Likely Finals Acute Cases
Emergency management of:
Airway
Abdo pain (acute)
Compartment syndrome / fat embolism
Coma
Compression of spinal cord / cauda equina
Confusional state / LOC
COPD excacerbation
Diabetic emergencies: DKA / HONK / Hypoglycaemia
DVT – Risk factors
Endocrine emergencies (non-diabetic) – addisons - SHAG
GI Bleed
Gynae pain / PV bleed
Headache
Hepatic failure
K+ states: Hyperkalaemia / hypokalaemia
Myocardial infarction - complications
Pneumothorax / tension pneumothorax
Poisoning
Pulmonary embolus
Renal failure (acute)
Respiratory failure – signs and symptoms
Septic arthritis
Shock: anaphylactic, cardiogenic, hypovolaemic, septic
Sickle cell crisis
Status asthmaticus
Status epilepticus
Stroke
Testicular torsion
Transfusion reaction
Airway management
Laryngeal mask airway
The laryngeal mask airway (LMA) is used in anaesthesia and in emergency medicine for airway
management. It is a tube with an inflatable cuff that is inserted into the pharynx. It causes less
pain and coughing than an endotracheal tube, and is much easier to insert. However, it does not
protect the lungs from aspiration, making it unsuitable for anybody at risk of this complication.
It is useful in situations where a patient is trapped in a sitting position, suspected of
trauma to the cervical spine (where tilting the head to maintain an open airway is
contraindicated), or when intubation is unsuccessful.
The laryngeal mask airway is a device that sits tightly over the top of the larynx. It avoids tracheal
intubation and can be used with spontaneous respiration or artificial ventilation. However, it may
not protect the airway from the aspiration of regurgitated material. It has found favour in day case
surgery. Patients who have been treated with the laryngeal mask airway claim it does not irritate
the throat as intubation typically does.
If an LMA is not suitable or appropriate, an endotracheal tube may be used to facilitate ventilation
and prevent aspiration.
The commonest and the most important complications are:
 regurgitation of gastric content and chances of aspiration.
 Inadequate patient anaesthesia may result in coughing, gagging, and bucking on attempted
LMA insertion.
 lingual nerve injury
 recurrent nerve paralysis
 larynx passing behind the thyroid and cricoid cartilage
 postoperative sore throat and dysphagia.
Endotracheal intubation
The tube is inserted into the trachea, generally via the mouth, but sometimes through the nares of
the nose (e.g. in extensive mouth surgery) or even through a tracheostomy. The process of
inserting an ETT is called intubation.
Intubation usually requires general anesthesia and muscle relaxation but can be achieved in the
awake patient with local anaesthesia or in an emergency without any anaesthesia, although this
is extremely uncomfortable and generally avoided in other circumstances.
It is usually performed by visualising the larynx by means of a hand-held laryngoscope that has a
variety of curved and straight blades. The intubation can also be performed "blind" or with the use
of the attendant's fingers (this is called digital intubation). A stylet can be used inside the
endotracheal tube. The malleable metal stylet is a bendable piece of metal inserted into the ETT
as to make the tube more stiff for easier insertion, this is then removed after the intubation and a
ventilator or self-inflating bag is attached to the ETT. The goal is to position the end of the ETT 2
centimeters above the bifurcation of the lungs or the carina. If inserted too far into the trachea it
often goes into the right main bronchus (the right main brochus is less angled that the left one).
Complications:
 Tension pneumothorax
 Oesophageal intubation
 Endobronchial intubation occurs if too long a tube is used and inserted into one of the
mainstem bronchi. The un-intubated lung does not contribute to gas exchange, and the large
volume of blood flowing through this lung results in a substantial right to left shunt.
 Signs are those of arterial hypoxaemia, including cyanosis and laboured breathing. In
addition, uptake of the inhalation anaesthetic agent may be impaired, resulting in an
unexpectedly light plane of anaesthesia.
 This problem may be avoided by trimming of the tube to the correct length and securing it
firmly. If too long a tube is used and it is tied around the back of the patient's neck, movement
of the tube during surgery may move the tip of the tube into a bronchus.
 Impaction of the tip of the tube against the tracheal wall - may result in respiratory
obstruction.
 Compression of the lumen of the tube by the cuff
 Stretching of the tracheal wall may be caused by over-inflation of the cuff. This may lead to
tracheitis, pressure necrosis of the tracheal wall or tracheal rupture.
Tracheostomy
A tracheostomy is most commonly performed in patients who have had difficulty weaning off a
ventilator, followed by those who have suffered trauma or some catastrophic neurologic insult.
Infectious and neoplastic processes are less common in diseases that require a surgical airway.
The advent of the antibiotic era coupled with great advances in anesthesia have made
tracheotomy the most commonly performed elective procedure.
To bypass obstruction
Congenital anomaly (eg, laryngeal hypoplasia, vascular web)
Foreign body that cannot be dislodged with Heimlich and basic cardiac life support
(BCLS) maneuvers
Supraglottic or glottic pathologic condition (eg, infection, neoplasm, bilateral vocal cord
paralysis)
Neck trauma that results in severe injury to the thyroid or cricoid cartilages, hyoid bone, or
great vessels.
Subcutaneous emphysema
Appears in face, neck, or chest
Readily dissecting air, especially through inflamed or traumatized tissue planes,
leading to massive soft tissue edema
Facial fractures that may lead to upper airway obstruction (eg, comminuted fractures of the
midface and mandible)
Edema
Trauma
Burns
Infection
Anaphylaxis
To provide a long-term route for mechanical ventilation in cases of respiratory failure
To provide pulmonary toilet
Inadequate cough due to chronic pain or weakness
Aspiration and the inability to handle secretions (The cuffed tube allows the trachea to
be sealed off from the esophagus and its refluxing contents. Thus, this
intervention can prevent aspiration and provide for the removal of any aspirated
substances. However, some would argue that the risk of aspiration is not actually
lessened, as secretions can leak around the cuffed tube and reach the lower
airway.)
Prophylaxis (as in preparation for extensive head and neck procedures and the convalescent
period)
Severe sleep apnea not amendable to continuous positive airway pressure (CPAP) devices or
other, less invasive surgery
Immediate complications
Apnea due to loss of hypoxic respiratory drive: This is mainly important in the awake patient.
Ventilatory support must be available.
Bleeding: Intraoperative bleeding arises from the cut edges of the very vascular thyroid gland
and from lacerated vessels in the field that should be cauterized or ligated. Care should
be taken to stop all thyroid bleeding before the cut edges are allowed to retract laterally,
which makes them difficult to expose.
Pneumothorax or pneumomediastinum: These can result from direct injury to the pleura or the
cupola of the lung (especially in children) or from high negative inspiratory pressures of
patients who are awake and distressed. Early recognition is critical, and routine
postoperative chest radiography should be considered after tracheotomy.
Injury to adjacent structures: The paratracheal structures vulnerable to injury are the recurrent
laryngeal nerves, the great vessels, and the esophagus. This danger is most prevalent in
children because the softness of the trachea hinders its identification if it is not distended
with a rigid object.
Postobstructive pulmonary edema: Although rare, a transient pulmonary edema can occur after
tracheostomy, which provides relief of upper airway obstruction.
Early complications
Early bleeding: This is usually the result of increased blood pressure as the patient emerges
from anesthesia (and relative hypotension) and begins to cough. Although this may
necessitate a return to the operating room, bleeding may be controlled with local packing
and hypertension control. Packing should involve antibiotic-impregnated gauze (eg,
iodophor), and the patient should be given antistaphylococcal antibiotics while the
packing is in place. Bloody secretions that issue from the tube may represent diffuse
tracheitis (most commonly), rundown bleeding from the skin or thyroid, or ulceration from
an ill-fitting tube or overzealous suctioning.
Plugging with mucus: The use of dual cannula tubes lessens this as a threat because the inner
cannula can be removed for cleaning while the outer cannula safely maintains patency of
the fresh tract. However, vigilance is still required, and all measures to thin and to remove
secretions should be undertaken.
Tracheitis: To some degree, tracheitis is present in all patients with fresh tracheostomies.
Again, humidification, minimization of the fraction of inspired oxygen (FIO 2) (because
high oxygen levels exacerbate drying), and irrigation are essential. Moreover, motion of
the tube within the trachea is extremely irritating and should be prevented with
stabilization of the ventilator circuitry so that torsion is minimized.
Cellulitis: The wound is colonized quickly; however, infection is unlikely if the incision has not
been closed tightly and drainage is allowed. Opening the wound and instituting
appropriate antibiotics should suffice to treat any early cellulitis.
Displacement
The need to replace a new tracheostomy tube is not uncommon. In this situation,
remember the access that the upper airway still affords. Bag ventilate the patient
and prepare for intubation if the tracheostomy tube cannot be replaced. Initial
management includes passing an object (eg, smaller tube, clear nasogastric tube
[which shows the fogging of respiration]) into the open wound.
A physician may attempt recannulation. This is facilitated with placement of the tube
over the fiberoptic laryngoscope and reentry of the trachea under direct vision.
However, endotracheal intubation remains the mainstay of airway management
and should not be ignored while an increasingly traumatized tracheostomy site is
labored over. Misplacement of the tracheostomy tube into the dreaded false
passage, usually in the pretracheal space, should be suspected in the presence
of difficult ventilation or passage of a suction catheter or if subcutaneous air or
pneumothorax develops.
Subcutaneous emphysema: This results from a tight closure of tissue around the tube, tight
packing material around the tube, or false passage of the tube into pretracheal tissue. It
can progress to pneumothorax, pneumomediastinum, or both and should be treated with
loosening of the closure or packing and with performance of a tube thoracotomy, if
necessary. Incidence of pneumothorax after tracheostomy is 0-4% in adults and 10-17%
in children; thus, postoperative chest radiography is recommended in children.
Atelectasis: An overly long tube can mimic a unilateral mainstem intubation, causing
atelectasis or collapse of the opposite lung.
Late complications
Bleeding
Bleeding more than 48 hours after the procedure may herald a tracheoinnominate
fistula caused by a low (farther along the trachea toward the carina)
tracheostomy or an ill-fitting long tube. One half of patients with significant
bleeding more than 48 hours after the procedure have a tracheoinnominate
erosion. This occurs in 0.6-0.7% of patients with tracheostomies, and the
mortality rate of this complication approaches 80% if treated aggressively.
Patients with an impending tracheoinnominate fistula may have a sentinel bleed
(ie, brief episode of brisk bright red blood from the tracheostomy site) hours or
days before catastrophic bleeding. Some physicians prefer to investigate all such
episodes of bleeding with a careful tracheobronchoscopy, looking for suggestive
areas in the appropriate area of the trachea.
If diagnosis is made only when catastrophic bleeding occurs, management includes
replacement of the tracheostomy tube with an endotracheal tube with the balloon
inflated distally to the site of the bleeding to protect the airway. If the balloon
does not tamponade the bleeding, a well-placed finger can temporize while the
thoracic surgery team mobilizes for median sternotomy to locate and to control
the bleeding vessel.
Occasionally, granulation tissue at the tip of the tracheostomy tube can bleed
vigorously. This can be identified via flexible laryngoscopy and can be treated
with excision or cautery via bronchoscope in the operating room.
Tracheomalacia: This is usually caused by a tube that fits poorly. Improved fit may allow
recovery of the softened cartilage.
Stenosis: Injury to the cricoid cartilage, the only circumferential ring in the trachea, can lead to
laryngeal stenosis. Stenosis typically occurs at the site of the tracheostomy or at the area
irritated by the cuff. Over the course of his life, Chevalier Jackson saw the incidence of
posttracheostomy stenosis drop from 75% to 2%. Modern high-volume low-pressure cuffs
have reduced the rate of this complication; however, care must still be taken not to
overinflate these cuffs and to deflate them periodically. Tracheal stenosis typically
develops several weeks after decannulation as a subacute distress, often mistaken for
bronchitis. Treatment is surgical and ranges from formal resection and reconstruction to
less invasive means of debridement or stenting for palliation.
Tracheoesophageal fistula: A tracheoesophageal fistula, which is typically caused by friction
between a posteriorly displaced tracheostomy tube or overinflated cuff and a rigid
nasogastric tube, almost always requires surgical repair, possibly with a muscle flap, skin
graft, or both. A tracheoesophageal fistula manifests as aspiration and subsequent
chemical pneumonitis and should be evaluated with a plain film (which may show an airfilled esophagus) or barium swallow, followed by bronchoscopy. Preoperative
management includes gastrostomy decompression and jejunostomy nutrition. This
complication occurs in less than 1% of patients with tracheostomy.
Tracheocutaneous fistula: Epithelialization of the tract from skin to trachea can result in a
nonhealing fistula. This can be repaired with coring out of the epithelial layer and
allowance of the wound to granulate in. Alternatively, a 3-layer closure can be performed
but is associated with more complications. A persistent tracheocutaneous fistula can
indicate proximal resistance or a remaining obstruction and should be evaluated via
direct laryngoscopy.
Granulation: This can occur at the site of the stoma and should be cauterized with silver nitrate.
It can also occur distally, where it may cause partial or complete obstruction or cause this
friable tissue to bleed. As granulation matures into fibrous scar, it can contribute to
stenosis.
Scarring: Both vertical and horizontal incisions heal with small but visible scars that can be
revised if they bother the patient.
Failure to decannulate: Sometimes, patients fail plugging trials or even decannulation for no
apparent reason. Possibilities to consider include obstructing granuloma previously held out of
the way with the tube, bilateral vocal cord paralysis, infractured cartilage, and anxiety. Evaluation
should include fiberoptic laryngoscopy and bronchoscopy through the stoma, with visual
inspection down at the carina, up at the glottis, and then through the nose to view the
hypopharynx and the supraglottis.
Cord compression / cona medularis / cauda equina
Cord compression
Spinal / root pain (early)
Spastic Weak legs (early)
Hyperreflexia
Sensory loss
Hesitancy (late)
Frequency (late)
Painless retention (late)
Conus medularis syndrome
Mnemonic: FULLAR
Faecal incontinence (early)
Urinary incontinence (early)
Lumbrosacral pain (early)
Leg weakness with LMN
presentation (flaccid)
Absent reflexes
Cauda equina syndrome
As conus medularis +
Assymetrical paralysis
Radicular pain down legs
FULLAR AR
Questions: SLOPS
Loss of Sphincter control (bowel / bladder)
Sensory Level
Onset: gradual or sudden
Progression
Spastic or flaccid
Causes: Tend to be age determined:
15-30yrs
30-50yrs
 Disc prolapse
 disc prolapse
 Trauma
 malignancy
 degen. spinal disease
 Ankylosing spondylitis





