to sit up and mobilise as soon as their condition permits
Prevention
There are several modifiable risk factors for stroke
- Modifiable by lifestyle change: smoking, alcohol, obesity, physical inactivity, diet

- Modifiable by medical intervention: hypertension, AF, diabetes, hyperlipidaemia, carotid

stenosis (endarterectomy at >70% occlusion)
Secondary prevention of stroke should include
- Antiplatelet therapy long term with clopidogrel or aspirin

- Lower blood pressure and cholesterol
- Anticoagulation for AF
- Carotid endarterectomy
Transient Ischaemic Attack (TIA)
A TIA is a focal neurological deficit due to inadequate blood supply that lasts for <24 hours
- Focal neurological deficit includes monocular visual field loss

- Typical presentation include limb weakness, expressive dysphasia, amaurosis fugax,
hemianopias, and sudden onset cerebellar signs
The risk of stroke following TIA can be estimated using ABCD2 scoring
- Age >60
- Blood pressure >140/90
- Clinical features of TIA (unilateral weakness = 2, no weakness = 1)
- Duration of symptoms (>60 minutes =2, 10 – 59 minutes = 1)
- Diabetes
The risk of a stroke is ~10% in the first 5 days following TIA, it decreases over time but remains up to
10% for 90 days
- ABCD2 >4 (or 2 or more TIAs within a week) should be treated with 300mg aspirin daily and
referred for specialist assessment within 24 hours
- ABCD2 <4 should be treated with 300mg aspirin daily and referred for specialist assessment
within one week
Malignant Spinal Cord Compression (MSCC)
Acute cord compression in cancer is a medical emergency, and if not treated promptly can
result in permanent disability
MSCC is a risk in any cancer that has bone involvement, with the vast majority of cases
occurring in the thoracic cord
- This is commonest in breast, prostate, lung, myeloma, and lymphoma
The signs and symptoms of different forms of spinal cord compression are summarised in
the table below
- Radicular pain frequently precedes neurological symptoms
Complete Anterior Posterior Lateral Cauda
Compression Compression Compression Compression Equina
(Brown-Sequard)
Loss of all Loss of pain and Loss of vibration Contralateral loss Saddle
sensation below temperature and position of pain and anaesthesia
level sensation below sensation below temperature
level level below level
Bilateral UMN Bilateral UMN Sparing of pain, Ipsilateral loss of Urinary

weakness below weakness below temperature and vibration and retention
level level touch position
Bladder and bowel Bladder and bowel Ipsilateral UMN Loss of anal
dysfunction dysfunction weakness sphincter
tone
Investigation should always include MRI where possible as this can accurately show the level
of the lesion. Occasionally it is necessary to use CT scanning or myelography
Management must be rapid to avoid permanent neurological impairment
- Dexamethasone 16 – 20mg should be given immediately to reduce peri-tumoural

oedema, this can be before MRI where suspicion is strong
- Surgical decompression and stabilisation of the spine should be considered in all
cases, but is often contraindicated in extensive disease
- Radiotherapy is used where surgery is not possible, or as an adjunct to surgery
Myasthenia Gravis (MG)
MG is an acquired autoimmune disease with antibodies against the nicotinic acetyl choline receptor
and/or muscle-specific tyrosine kinase
- This leads to muscle weakness with easy fatigability improving at rest

There is a strong association between MG and thymoma, as well as aggravation/induction of disease
with penicillamine
Presentation
The clinical presentation ranges from mild weakness of limited muscle groups (Class I or ocular)
through to severe weakness of multiple muscle groups (Class V or generalised)
Common symptoms include
- Painless muscle fatigue following exercise e.g. voice becomes progressively less audible as
the patient talks, patient cannot sustain upward gaze. Weakness is more marked in proximal
muscles, but can include
o Weakness of the small muscles of the hand (finger extensors)
o Bulbar weakness causing nasal and slurred speech as well as dysphagia
o Facial muscle weakness
o Muscles of mastication may be weak, meaning that eating is difficult and the jaw
may drop (patients often sit with their chin on their hand)
o Weakness of the flexors and extensors of the head
- Ptosis
- Diplopia due to ophthalmoplegia
On examination there is no wasting or fasciculation, tone is normal, sensation is normal, and tendon
reflexes are normal
- To induce symptoms it is necessary to fatigue the patient with repetitive movements

