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					A&E OBJECTIVES
SHOCK
(from Lecture notes on emergency medicine by Moulton & Yates)
Shock is a term used for inadequate perfusion of the vital tissues in the body. There are potential
areas in the body that can be affected which would result in shock. This includes the pump (heart),
delivery system (blood vessels) and the fluid itself (blood). There are three basic types of shock:
 Central– pump failure (cardiogenic)
 Hypovolaemic– decreased blood volume
 Distributive– leaky or dilated blood vessels.
As well as this there are other types of shock, which are mainly due to the effects on the
maldistribution of fluid. These include:
 Anaphylactic
 Neurogenic
 Septic

General features to look for in shock:
Cold and clammy limbs (cardiogenic or hypovalaemia)
Warm and well perfused limbs with a bounding pulse(septic)
Decrease in skin turgor
Postural hypotension
Anaphylactic features – history, urticaria, angio-oedema, wheeze
Tachycardia (not always, e.g. may be on a beta-blocker)
Hypotension (blood pressure may be normal)
Increased respiratory rate to compensate for acidosis.
Urine output (excellent if inpatient and monitoring)
Mental state will change if severely shocked

Hypovolaemic shock:
Shock due to the loss of blood or other body fluid. Signs to look for vary according to the volume of
blood lost. Some signs may appear normal even with significant volume losses due to the
compensatory mechanisms of the body (sympathetic nervous system increasing heart rate and
vascular tone and renin-angiotensin system). Changes in the signs are shown below:
Blood loss (%)      <15%                 15-30%                30-40%              40%
Blood pressure      Normal               Normal                Decreased           Decreased
Heart rate          Normal               Raised                Rapid               Very rapid
Respiratory rate    Normal               Raised                Rapid               Very rapid
Causes:
Bleeding  trauma, ruptured arotic aneurysm, ruptured ectopic pregnancy (always ask women
LMP), GI haemorrhage
Fluid loss  vomiting (GI obstruction), diarrhoea, burns, third-spacing (pancreatitis), heat
exhaustion

Management of shock: (from cheese and onion)
ABC including high flow oxygen
Raise foot of the bed
IV access - both arms, wide bore. Get help >2mins
Identify and treat underlying cause
Infuse crystalloid fast to raise BP (unless cardiogenic, see later)
Seek expert help early
Investigations – FBC, U+E, ABG, glucose, CRP, cross-match and check clotting, blood cultures,
urine culture, ECG, CXR, others (lactate, echo, abdo CT, USS)
Consider arterial line, central venosu line and bladder catheter (aim for flow greater than 30ml/h)
Further management:
Treat underlying cause
Fluid replacement as dictated by BP, CVP, urine output
Don’t overload with fluids if cardiogenic, consider inotropes

Peripheral IV access (wide bore) can achieve better flow rates than a central line
If cause unknown then treat as hypovolaemia.
If ruptured AAA aim for a sytolic BP of 90mmHg
If severe blood loss or more than 1L of fluid required to maintain BP consider a specific blood or
O-ve blood.
Correct electrolyte abnormalities. Acidosis usually responds to fluid replacement

Cardiogenic shock:
This is due to any affect on the heart that will result in hypotension and inability to circulate the
fluid around the body. The effect is a ‘forward failure’. Without external factors the cause is usually
down to the inadequacy of the cardiac muscle. It can occur as a sudden onset or a progressive onset
depending on the cause.
Causes  arrhythmias, cardiac tamponade, tension pneumothorax, MI, myocariditis, myocardial
depression (drugs, hypoxia, acidosis, sepsis), valve destruction (endocarditis), pulmonary embolus,
aortic dissection.
Management:
ABC + Oxygen
Diamorphine (2.5-5mg for pain and anxiety)
Investigations ECG, U+E, CK, ABG, CXR, echo, CT thorax (for aortic dissection if indicated),
V/Q scan for PE.
Monitor  BP, CVP, ABG, ECG, urine output. Do ECG every hour until diagnosis made. Consider
Swan-Ganz catheter to assess pulmonary wedge pressure and cardiac output. Catheterise for
accurate urine output.
Correct arrhythmias, U+E abnormality or acid-base inbalance
Optimize filling pressure – if available measure pulmonary capillary wedge pressure (PCWP):
If PCWP < 15mmHg fluid load – give a plasma expander 100ml every 15min IV aim for PCWP of
15-20mmHg
If PCWP > 15 mmHg fluid load – inotropic support e.g. dobutamine (2.5-10mcg/kg/min IVI) aim
for systolic BP> 80mmHg
Consider ‘renal dose’ dopamine – 2-5mcg/kg/min IVI via central line only.
Consider intra-aortic balloon pump if you expect underlying condition to improve or awaiting
surgery (this allows more blood to fill back into the heart)
Look for and treat any reversible cause such as MI, PE (thrombolysis) or surgery for acute VSD,
mitral or aortic incompetence.