Investigations
Management
STAT MRI
Cross match / G+S
FBC + clotting
IV Access
Urgent neurosurgery
referral









50+ yrs
Osteoporosis
Paget’s
Malignancy
Myeloma degenerative
ESR ( in myeloma,
infections, cancer)
Syphilis serology, B12
Nil by mouth
DVT prophylaxis
Consider catheterisation
Confusional state / LOC
You can think of the causes with the mnemonic AEIOU TIPS
 Alcohol
 Endocrine (e.g. Addisons) / encephalopathy
 Insulin (DM: Hypoglycaemia, DKA, HONK)
 Overdose / oxygen (hypoxia)
 Uraemia
 Trauma / tumour / temperature
 Infection (meningitis, septicaemia)
 Post-ictal / psychosomatic
 Subdural / subarachnoid haemorrhagediu
You can also categorise
them by Airway cause,
Breathing cause, Circ cause,
disability (neuro) cause and
exposure cause.
In the elderly do not forget the four Ps: Poo (constipation), Pee (UTI), Pneumonia and
Polypharmacy
Immediately: ABC then DEFG: Don’t Ever Forget Glucose (BM) + tests below & IV access
BM
ABG
FBC
U+E, LFT
ESR, CRP
Blood culture
Ethanol
Hypo / hyperglycaemia – followup with urinary ketones as appropriate
Hypoxia, CO2 narcosis, acidosis
Infection
Hepatic / uraemic encephalopathy / hyponatraemia or other imbalance
Infection – potential meningitis
Infection – only if systemic signs (hyperthermia)
LFT & GGT
Toxic screen
CXR
Spine X-ray
CT
Overdose, poisoning – salicylates and paracetamol at least
May reveal cause of hypoxia
Eliminate C spine injuries – must view C1 – T1
Neurological causes
Brief examination…
 GCS (or AVPU – see box)
 Full set basic obs (inc temperature)
 Respiratory pattern and rate
 Visual fields (test with visual threat)
 Pupils – size, reactivity, gaze direction
 Extra-ocular movement (not if C spine
danger) Dolls-head movement (brainstem)
 Fundoscopy
 Neck stiffness
 Tone and reflexes
 SKIN for needlemarks, self-harm, trauma
 CSF from nose or ears
 Abdomen – signs of chronic liver disease
or internal bleed
 Cardiovascular exam + ECG
…and focussed history
 Speed of onset
 Recent complaints: headache, fever,
vertigo, depression.
 Suicide note
 Recent illness: sinusitis, otitis, Neuro /
ENT surgery
 PMH: DM, asthma, BP, cancer,
epilepsy, psychiatric
 Drugs (alcohol, recreational) or toxins
 Exotic travel
AVPU is a basic, abbreviated coma scale
A= alert
V= responds to vocal stimuli
P= responds to pain (approx GCS 8)
U= unresponsive
Treat specific causes
 Opioid OD: naloxone
 Benzodiazepine OD: flumazenil
 Thiamine: if Wernicke’s encephalopathy possible
 In poisoning, remember to call the poisons centre (number in BNF)
 Hyperglycaemia: insulin + saline
 Hypoglycaemia: glucose
 CO: High flow O2
 Meningococcal septicaemia
Continuing Care
 Regular reassessment of GCS: a change of 2 points necessitates a review of management.
 Should be intubated with oxygen and on ITU
 Maintain careful monitoring of Fluids. Catheterise.
 Daily bloods
 At least hourly obs.
 Regular movement is necessary to avoid pressure sores (more of a nursing priority).
Diabetic emergenicies
DKA
Both Ketones and acidosis are required for this diagnosis. BM is not required.
PC: SLOW ONSET -  conscious level / coma; lethargy; anorexia; hyperventilation; ketotic
breath; dehydration; abdo pain (mainly children)
Immediately: (ABC) then BM, O2 Sats, Temp, ABG, IV access; Urine ketones (catheter if req)
Differentials:
Overdose (e.g. aspirin)
Lactic acidosis (elderly diabetics)
Investigations
Glucose
HCO3Amylase
Osmolality
Management: SKIDS
 Saline: 0.9% (1L over 30 mins; 1L 1˚; 1L 2˚; 1L 4˚; 1L 6˚)
 K+: With 2nd and subsequent bags (see right)
 Insulin: 4-8 Units if BM > 20
 Dextrose: Swap from saline to 5% dextrose when BM <15
 Sliding scale
Blood culture
FBC
Salicylate levels
K+ to add per L of IV fluid
Serum K+
KCl to add
<3
40 mmol
3-4
30 mmol
4-5
20 mmol
Sliding Scale
BM
Insulin
Insulin*
Note that the number of units of soluble insulin
0 - 3.9
0.5**
1**
given normally (green column) is 1/4 that of the
4 – 7.9
1
2
figure in bold in the BM column.
8 – 11.9
2
4
12 – 15.9
3
6
*This value is doubled in infection / insulin
16+
4
8
resistance.
* If infection or insulin resistance; ** Zero units is NEVER put on a sliding scale!