The most common pattern of disease is to spread from ocular to generalised within a year from
onset, progressing to maximal weakness is around 40 years.
Respiratory compromise in MG can be fatal due to weakness of the muscles of ventilation leading to
acute respiratory failure. Patients with neuromuscular respiratory failure do not look distressed, and
changes in blood gas occur very late (gas transfer is good)
- It is important to monitor vital capacity, tidal volume and blood gasses in these patients to
ensure that early intervention with ventilation occurs when needed
- FVC <15ml/kg or >20% drop in FVC is an indication for intensive care monitoring
Investigations
The ice test can be used first-line to distinguish MG from other causes of ptosis, alleviating the ptosis
when ice is applied over the eye for three minutes
Laboratory investigations should include MG serology (nAChR and MuSK antibodies) as well as
muscle-specific enzymes to rule out myopathy
Neurophysiological tests can include
- Repetitive nerve stimulation

- Single fibre EMG
The Tenilson test can be used to confirm diagnosis, but is often not required as trial doses of
pyridostigmine carry less risk of bradycardia
- IV administration of a short-acting acetylcholinesterase inhibitor e.g. edrophonium chloride

leading to objective improvement in muscle strength
All patients should have CT thorax to exclude underlying thymoma
Management
Medical treatment of myasthenia can include the following
- Long acting acetylcholinesterase inhibitors e.g. pyridostigmine are first line

- Steroids are indicated in patients that are not adequately controlled on cholinesterase
inhibitors. These should be slowly tapered off when remission occurs
- Immunosuppressants are used alongside steroids. This is usually azathioprine but can
include methotrexate, MMF, and rituximab
In Myasthenic crisis there can be plasma exchange (50ml/kg for 10/7) and IVIg (2g/kg for 5/7)
alongside corticosteroids
Thymectomy is important if thymoma is present. Thymectomy can also be beneficial in resistant

disease in the absence of thymoma
Guillain-Barre Syndrome (AIDP/ GBS)
GBS is a disorder causing demyelination ± axonal degeneration resulting in acute, ascending and
progressive neuropathy
- This is characterised by weakness, paraesthesiae and diminished reflexes
The majority of patients have a history of preceding infection (1 – 3 weeks prior to onset of
weakness), usually of the respiratory or GI tract; this association suggests that there is a cross-
reaction of antibodies against peripheral nerve tissue
- Organisms involved include C.jejuni, EBV, CMV, and mycoplasma
Presentation
The commonest presenting complaint of GBS is weakness starting in the lower extremities
- Weakness is usually ascending, progressive and symmetrical

- Maximum severity is usually reached within 2 weeks after the initial onset of symptoms, and
usually stops progressing after 5 weeks
There may also be neuropathic pain, autonomic symptoms, and paraesthesiae starting in the lower
extremities
On examination the following signs may be present
- Hypotonia
- Altered sensation
- Reduced/ absent reflexes
- ~30% will have autonomic features
Investigations
Diagnosis is usually made on clinical grounds; however, the following investigations may be useful to
exclude other conditions
- Routine blood tests including U+Es, as there may be SIADH