Always consider a bolus when starting a sliding scale
50 U actrapid made up to 50 ml with 0.9% saline – this provides 1 U / ml concentration. This
is placed in a syringe driver set to deliver the appropriate amount per hour.
Every hour the nurses will take a BM and reset the driver to deliver the amount of insulin you
have written up for the appropriate BM
If BM does not come down the consider another bolus or increasing slightly the amounts of
insulin written up for a given BM on the sliding scale (e.g. go up a unit or two)
Stopping a sliding scale
 The scale should be continued until there are no ketones and BM<10
 Consult with the diabetic specialist nurse.
 It is ideally stopped at breakfast
 Take a BM and give long-lasting insulin appropriately before breakfast
 After breakfast, stop the sliding scale infusion – the effect will cease almost immediately
so alternate insulin cover must be in place.
 Keep patient in for another 24 hours for observation.
The extended insulin regime:
BM often drops faster than ketones and is a poor (and dangerous) substitute for ketone levels.
Running the patient on 10% or 20% dextrose with appropriate insulin will ensure the ketone levels
drop while preventing hypoglycaemia. Helps prevent recurrence of DKA.
Establish the cause of the DKA
HONK
Management
Mnemonic: HIS HONK
 Heparin – (High risk of DVT)
 Insulin: 1 Unit / hour
 Saline: at half the rate for DKA
Alternate Mnemonic: SIDs HONK*
 Saline: at half the rate for DKA
 Insulin: 1 Unit / hour
 DVT prophylaxis (high risk) – heparin
*NB: Sid is obviously a goose…
Hypoglycaemia
The definition of hypoglycaemia is plasma glucose <2.5 g / dl. Symptoms arise at varying points
person to person.
Causes: alcohol (even in non-diabetics), insulin, long-acting sulphonylurea, unexpected
exercise, Addisons, insulinoma, prolonged starvation, dumping syndrome, aspirin OD.
Symptoms include: pale+sweating, hunger (though sometimes food refusal), nausea, tremor,
drowsiness, seizures, hemiplegia, coma, mutism, mannerisms, personality change (e.g.
aggression).
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
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Take BM
Take blood: before treatment for: glucose, insulin, C-peptide, salycylate levels.
If alcohol related or malnourished give 1-2 mg / kg thiamine before glucose to avoid
Wernike’s
If not in coma: Give hypostop or similar oral glucose. Outside hospital give oral sugar + long
acting starch (e.g. jam sandwich)
If in coma: give 20-30g dextrose IV (200-300 ml of 10% dextrose). 50% dextrose harms
veins. An alternative is glycogen IV/IM 1 g. Expect prompt recovery for either. Follow with
sugary drinks and a meal.
Investigate the cause
DVT
PE is a consequence of DVT – risk factors for DVT include NO PILLS
The following are NOT risk factors for DVT
 Neoplasm
 Oral contraceptive pill
 Smoking
 Hypertension
 Pregnancy
 Intravenous drug use
 Hypercholesterol / lipidaemia
 Long distance road/air travel
 Lower limb fractures
 Surgery (major)
Investigations
 D-Dimer
 Thrombophilia tests if FH,
no risk factors of recurrent
 Compression ultrasound
Prevention
Treatment
Management
 Stop OCP 4 wks pre-op
 LMW heparin 1.5 mg/kg/d
 TED stockings
 Switch to warfarin for 3
months to INR 2-3
 Prophylactic heparin
 Early mobilisation
Headache
As with all pain, ask the full range of questions in SOCRATES (see appendix x). Associated
symptoms are listed below.
Acute / severe
Meningococcal septicaemia
Pre-eclampsia
Glaucoma (closed angle)
Raised intracranial pressure
Subarachnoid haemorrhage
Giant cell (temporal) arteritis
Recurrent
Tension headache
Migraine
Cluster headache
Space occupying lesion
Features
Fever (± other signs of sepsis), neck stiffness, ?petechial rash
In pregnancy
Eye pain + redness, tears, fixed dilated pupil, decreased acuity,
haloes around lights
 systolic BP, widened pulse pressure, bradicardia, nausea.
‘Like being hit by a cricket bat’ – sudden, severe.
Jaw claudication, scalp tenderness, Trismus, ESR, Loss of
vision.
May be very severe, pain typically ‘like a band’ around the head
or like a weight on the head, often goes away on holiday.
Aura, photopsia, nausea
‘clusters’ of headaches over weeks / months that disappear for
a period before returning. Unilateral with one red eye + tearing.
Typically pain in mornings, increasing severity over months
Mnemonic: MEG IS A FUNNY FEMALE JESTER
Causes (acute severe)
Questions (all headaches)
M Meningococcal
F Fever
E Pre-Eclampsia
U Aura / photopsia / haloes
G Glaucoma
N Nausea
I Intracranial pressure
N Neck stiffness
S Subarachnoid haem.
Y Young? – first severe
A Arteritis (giant cell)
headache >35 is sinister.
Questions (all headaches)
F Fit / collapse
E Eye – loss of vision
M Memory / mental changes
A Abrupt onset
L Loss of consciousness
E Eye pain, redness, tears
Causes (acute severe)
Essential components of the examination
J Jaw claudication
 GCS, MMSE
 Otoscopy
E Raised ESR*
 Focal neurology
 Temperature
S Scalp tenderness
 Scalp + sinuses for
 Meningism / neck
T Trismus
tenderness / fractures
tenderness
E Event e.g. trauma
 Pupils
 Rashes
R Rash
 Fundoscopy
 BP
*OK – this is an investigation and not a question…
Immediately: ABC then BP, temp, urine dip if pregnant, IV access
Investigations:


CT/MRI head or LP
Blood cultures


ESR
LFTs
Management: meningitis
Mnemonic: ABC HUBS
 ABC & admit immediately
 Place head-up
 1200 mg benzylpenicillin
by slow IV or IM 1 g
Cefotaxime if penicillin
allergic
 Steroid - dexamethasone
Management: SAH
 ABC & admit immediately
 Observation / analgesia
 Prevention of further
ischaemia: 3L fluids
minimum + nimlodipine
 Prevention of re-bleed –
clipping of aneurysm
Management: ICP
Mnemonic: ABC ERMMM…
 ABC & admit immediately
 Elevate head of bed to 40˚
 Restrict fluids <1.5L / 24h
 Mannitol 20% 1-2g / Kg
over 10-20 mins*
 Monitor
 Make diagnosis for
definitive management
*this takes 10-20 mins to work – if intubated can also hyperventilate to PaCO2 <3.5 – this yields
almost immediate reduction in ICP.
Pre-eclampsia
Diagnosis is based on: BURPP
O/E remember:
 BP>160/110mmHg on 2 occasions
 High BP / Urine dip
 U+E’s: raised creatinine
 Facial oedema
 Raised ALT/AST, deranged clotting factors  Confusion (severe PET)
(hepatitic picture)
 Hyperreflexia and clonus
 Protein (urinary) >300mg/24hours
 Papilloedema
 Platelets low
 Foetal Doppler / Cardiotocography (CTG)
Management:



ABC & Ob/Gyn referral
IV Access, BP, Urine dip
Treat hypertension
(methyldopa or CCB /
labetalol) ACE I contraind.



Monitor maternal health
Monitor fetal health (CTG /
fetal movement chart)
Delivery (± steroids as
required)
General info for supplemental questions
Neck
Stiffness
Meningitis
Triad
QuickTime™ and a
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Fever
Headache
An important physically
demonstrable sign of meningitis
is Kernig's sign. Severe
stiffness of the hamstrings
causes an inability to straighten
the leg when the hip is flexed to
90 degrees. The back of the
thigh muscle can be felt in
spasm.
Cushing’s triad is the triad of signs that may indicate raised intracranial pressure – papilloedema
is often cited but is a very late sign. Others are headache, vomiting, drowsiness and fever.
Pulse Pressure is the difference between
systolic and diastolic blood pressures
Widening Pulse
Pressure
Monroe-Kelly doctrine
Cushing’s
Triad
 Sys BP
Bradycardia
The cranium and the vertebral body, along with
the relatively inelastic dura, form a rigid
container, such that the increase in any of its
contents --- brain, blood, or CSF --- will increase
the ICP. In addition, any increase in one of the
components must be at the expense of the other
two.
Pathogenesis of Pre-eclampsia

Not fully understood yet.

What is known is that problem is fundamentally poor placental perfusion. It is thought this poor
placental perfusion may either be due to a problem with trophoblast implantation and/or due to maternal
microvascular disease, but whatever the cause, the blueprint for pre-eclampsia is set early in
pregnancy.

The lack of placental perfusion leads to the release of vasoconstrictors such as thromboxane, a relative
lack of vasodilators such as prostacyclin and women with PET seem to be more sensitive to
vasoconstrictors in general.

This creates a high pressure system and in the placenta this damages the endothelium to cause
microthrombi of trophoblastic tissue, which in turn leads to increased coagulation and also precipitate
end-organ damage.

This end organ damage includes:

CVS: High TPR leads eventually to LVF, which in turn causes pulmonary oedema and ARDS.

Kidneys: There is swelling of glomerular endothelial cells which blocks the capillaries and leads to
leakiness of the kidneys which manifests as proteinuria and reduced renal function

Liver: Fibrin deposits accumulate in the liver and this causes hepatocellular damage, which can result
in DIC. The liver becomes distended and sub-capsular hemorrhage can also occur.

Increased cerebral vascular resistance leads to visual disturbance, headache, eclampsia and increased
risk of CVA.
 Placenta: High resistance and poor perfusion leads to oligohydramnios and IUGR.
Endocrine emergencies (non-diabetic)
Addisonian crisis
Addison’s disease is the primary adrenal insufficiency. Adrenal hormones will be lacking and this
may result in an Addisonian crisis.
Tuberculosis
Surgical removal of adrenals
Meningococcal septicaemia
Causes:
Autoimmune disease
Steroid therapy
Most reliable are in bold
Symptoms
Weight loss
Anorexia
Signs
Pigmentation: esp palmar creases
Depression
Confusion
Weakness
Myalgia
Diarrhoea
N&V
Syncope
Joint / back
Postural Hypotension
Buccal pigmentation
Loss of weight
Loss body hair
Gen. Wasting
Vitiligo
Dehydration
The immediate management of Addisonian crisis
Take blood for cortisol levels. Do not await results.
There are several priorities:

-60 mins. 100 mg IM 6 hourly thereafter
until clinically stable.
 Fluid & salt replacement: 1L normal saline IV over 30-60 mins. 2 units over next 12 h thereafter.
 Glucose replacement: IV glucose as required (5% dextrose is not sufficient).
Initiate tests for TB (the commonest cause of Addisonian crisis after primary Addison’s
syndrome).
 Sputum culture and microscopy (for AAFB – alcohol acid fast bacilli)
 Tuberculin (Mantoux) test
 Chest X-ray
Mnemonic: SHAG – saline, hydrocortisone, AAFB, glucose
The confirming test for primary Addison’s disease is the synthacthen test measuring response to
a synthetic ACTH analogue.
K+ States
Hyperkalaemia
K+ > 6 is a medical emergency
Possible clinical features include:
cardiac arrhythmias, e.g. asystole: hyperkalaemia is usually asymptomatic until cardiac
toxicity intervenes.
other features include peripheral muscle weakness(less common), confusion and
respiratory paralysis.
Note that emergency treatment is necessary if the serum potassium rises above 7.0 mmol/l or if
there are ECG changes associated with hyperkalaemia.
The ECG changes involved in hyperkalaemia are variable but may involve:
peaked T waves
widened QRS complex
increased PR interval
asystole
Management
 Levels – confirm the reading is real and not due to artifact e.g. haemolysis of the sample
 Calcium gluconate (for cardiovascular protection – does not affect K+ levels) 10 ml of 10%
given over 2 mins.
 Salbutamol Nebs (2.5 mg) Moves K+ into cells
 Insulin + Dextrose (20 U + 50ml of 50% dextrose)* Moves K+ into cells


Calcium resonium (binds K+ in the gut) 15 mg over 8h in PO in water or 30 mg PR
Dialysis if unresponsive to medical treatment or if K+ > 7
Mnemonic: GRIDDLeS – Gluconate; Resonium; Insulin + Dextrose; Dialysis; Levels; Salbutamol
*250ml of 20% dextrose is less damaging to veins but takes longer to deliver.
Hypokaleamia





peripheral muscle weakness - may also occur in hyperkalaemia
polyuria
polydipsia
cramps, tetany
tiredness
K+ <3 in a patient taking thiazides rarely requires treatment
K+ <2.5 – 3 not taking diuretics is treated by 80 mmol / 24 hours K+ (Sando-K, 2 tabs TDS/QDS)
K+ <2.5 always requires treatment (or advice from a senior)
 Cautious IV K+: 1 L of 20 mmol/L (or 500 ml of 40 mmol/L) over 1 hour then repeat levels
Gastrointesinal bleed
Gynae Pain / PV bleed
In pregnancy
In 50% of women presenting with vaginal bleeding in pregnancy, the pregnancy will continue as
normal.
In early pregnancy (<20 weeks), think of:
 Ectopic pregnancy
 Miscarriage: threatened, inevitable,
missed/silent.
 Molar pregnancy
In later pregnancy think of:
 Placenta praevia
 Placental abruption
Unrelated to pregnancy
 Cervical lesions e.g. cervical ectropion.
 If pain only think of appendicitis, UTI and renal stones.
Asking about the bleeding
 Is the patient pregnant (test if not absolutely sure)
 If pregnant, has intrauterine pregnancy been confirmed on ultrasound.
 Is it heavier than a normal period
 How much blood (how many pads)
 Have any clots been passed (think of vaginal shock)
Ectopic pregnancy:
Any pregnancy outside the uterus. Ask if the patient has had an ultrasound scan yet – if so and
this has confirmed an intrauterine pregnancy then this diagnosis is excluded.