- Urinalysis, CXR and stool culture can be used to detect any triggering infection
- Lumbar puncture in GBS will show elevated CSF protein
- Nerve conduction studies are the most useful confirmatory test, showing a slowing of
conduction
- Immunoglobulin levels should be checked, as patients with IgA deficiency may experience
anaphylaxis when given IVIg
There should be regular spirometry as respiratory muscle weakness is common, and is an indication
for ITU admission
Management
Plasma exchange or IVIg should be used in all patients. There should also be DVT prophylaxis
- Corticosteroids should not be given
90% of patients will make a full recovery (~80% within weeks to months), but persistent fatigue is
common and ~10% will require a walking aid for >1 year
- Death occurs in ~10%, this is more common in older patients with axonal damage and a
need for ventilatory support
Motor Neurone Disease
Motor Neurone disease (MND) is a progressive paralysing disease, there are several forms
- Amyotrophic lateral sclerosis (ALS) is the commonest form

- Progressive bulbar palsy is where the first effects of the condition are seen in the muscles
used for talking and swallowing
- Progressive muscular atrophy is where the effects are solely in the lower motor neurones,
and the progression of the condition is much slower than in ALS
- Primary lateral sclerosis is where the effects are solely in the upper motor neurones
MND is due to a degeneration of the anterior horn cells of the spinal cord and the motor cranial
nuclei, leading to a mixed LMN and UMN dysfunction
The aetiology of the condition is unknown
- Around 5% of cases are inherited in an autosomal dominant pattern, with some of these
cases having a mutation in the SOD1 gene
- There may be an abnormality of mitochondrial functioning causing oxidative stress in motor
neurones
Presentation
MND has peak onset in middle age, and tends to affect males more than females. Symptoms differ
dependent on the cause of MND
ALS presents with progressive weakness (generally starting asymmetrically in the upper limbs)
affecting the bulbar (LMN v pseudo-bulbar (UMN)), limb, thoracic and abdominal muscles
- Patients may complain of clumsiness, muscle cramps, foot drop, and tendency to trip
- With bulbar onset there may be slurring of speech, tongue fasciculation, dysphagia, and
emotional lability
Pain and sensory disturbance are not common features of the disease, and there is no cognitive
impairment
Signs that can indicate MND include
- Assymetrical distal weakness

- Brisk reflexes, hypertonia, and up-going plantars in a wasted limb
- Fasciculations
- Absence of sensory signs
Investigations
There are no specific diagnostic tests for MND, but investigations can include the following
- Electrophysiological studies, with EMG showing fibrillation and fasciculations and with NCS
showing normal function
- Respiratory function testing, with both measurement of FVC and SpO 2 at rest
o If SpO2 <94% on air, perform ABG to assess need for NIV
- CT/MRI
- Muscle biopsy
- Blood tests can include B12/folate, HIV serology, Lyme disease serology, CKMB
Diagnosis of MND can be made in the following circumstance
- Presence of
o LMN dysfunction evidenced by clinical, electrophysiological, or neuropathological
examination
o UMN dysfunction evidenced by clinical evaluation
o Progressive spread of symptoms
- Absence of
o Electrophysiological and pathological evidence of other disease processes
o Neuroimaging evidence of other disease processes
Management
MND is an incurable condition with an average survival from diagnosis of 2 – 4 years, however there
are many aspects of the patients’ care that should be addressed
- An MDT approach is essential including regular physical, occupational, and speech therapy
- Insertion of a PEG/RIG or NG tube is important when patients have lost >10% of body weight
or have a BMI <18.5
- When respiratory function is impaired, there should be regular physiotherapy to clear
secretions. Assisted ventilation with NIV (PPV) is required when respiratory function declines
o Respiratory involvement is suggested by breathlessness, poor sleep, excessive
daytime somnolence, and morning headaches
o FVC should be measured regularly
o NIV should include palliative care input, and is gradually built up as necessary
Medications can be given for symptomatic relief
- Drooling can be reduced with anticholinergics e.g. hyoscine

- Muscle cramps and spasticity can be reduced with agents such as diazepam, baclofen, and
tizanidine
- Depression should be treated adequately
- Pain should always be asked about and treated adequately, this includes the use of opioids
There is only one drug with proven disease-modifying efficacy
- Riluzole is a glutamase-release inhibitor, this is given at 50mg BD
Spinal Muscular Atrophy (SMA)
SMA is a disorder of degeneration of motor nerve cell bodies in the anterior horn of the spinal cord,
and is therefore a solely LMN disorder
- Most cases in childhood are autosomal recessive, however in adulthood there are variable
inheritance patterns
The onset of the condition is both proximal and distal