Ovary
Fallopian tubes (accounts for 95%):
Fimbrial, ampullary (most common), isthmic
and corneal.
Cervix
Broad ligament
Abdomen
Predisposing factors:
Miscarriage is loss of pregnancy before 24 weeks. There are a number of types:
 Threatened: This is when there is PV bleeding (no pain) before 24 weeks gestation, the os is
closed and a viable intrauterine pregnancy is seen on USS
 Inevitable: This is when there has been/is imminent loss of the products of conception
through an open cervix. An inevitable miscarriage can be incomplete (products have not
completely been lost) or complete (all the products of conception have been expelled from the
uterus).
 Missed miscarriage: This is when there is loss of the pregnancy with the os closed and
complete retention of products of conception.
Myocardial infarction
Infarction - tissue death by ischaemia most often resulting from occlusion of a coronary vessel by
an embolus. The most common source of emboli come is the rupture of an atherosclerotic plaque
STEMI: ST elevation myocardial infarction (Q wave MI)
NSTEMI: non ST elevation MI (‘unstable angina’, non Q wave MI)



Presentation varies from severe central chest pain to asymptomatic (latter more common in
the elderly and in diabetics)
Pain is NOT relieved by nitrates or rest (compare angina)
Associated symptoms - dyspnoea, sweating, nausea. May be present without pain.
Pathology
 Coagulation necrosis
 Inflammation
 Granulation tissue
 Scar tissue formation
 Remodelling
Infarct size depends upon
 Extent and duration of occlusion
 Site of occlusion within coronary tree
 Existence of collaterals
 Oxygen demand of myocardium.
Investigations:
ECG – ST segment elevation, T wave inversion, Q wave increased
 These changes may take up to 24 hours to become apparent
Cardiac Cellular Enzymes
 Creatine Kinase MB: levels rise rapidly to peak at 24hrs. Near normal in 3d
 Lactate dehydrogenase: peak in 3d, Near normal in 8d
Cardiac Troponins I and T: More sensitive and specific to acute MI than enzymes above – take
3-12 hours to become apparent but are detectable as rasied for weeks post attack.
Complications (mnemonic: Sudden Death For Mr DRAPAS)
 Sudden Death
 Cardiac Failure







Mitral regurgitation
Dresslers syndrome
Rupture of ventricular wall
Arrhythmia - tachycardia, fibrillation, locks
Pericarditis
Aneurysm
Cardiogenic Shock
General Management
 Oxygen
 Opiates (e.g. allopurinol) to control pain
Treatment of acute NSTEMI:
Mainly antithrombotic therapy to stabilise the underlying coronary thrombus and anti-ischaemic
therapy to improve balance between oxygen supply and demand
 Aspirin – inhibits platelet synthesis of thromboxane A2 – platelet activator.
 IV heparin – increases the efficiency of the bodies own anti-thrombotic mechanisms. Binds
to ATIII and increases its potency for thrombin (factor IIa) inactivation (factor Xa inactivation
in low MW heparin).
 Clopidogrel – aspirin only blocks one platelet activating pathway – concomitant treatment
with clopidogrel is more effective – this drug inhibits ADP mediated platelet activation.
 GP IIB/IIIA inhibitor (for high risk patients) – block the final common pathway of platelet
activation. e.g. abciximab (a monoclonal antibody)
 Nitroglycerin – an anti-ischaemic used in same way as for angina

– anti-ischaemic used in same way as for angina
Treatment of acute STEMI:
Focus is to quickly restore blood flow through occluded coronary arteries.
 Fibrinolytic (thrombolytic) therapy – these drugs function by stimulating the natural
fibrinolytic system of the body. They transform inactive plasminogen into the active protease
plasmin which degrades the alpha helix of fibrin. Newer dugs such a tPA, rPA and TNK-tPA
bind preferentially to fibrin in formed thrombi and generate plasmin locally to that site rather
than all around the system as older drugs (e.g. streptokinase) did.
 PCI (percutaneous coronary intervention) is an alternative to fibrinolytic therapy. This
requires more expertise and better facilities than fibrinolytic therapy but has a better outcome.
 Aspirin – inhibits platelet synthesis of thromboxane A2 – platelet activator.
 Clopidogrel – if aspirin is contraindicated. This drug inhibits ADP mediated platelet
activation.
 IV heparin – increases the efficiency of the bodies own anti-thrombotic mechanisms. Binds
to ATIII and increases its potency for thrombin (factor IIa) inactivation (factor Xa inactivation
in low MW heparin).

-blockers – anti ischaemic - primarily reduce oxygen demand but also protect against
arrhythmias and reinfarction.
Adjuncts for both NSTEMI and STEMI:
 ACE inhibitors:
HMG-CoA reductase inhibitors (‘statins’)
Pneumothorax / tension pneumothorax
Sudden onset dyspnoea and/or pleuritic chest pain
Non-tension pneumothorax
 ABC then IV access + chest X-ray
 Aspiration  consider repeat if
unsuccessful
 Chest drain
Tension pneumothorax
 Airway
 Emergency aspiration via wide-bore
venflon / needle in 2nd intercostal space
mid-clav line.
 Oxygen and Chest drain
 Chest X-ray
Poisoning
Sign
Hypoventilation
Hyperventilation
Bradycardia
Tacharrythmia
Pinpoint pupils
Dilated pupils
Hypertension
Hyperthermia
Pyramidal signs,
ataxia, hypotonia,
hyperreflexia,
extensor plantars
Consider
Opiates, ethanol, benzodiazapines
Metabolic acidosis (aspirin, paracetamol), gastric aspiration, CO 2
Opiates,  blockers, digoxin
Tricyclics, anti-cholinergics, caffeine, theophilline, lithium, digoxin
Opiates, organophosphates
Methanol, anticholinergics, tricyclics, LSD
Ecstacy, amphetamines, cocaine
Ecstacy, amphetamines, anti-cholinergics
Drug
Opiates
Paracetamol / aspirin
Tricyclics
Ecstacy
Signs
Bradycardia, hypoventilation, pinpoint pupils
Hyperventilatation
Tachyarrythmia, dilated pupils, tone + reflex changes, pyramidal signs
Hypertension, hyperthermia
Tricyclics or anti-cholinergics
Participate in the management of the commoner poisonings
Always record:
 GCS
 Respiratory rate
 Heart rate
 Pupil dilatation (even if normal)
 Blood pressure
 Temperature
 Tone & reflexes
Investigations
 BM
 ABG
 U+E, LFT + INR
 Urine screen
 ECG (characteristic in some poisonings)
 Salicylate
 Paracetamol level 4 hrs post ingestion, and
again 4 hrs later.
Salicylate and paracetamol levels are always ordered at some trusts in any OD
Always contact the local poisons unit (telephone number in BNF) and check TOXBASE.
Priorities are
 Resuscitation – ABC + IV access
 Intubate if GCS <8 and non-responsive to naloxone (opiates) or flumazenil (benzodiazepines)
 Fluids if hypotensive






Control of hyperthermia (e.g. remove clothing, cold sponging ± electric fan, 4ºC IV fluids)
Prevention of further absorption of the poison
Note: There are no proven benefits to any of these techniques and risks associated include
aspiration and subsequent lung complications that may be more dangerous than the effects
of the poison. These techniques should be discussed with seniors before use.
Gastric lavage: If it has been <1 hour since the poisoning then gastric lavage may be useful –
contraindicated for corrosive substances or hydrocarbons. Reduces absorption.
Activated charcoal: Only really effective if given within 1 hour. Reduces absorption of toxins
that have carbon side chains e.g. . Of no use others e.g. iron. For some poisons, activated
charcoal may be given 2 hourly – reduces enterohepatic cycling. May be easier to give via
NG tube as it has a foul taste.
Total Bowel Irrigation (TBI): this aims to fill the whole bowel with water to dilute the poison
and help it be excreted quickly.
 Specific management (see below)
For control of fits, benzodiazepines may be given – consider PR if IV access is difficult
Always contact the local poisons unit – telephone number in BNF.
Toxin
Opiate
Aspirin
Immediate action
Check and monitor breathing
Paracetamol
Gastric lavage if within 4 hours
Paracetamol levels at 4 hours*
Antidepressants
Activated charcoal
Benzodiazepines
Protect airway
Digoxin
Lithium
Check K+ and ECG
Gastric lavage
CO2
ABG, ECG, 100% O2
Antidote
Naloxone (short half-life)
Alkaline diuresis, haemodialysis
N-acetylcysteine (NAC)*
Diazepam for convulsions
Cardiac monitoring
Flumazenil if severe
Atropine (3 mg), glucagons 7 mg IM,
consider pacing.
Digibind ® binding antibody
Diuresis, dialysis
Diazepam for fits, consider hyperbaric
oxygen if available.
*NAC has an unpleasant side effect profile and is not automatically indicated in all overdose.
Take paracetamol levels 4 hours post ingestion (or later if presentation is after 4 hours) and
measure serum level against time post OD on the graph in the BNF – this will tell you whether to
give or withhold NAC. Junior doctors should always seek a senior opinion.
The BNF table has 2 levels – the upper line is for the majority of patients – the lower level is for
those who already are receiving enzyme inducing drugs, malnourished (e.g. alcoholics) or for
some other patient groups (see BNF for details).
History taking:
If the patient is responsive and coherent then a history can be taken after ABC assessment. If this
is not the case then try to get a history from family, friends, ambulance crew or anyone else who
may be able to provide details. Empty tablet bottles may give a clue to what has been taken.
 What did they take: all drugs including alcohol; how much?
 When did they take them?
 Why did they take them: assess suicidal ideation.
If you need to take a poisoning history in an OSCPE station or long case then you can prevent
forgetting anything by making a table in the notes, e.g.:
Drug
No. Pills
Dose
Tot. dose
Time
Paracetamol
12
500 mg
6g
08.30
Paracetamol
10
500 mg
5g
10.00
Ferrous sulphate
20
Unknown
08.30
Get help from:
 TOXBASE: www.spib.axl.co.uk
 BNF: Section on poisoning emergencies at the front
 National poisons centre: Telephone number in BNF
 Seniors!
Make an assessment of the underlying social and psychiatric factors in deliberate selfharm and the likelihood of a repetition
In some trusts (including Walsgrave) a formal psychiatric assessment is required of any patient
who has deliberately taken an overdose – remember to check local trust policies. Such
assessment may be requested when the patient is stabilized.




Risk factors for self-harm
Demographic / epidemiology
 Previous Hx self-harm
 Younger
 Female > Male
 Low SES
 Divorced and younger single
 Teenage wives
Illness related
Psychiatric illness less common, less severe
Personality disorder (especially
borderline)
Alcohol dependence
Poor physical health
Other
 Early parental loss
 Parental neglect or abuse
 Long term social problems: family,
employment, financial
Risk factors for suicide
Demographic / epidemiology
 Previous Hx Suicide or self-harm
 Older*
 Male > Female
 Single, separated, widowed
 Unemployed
Illness related
 Psychiatric illness common, severe
 Depressive illness
 Alcohol abuse
 Drug abuse
 Schizophrenia
 Personality disorder
 Chronic pain or epilepsy
Other
 Threats of suicide
 Proposed plan
 Preparatory acts (e.g. saving pills) or
‘putting affairs in order’
* It is important that attempted suicide should always be taken seriously in the elderly[1]. Attempts in the elderly are a much
stronger predictor of subsequent completed suicide compared with attempts in younger people, with a ratio of attempts to
completion estimated to be around 4:1 compared with between 8 and 200:1 for young people who attempt suicide[1].
Suicidal behaviour in the elderly is undertaken with greater intent (less often expressed) and with greater lethality than in
younger age groups. Significant factors include: bereavement, social isolation and loneliness with depressive illness as
the most important predictor[1]. [1] H Cattell. Suicide in the elderly. Advan. in Psychiatr. Treat. 2000; 6: 102-8.
Pneumonia / pulmonary embolism
Pneumonia
Pulmonary Embolism
Pneumonia
Pulmonary Embolism
Gradual (over days)
Sudden
Dyspnoea
Potentially present
Potentially present
Cough
Heamoptysis
Potentially present
Potentially present
Potentially present
Pleuritic chest pain
Potentially present
Potentially present
Usually absent
Potentially present
Usually absent
Potentially present
Potentially present
Potentially present
Potentially present
Usually 
Usually 
Potentially present
Potentially present
Potentially present
Usually absent
Potentially present
 (unreliable)
Stony dull
Potentially present
Usually absent
Potentially present
Potentially present
Potentially present
Potentially present
Usually absent
Usually absent
Potentially present
Potentially present
Potentially present
Potentially present
Smokers, COPD,
Heart failure / Cystic fibrosis
CXR, ABG, Blood/sputum cult.
Surgery, Immobility
Hypercoagulability
CXR, ABG, D-dimers
Onset
Dizziness
Syncope
Fever
Confusion
Tachypnoea
Tactile vocal fremitus
Percussion note
Bronchial breathing
Crackles
Whispering pectoriloquy
Pleural friction rub
Tachycardia
Hypotension
Raised JVP
Risk factors
Investigations



Usually absent
The more useful distinguishing characteristics are in bold.
Tachypnoea + cyanosis are signs of respiratory failure
Pyrexia, rigors or prostration are signs of systemic disease – always take blood culture.
PE is a consequence of DVT – risk factors for DVT include NO PILLS
The following are NOT risk factors for DVT
 Neoplasm
 Oral contraceptive pill
 Smoking
 Hypertension
 Pregnancy
 Intravenous drug use
 Hypercholesterol / lipidaemia
 Long distance road/air travel
 Lower limb fractures

Surgery (major)
Investigation of PE
 D-dimers (excludes if negative in a low risk
patient)
 FBC
 Clotting
Management of PE: SOD HIM
 Sit upright
 O2 at high concentration
 D-dimers







Contraindications to streptokinase:
 Recent haemorrhage, trauma, or surgery
(including dental extraction),
 coagulation defects, bleeding diatheses,
 aortic dissection, coma, history of
cerebrovascular disease
 recent symptoms of possible peptic
ulceration, heavy vaginal bleeding,
 previous allergic reactions to either
streptokinase or anistreplase (no longer
available).
Arterial blood gas
Chest X ray
ECG
V:Q scan / CT pulmonary angiogram
Heparin IV
IV streptokinase if no improvement after 60
mins and no contraindications)
Morphine
Alternatives:
 Reteplase
 Alteplase
The Wells Score:
This is a scoring system that attempts to grade patients into low, moderate and high risk of DVT.
1 point for each of the following points of history / examination
History
 Active cancer (treatment within 6 months)
 Bedridden (>3 days) or major surgery + GA within 12 wks
 Recent plaster (cast), paralysis or paresis
 Prior DVT
Examination:
 Pitting oedema (confined to symptomatic leg)
 Leg swelling affecting whole limb.
 Diameter of calf (10 cm below tibial tuberosity) 3+ cm greater on affected leg.
 Tenderness along the anatomy of the deep venous circulation
-2 points if any other diagnosis is equally likely
<1: Low risk
1-2: Moderate risk
3+: High risk
Respiratory failure
Presentation will be that of the cause for the failure together with symptoms and signs of either
hypoxia (type 1) or hypoxia and hypercapnia (type 2).