Kennedy’s Disease
Kennedy’s disease is an X-linked condition due to a mutation in an androgen receptor gene. This
causes a progressive lower motor neuronopathy
- It presents with weakness and wasting of the face and upper limbs. Predominantly affecting
bulbar muscles
- There are additional features of androgen insensitivity e.g. gynaecomastia and infertility
Multifocal Motor Neuropathy
Multifocal motor neuronopathy is a motor syndrome that can closely mimic MND
- Onset is typically in early adulthood with asymmetrical involvement of the upper limbs
- Wasting and brisk reflexes are not predominant features
The key to diagnosis is a conduction block in motor nerve conduction studies
- This is a treatable condition

The Acutely Ill Patient: Key Investigations

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The Acutely Ill Patient: Key Investigations

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Hannah Cooke, 2016/17

The Acutely Ill Patient

ABGs are indicated in many circumstances

Contraindications and cautions to ABG sampling include

- Sampling from an arm with an IV infusion in progress

Complications of ABG include

- Vascular thrombosis or spasm

First, clarify the following with the patient

Ulnar circulation is assessed using the modified Allen’s test

Collect and prepare equipment

The steps in performing an ABG are listed below

Factor Reference Range

Base Excess +/- 2

PaO2 11.0 – 13.0

PaCO2 4.7 – 6.0

Other factors that can be measured include

1. Is the patient adequately oxygenated?

- Alveolar-arterial oxygen gradient

Respiratory Hypoventilation (T2RF) Hyperventilation

- Lung disease - Anxiety

Low/normal anion gap (losing HCO3-)

Following CPR, there is generally a mixed respiratory and metabolic acidosis

Venous Blood Gas

- VBGs can only give accurate information about metabolic derangement

When analysing VBG results, it is important to remember the following

- pH is 0.02 – 0.04 lower

NEW score Clinical Risk Monitoring Frequency Clinical Response

1–4 Low 4 – 6 hourly Assessment needed by registered

The following features are assessed and scored

PEW Score Clinical Response

A 12 lead ECG should be reported in a set method, covering the following

- Rate and rhythm

Arrhythmias can be detected on the rhythm strip

1. Rate will usually be normal to fast

In atrial fibrillation, there will be an absence of p waves on the ECG trace

This p wave fragmentation manifests as a wondering baseline on the trace. As there is no

Paroxysmal Atrial Tachycardia

This is often an adverse effect of digoxin

- Other adverse effect is ‘reverse tick’ T waves on ECG

WPW syndrome is a congenital supraventricular tachycardia due to an accessory pathway between

1. Fast rate >200bpm

1. Very fast rate

1. Rate will be bradycardic ~50bpm

This does not typically require any treatment

1. Rate will be bradycardic, but not drastically

1. Rate will be bradycardic, around 30bpm

1. Rate will be bradycardic, around 30bpm

- If Lead I and II are positive, there is no axis deviation

- II, III and AVF will be negative

- III and AVF will be positive

Left Axis Deviation Right Axis Deviation

- ST elevation is defined as anything >2 small squares

ST depression indicates ischaemia, the same territories as above apply.

Widespread ST elevation with a saddle shaped ST segment indicates pericarditis

Bundle Branch Block

- The changes of bundle branch block are best seen in V1

In right bundle branch block there is an RSR pattern in V1, V2 and V3

Right bundle branch block can be due to cor pulmonale and PE

- The red electrode is placed on the right arm, RA

The ECG electrodes are placed on the chest as shown below

- V1 is placed on the right sternal edge, 4th intercostal space

- V2 is placed on the left sternal edge, 4th intercostal space

- Check ID and date