Hypoxia: PaO2 <8 kPa
If long standing:
Dyspnoea

Hypercapnia: PaCO2 >6 kPa
Headache
 Tremor / flap






Restlessness
Agitation
Confusion
Central cyanosis


Polycythaemia
Pulmonary
hypertension
Cor pulmonale


Peripheral
vasodilatation
Tachycardia
Bounding pulse




Papilloedema
Confusion
Drowsiness
Coma
Causes
Type 1 resp failure
PaO2 <8 kPa; PaCO2 normal/
Type 2 respiratory failure: PaO2 <8 kPa; PaCO2 >6 kPa
Pulmonary disease:
Neuromuscular:
Asthma
Cervical cord lesion
COPD
Poliomyelitis
Pneumonia
Gullaine Barré
Pulm fibrosis
Myasthenia gravis
Obstructive sleep apnoea
Muscular dystrophies
Reduced Respir. drive
Diaphragmatic paralysis
Thoracic wall disease
Right  left shunt
Sedative drugs
Cyanotic congenital heart
CNS tumour
Flail chest
disease
Trauma
Kyphoscoliosis
Mnemonic for type 1 causes: A PEPPER – Asthma; PE; pneumonia, pulm oedema; emphysema;
RightLeft shunt.
Pneumonia
Pulm oedema
PE
Asthma
Emphysema
Fibrosing alveolitis
Management
Investigations to ascertain cause:
Bloods: FBC, U&E, CRP, ABG
Radiology: CXR
Microbiology: Blood / sputum culture (if febrile)
Spirometry
Treat underlying cause
Give oxygen appropriately
So what system should I use?
Well but slightly low SATs
Long term home oxygen
Asthma / LVF / pneumonia
COPD
Nasal cannulae (24-28% dependent on flow / resp rate)
Hudson mask if required FiO2 <50% (approx 50% with 15L / min flow)
Add a reservoir bag if required FiO2 >50-70% (at 15 L / min flow)
Venturi mask – 24, 28 or 35% as tolerated
Hypoxia kills faster than hypercapnia and CO2 retainers are rare (even in those with COPD) –
if in doubt start O2 at 35% and move from there.
If ABG shows >1.5 kPa increase in PaCO2, consider a respiratory stimulant (e.g. doxapram 1.5
– 4 mg / min IV) or assisted ventilation (e.g. NIPPV – non-invasive positive pressure ventilation).
An arterial blood gas sample is taken usually from radial artery at wrist or brachial artery in cubital
fossa. Sample is kept in ice and must be processed within 30 minutes. Reference ranges are:
pH:
pCO2:
pO2:
[HCO3-]:
7.35 – 7.45
4.7 – 6.0 kPa
>10.6 kPa
22-25 mmol/L (standardised bicarbonate)
Base excess:
+/- 2 mmol/L
If the problem is respiratory then pH and pCO2 change in the opposite directions (mnemonic
ROD)
 Respiratory acidosis:  pH,  pCO2
 Respiratory alkalosis:  pH,  pCO2
If the problem is metabolic then pH and pCO2 change in the same direction.
 Metabolic acidosis:  pH,  pCO2
 Metabolic alkalosis:  pH,  pCO2
It is also important to look at the FiO2 value – this is a value input by the user of the blood gas
machine. It is the concentration of O2 the patient was receiving at the time the sample was taken
(e.g. .21 in normal air)
Background box: useful facts about ABGs
 The blood gas syringe and needle – what is special about them: The syringe and needle
come in a package together – the syringe contains vacuum and heparin – it will draw blood
into itself with the heparin preventing clotting.
 Allens test can be performed before taking an ABG from the radial artery – it ensures patenct
of the collateral supply from the ulnar atery: Press hard upon the patients radial and ulnar
arteries and get the patient to make a fist, hold for a few seconds then relax – the palm will go
white. If the grip on the ulnar artery is released and the palm goes red again then the
collateral supply is OK and you may proceed to take blood from the radial artery.
The pulse oximeter allows non-invasive measurement of peripheral O2 saturation (‘sats’) by way
of a probe attached to fingertip or earlobe. Results <90% require attention; <80% is clearly
abnormal and action is required unless this is normal for the patient (e.g. COPD).
Results from a pulse oximeter must be treated with caution – the following can result in erroneous
readings:
 Cold peripheries (poor perfusion)
 Skin pigmentation
Take an ABG when indicated
 Excess light
 CO poisoning (cherry red coulour)
 Methaemaglobnaemia
 Nail varnish
Assess the cause and severity of respiratory failure and initiate management
The purpose of the lungs is gaseous exchange – this process requires the following:
 Pumping of blood to the lungs by the heart
 Inspiration and expiration – powered by muscle and controlled by the respiratory centre of the
medulla. Impulses conveyed down the spinal cord and through peripheral nerves.
 A suitable environment for exchange at the alveoli (V:Q matching, no barriers to diffusion)
Shock
Immediately: ABC then BP, Temp, ABG, 2x IV Access, ECG
Causes
Signs
Mnemonic: O CRAPP
Oliguria
Capillary refill prolonged
Reduced BP (<90 systolic)
Air hunger
Pulse 
Pallor
Management
Mnemonic: RICH
Raise foot of bed
ID cause if possible
Crystalloids stat to BP (but see
cardiogenic shock)
Get Help early
Anaphylactic Shock
Anaphylactic: Type 1 IgE mediated release of histamine and other products resulting in capillary leakage.
Anaphylactoid: Direct release of mediators from inflammatory cells resulting in capillary leakage.
PC: Wheeze, cyanosis, oedema (lids, tongue, larynx), pruritis, tachycardia, hypotension
Immediately: (ABC) including definitive airway if needed + 100% oxygen
Management: ABC CRASH FLUIDS
Chlorpheniramine (Chlorphenamine 10 mg IV - antihistamine) given after hydrocortisone
Raise feet to improve circulation
Adrenaline IM 0.5 mg (0.5 ml of 1:1000) – repeat every 5 min if required
Secure IV access
Hydrocortisone 200 mg IV
Fluids – challenge with 500 ml normal saline at 15 minute intervals until BP response. May need
up to 2L
Common precipitants
Iatrogenic
 Drugs e.g. penicillin
 Contrast media
 Latex
Food
 Peanuts
 Eggs
 Fish
 Strawberries
Other
 Stings
 Semen
Cardiogenic Shock
Immediately: ABC then BP, Temp, ABG, IV Access, ECG
This is the one type of shock in which fluids may be dangerous
Causes: MATTED
Myocardial infarction
Arrhythmia
Tamponade
Tension pneumothorax
Endocarditis (valve destr.)
Aortic dissection
Sickle cell crisis
Management
Mnemonic: ABC SOD IT
Senior help – urgently
Oxygen
Diamorphine
Investigations
Timing (arrythmias)
Investigations
U+E; CK; ABG
ECG
Chest X-ray
Echo
CT thorax (dissection)
V:Q scan (exclude PE)
Causes:
 Cold
 Dehydration
 Infection
 Ischaemia (e.g. exercise)
 Hypoxia (e.g.anaesthesia)
Investigations
 Check for
hepatospelenomegaly
 FBC (Hb )
 INR / clotting
 LFT (bilirubin )
 Electrophoresis
Management
Mnemonic:
ABC ALL STAFF CHOW
 Analgesia (opioid)
 Check Liver / spleen size
 Salbutamol if wheezy
 Consider Transfusion
 Antibiotics if fever and
inflam markers / WCC
 Fluids
 Crossmatch
 Haematology opinion
 Oxygen
 Warmth
Presentations
 Fits / CNS symptoms
 Painful swelling of hands /
feet
 Hepatosplenomegaly +
RUQ pain
 Lethargy + pallor
Sequelae
 Osteomyelitis
 Leg ulcers
 Renal failure
Chronic management:
 Immunisation: Pneumococcal + NHS (neisseria, heamophilae influenzae, strep)
 Prophylactic antibiotics
 Hydroxyuria if frequent crises
There is an argument for performing a sickling test on all patients of African descent pre-op.
Status asthmaticus
PC: Acute onset shortness of wheezy breathlessness
Immediately: (ABC) then PEFR, O2 Sats, Temp, ABG, IV access
Differentials:
Acute exacerbation of COPD
Pulmonary oedema / embolism
URT obstruction
Anaphylaxis
Investigations
FBC
U+E
Chest X-ray
D-Dimers
V:Q scan;
Pulmonary angiogram
Severe asthma is a PURE BEAST
Signs of severe asthma (PURE)
 Pulse rate > 110 / min
 Unable to complete sentences
 Respiratory rate > 25 / min
 Expiratory peak flow <1/2 predicted / normal
Signs of life-threatening asthma (BEAST)
 Bradycardia; BP 
 Exhaustion; confusion, coma
 ABG: PaO2 <8; PaCO2 normal or elevated
 Silent chest
 Third of normal PEFR or less
Management: SO SHIT
 Sit the patient up
 Oxygen (100%)
 Salbutamol (Nebulised through oxygen) 5 mg – back to back if needed.
 Hydrocortisone IM
 Ipratropium bromide (Nebulised through oxygen) 0.5 mg
 Theophiline (aminophyline – with senior advice)
Status epilepticus
Tonic-clonic status epilepticus is a condition in which prolonged or recurrent tonic-clonic
seizures occur over 30 minutes without the patient regaining consciousness. This is a
medical emergency because of the 20% mortality and the high rates of neurological and systemic
morbidity.
The condition does not imply that the patient is epileptic – there are other causes. A common
cause is the withdrawal of drugs, for example, anticonvulsants and alcohol. Others include:
 Hypoglycaemia
 Encephalitis
 Electrolyte imbalance
 Hypocalcaemia
 Acute meningitis
 Cerebral tumour
 Hypomagnesaemia
 Fever (esp children)
 Eclampsia
Mnemonic: GATE to FAME
 Glucose
 Alcohol / drugs
 Tumour
 Eclampsia
 Fever
 Anticonvulsant
 Meningitis
 Electrolytes / Calcium
Immediately
 ABC
 BM Glucose
 O2 Sats,
 Temp
 IV access
Basic management
Mnemonic: OI FLID RAP
 Oxygen, Investigations
 Fluids
 Lorazepam IV
 Or Diazepam rectally
 Again – repeat after 10
mins if no change
 Phenytoin
ENSURE anaesthetist is aware of situation if a second dose of benzodiazepine is needed.
Investigations: ABG. U+E, Ca2+, ESR / CRP, anticonvulsant levels, CT/MRI ASAP
Adult
Initial management (0-10 minutes):

ABC - maintain airway, ensure breathing,
cardiovascular resuscitation if necessary

Always give oxygen to prevent hypoxia
Second line management (0-60 min):

Emergency investigations aimed at determining
the cause of the epilepsy:

Electrolytes, glucose

Renal and liver function tests

Calcium and magnesium

Anticonvulsant levels

Keep 50 ml of blood for future anaylsis

Regular cardiovascular monitoring:

Pulse, blood pressure, ECG

Regular biochemical monitoring:

Urea and electrolytes

Blood count and clotting

Blood gases and pH

Hydration should be maintained with an intravenous
infusion

If hypoglycaemia is demonstrated or suspected give
Child
Initial management:
After ensuring a patent airway with 100% oxygen and
having checked for hypoglycaemia, the first drug to
consider depends upon whether vascular access has been
obtained.
The preferred treatment is:
lorazepam 0.1 mg/kg intravenous or intraosseous
wait up to 10 minutes; if still fitting repeat the dose once
only
If no vascular access:
diazepam 0.5 mg/kg rectally
wait up to 10 minutes; if still fitting AND vascular access
now obtained, give lorazepam 0.1 mg/kg (but once only if
used after giving rectal diazepam)
N.B. if lorazepam cannot be found remember to check the
fridge as it should be kept there.
second line management:
If still fitting after first line drugs, then:

if less than 6 months; paraldehyde 0.3 ml/kg rectally

if greater than 6 months; paraldehyde 0.4 ml/kg
rectally
Paraldehyde should not be used in liver disease. It takes
50 ml of 50% glucose with 250 mg of thiamine
intravenously (thiamine to avoid Wernicke’s syndr.)

Give emergency anticonvulsant medication




Third line management (0-90 minutes):
Determine the cause of the epilepsy:
Consider MRI/CT scan
Lumbar puncture may be required but care must be
taken that intracranial pressure is not raised and
facilities for resuscitation should be available
If stopping anticonvulsant treatment has precipitated
status then the drug should be restarted
Treat the complications of status, often hypotension
necessitates the use of intravenous dopamine
infusions
Continue anticonvulsant medication








Fourth line management (30-90 mins):
If seizures continue despite the above measures then
the patient should be transferred to intensive care
where they should be ventilated and anaesthetised
Aim for burst suppression on continuous EEG
monitoring
Continuous intracranial pressure monitoring may be
required
Long-term anticonvulsant medication is given in
addition to the general anaesthetic agents
10-15 minutes to act and the effects last 2-4 hours.
Intramuscular paraldehyde causes severe pain and may
cause abscess formation. It is not recommended.
Third line drugs are:

phenytoin 18 mg/kg intravenous or intraosseous over
20 minutes

Rate of infusion not to exceed 1 mg/kg/min

Concentration of infusion not to exceed 10 mg/ml

Mix with 0.9% sodium chloride

Ensure cardiac monitoring as risk of arrhythmias and
hypotension

If already on phenytoin:

phenobarbitone 15-20 mg/kg intravenous or
intraosseous over 10 minutes

If child remains fitting despite all earlier measures:
rapid sequence induction with thiopentone 4 mg/kg
intravenous or intraosseous
Testicular torsion
PC: swollen scrotum + intense pain
Differentials:
 Epididymo-orchitis
 Torsion of Hydatid of Morgagni
 Ideopathic scrotal oedema
Management:
 Urology referrral
 Sugical exploration and management.
Testicular torsion can result in loss of the testicle within four hours through ischaemia so
this diagnosis is an emergency – if in doubt refer to urology registrar - the scrotum must be
explored surgically if there is any uncertainty about the diagnosis.
Torsion occurs most often in adolescents. The typical presentation is with a tender, swollen
scrotum and lower abdominal pain; symptoms are however variable and often much less marked
in young children and neonates. The incidence of torsion is higher for undescended testes.
Epididymo-orchitis is inflammation of the testicle and occurs most often in 3rd – 4th decade.
 Acute orchitis (testis) is usually viral in origin (e.g. mumps, Coxsackie)
 Acute epydidymitis (epydidymis) is usually bacterial in origin. If following catheterization or
urinary tract surgery then suspect E.coli. Otherwise suspect Chlamidia trachomatis (or rarely
TB).


Chronic orchitis is most likely to be misdiagnosed cancer. Syphilis is a very rare possibility.
Chronic epydidymitis is likely to be due to TB but an inflammatory response to extravasated
sperm is possible post vasectomy (seminal granuloma).
Torsion
Typical age of onset younger.
The testis lies horizontally, high in the neck of
the scrotum. In the early stages, the cord may
be palpably thickened. Later, palpation is
difficult as the overlying scrotal skin becomes
red and oedematous.
Systemic features less likely
The cremasteric reflex is absent.
Pain is not relieved by elevating the twisted
testis - negative Prehn's sign.
Epididymo-orchitis
Typical age of onset older.
The epididymis is tender and swollen, and the
overlying scrotal skin, red and warm. Initially,
the epididymis is palpable separately from the
testis but becomes more difficult as the
infection becomes established and
inflammation spreads to the testis.
May be systemic features such as fever and
rigors in severe cases
The cremasteric reflex may be present.
Tenderness may be relieved by elevating the
scrotum - Prehn's sign.
The cremasteric reflex is dependent upon the nerve roots L1 and L2. This reflex is elicited by
stroking (with the nails) the superior and medial part of the thigh in a downward direction. The
normal response in males is a contraction (often small and hard to see) of the cremasteric muscle
that pulls up the scrotum and testis on the side stroked.
In children, the reflex may be overexaggerated.
Transfusion reaction
Acute Transfusion reaction (wrong ABO type): Mnemonic FFFFFlip…
 Fever
 Flushing
 Fast heart
 Falling BP
 Flipping painful (back, chest, loin, infusion site).
Management: mnemonic SHIT
 Stop the transfusion
 Check ID and name on unit
 Call haematologist
 Take unit, FBC, U+E, clotting and cultures to lab
Complications: DIC
 Extensive bruising, bleeding anywhere (esp old venepuncture sites)
 Give 2 units FFP and seek senior advice
O patient given A blood is worst – 10% mortality. Give supportive care and seek advice.
Multiply transfused patient given platelets
 Not very serious – febrile non-haemolytic transfusion reaction.
 Fever, rash, nausea.
General info for supplemental questions
What antigens are on the surface of the RBC?
Residual H antigen is always present – it is the root of the ABO antigen system – others as
below.
Type
RBC antigen
Antibody
O
H
anti A & B
A
H, A
anti B
B
H, B
anti A
AB
H, A, B
-
What does negative and positive refer to?
To the absence or presence of Rhesus D antigen. As well as Rhesus D there are Rhesus C and
E alleles. Rhesus D is the most antigenic of the three and is either absent or present – the other
two are always present in one of the two alleles (C or c and E or e).
What transfusions are safe?
Patient
Type O
Type A
Donor
O
O, A
Type B
O, B
Type AB
O, A, B
Rhesus Rhesus -
Rhesus +
Rh – or +
In theory, Rh+ blood could be given once to an Rh- person who had not been exposed to it before
– 70% would then seroconvert and could not be given it again. To prevent seroconversion, anti-D
could be given. This would be done to correct accidental Rh+ administration of one unit. In
amounts more than one unit it would result in coagulation.
When a sample is sent for crossmatch, what tests are carried out?
 The ABO group is ascertained
 The Rhesus D status is obtained – these two give a 98% chance of safe transfusion.
 Other Rh groups may be tested for non-Caucasians & in multiple transfusions.
 An antibody screen is performed (to detect antibodies such as anti-Kell)
 A cross match is performed - patient plasma is mixed with donor red cells to see if a reaction
(indicative of rarer antibody in patient plasma) occurs.
What does the result ‘antibody screen positive’ mean? What action is taken?
 The patients blood has antibody to non ABO/Rh antigen – crossmatch cannot proceed
(would take too long) blood cannot be given.
 Gain help from consultant for immediate patient management (e.g. control of bleed)
 Perform an antibody identification test – this is done against 12 types of characterised
erythrocytes – the pattern of wells reacting will yield a probable antigen – this takes several
hours at least.
 Test many (at least 12) ABO & Rh matching packs – if any are negative for the putative
antigen then crossmatch.
What information is required on the transfusion request form and sample?
 Name, DOB and Address to be taken from patient (not notes) to confirm correct person
 Hospital number from wristband
 Reason for transfusion – the MSBOS (maximum surgical blood ordering schedule) will tell
you how much blood can be requested routinely.
 Where and when the blood is required
 Other relevant clinical details e.g. prev pregnancy, prev transfusion.
 Legible Drs name, signature and Bleep.
 Bottle should have, patient full name, DOB, hosp no., date, Drs name & Bleep.
List blood products appropriate for:
None unless angina is present – give iron instead.
Severe Fe deficiency anaemia
Erythrocytes can be given in other anaemias.
Upper Gi haemorrhage, low BP
Saline to boost volume
Red cells for oxygen capacity
and tachycardia (shock)
Overcoagulated with warfarin
(INR 8.5) with bruising.
Overcoagulated with warfarin
(INR 8.5) with intracranial bleed..
DIC, low fibrinogen, low
platelets.
Haemophilia + haemarthrosis
None
Vitamin K – takes 10-12 hours
Prothrombinase complex (powder made up to 10-20 ml) to
help resolve bleed – contains factors II, VII, IX and X in
amounts to specifically match likely deficit. By contrast, FFP
is very high volume and low in factor VII.
Correct underlying cause
Cryoprecipitate*, platelets, FFP.
Recombinant factor VIII (haem A) or IX (haem B)
What tests are carried out on donated blood?
Hep B & C, HIV, syphilis, CMV. Also ABO and Rh grouping.
What products can be made from 500 ml donated blood?
Erythrocytes (optimum additive solution can be added to reduce viscosity) stored @ 4°C
Platelets – 5 bags are pooled together for 1 adult dose. Stored at room temperature.
Fresh frozen plasma stored at –40°C
Albumin – made by fractionation of pooled plasma.
*Cryoprecipitate contains factor VIII, fibrinogen and von Willebrands factor – made by slow
thawing of FFP.