PCWP – this gives us an indirect measure of the left atrial pressure. We can not access the left
atrium that easily so what we do is pass a Swan-Ganz catheeter into a preipheral vein, into the right
atrium, through the right ventricle into the pulmonary artery and then into one of its branches. There
is a balloon which is inflated at its tip and can help assess the PCWP as well as cardiac output
through thermodilution techniques.

Cardiac tamponade has slightly different but interesting signs. There is hypotension, raised JVP
unless hypovolaemic (due to squeezing of the heart), muffled heart sounds, pulsus paradoxicus (a
loss of blood pressure of 10-12mmHg duyring inspiration – lung squeezes heart), breathlessness. If
there is a tamponade look for a cause of pericardial effusion –MI, trauma, neoplasia or renal failure.
If there is a collapsed patient with a tamponade, attempt pericardiocentesis. It may buy time but is
not definitive.
Septic shock:
This is a common cause of collapse, especially in elderly and children. It can be overlooked
because:
 The temperature is not always raised
 The WCC may be normal or low
 Blood cultures can come back negative.
The main problem in septic shock is like any other type of shock, which is inadequate tissue
perfusion.
There are many terms used in relation to this type of condition and they are all explained below:
Systemic inflammatory response syndrome (SIRS)  the presence of two or more of the following
features:
- temperature either >38C or <36C
- tachycardia >90bpm
- respiratory rate > 20breaths/min or PaCO2 < 4.3 kPa
- WBC >12*109/L or <4*109/L or <10% immature forms.
SIRS occurs through the activation of cytokines, free radical production and release of vasoactive
mediators. There does not have to be an infection present.
Sepsis  SIRS occuring in the presence of infection
Severe sepsis  sepsis with evidence of organ hypoperfusion. E.g. oligouria, hypoxaemia, altered
cerebral function, lactic acidosis etc.
Septic shock  severe sepsis with hypotension – systolic BP<90mmHg
Septicaemia  presence of multiplying bacteria in the blood. It is an old term.

Investigations  same but also cultures (urine and blood), FBC and temperature.
Management:
Same as for hypovolaemic shock but also specific treatment for the infection.
Start broad spectrum IV antibiotics that are most likely for the source of the infection.
Treat empirically if source of infection is unknown. E.g. cefuroxime and gentamicin (less if in renal
failure).
Check locations for sepsis – urinary tract, chest, intra-abdominal, neutropenic, skin or bone soruce
or unknown.
If unknown and if necessary give broad spectrum antipseudomonal beta-lactam antibacterial such as
piperacillin enhanced with tazobactam.

Anaphylactic shock:
Tissue hypoperfusion that occurs as a result of tpye I IgE-mediated hypersensitivity reaction. This
leads to a release of histamine and other cytokines which causes capillary leak, wheeze, cyanosis,
oedema (larynx, lids, tongue, lips) and urticaria. There are triggers which will usually cause this
such as:
Drugs  penicillin and contrast media
Latex
Stings, eggs, fish, peanuts, strawberries, semen
Clinical features:
Itching, erythema, urticaria, oedema
Wheeze, laryngeal obstruction, cyanosis
Tachycardia, hypotension
Management:
Secure the airway – 100% oxygen, intubate if obstruction imminent
Remove cause, raise feet
Give adrenaline IM (0.5mg)
Repeat every 5min if needed as guided by pulse, BP and respiratory function
Secure IV access
Chlorpheniramine 10mg IV and hydrocortisone 200mg IV
IVI 0.9% saline. Titrate against BP
If wheeze, treat for asthma
If still hypotensive admit to ITU, IVI adrenaline, aminophylline and nebulized salbutamol.
IV dose of adrenaline is different to IM.

Further management:
Admit to ward and monitor ECG
Continue chlorpheniramine 4mg/6h PO if itching
Medic-alert bracelet for naming culprit allergen
Teach about self-injected adrenaline if there is an attack.
Skin-prick tests to identify which allergens to avoid.
ACUTE CONFUSION
(from cheese and onion)
This is also covered in neurology and psychiatry objectives.
It is otherwise known as delirium.
Causes:
Infection – pneumonia, UTI, wound, IV lines
Drugs – opiates anticonvulsants, L-dopa, sedatives, recreational, post-GA
Alcohol withdrawal – (2-5days post withdrawal), raised LFT’s, raised MCV and history of abuse.
Also drug withdrawal.
Metabolic – hypoglycaemia, uraemia, liver failure, U&E imbalance, anaemia
Hypoxia – respiratory or cardiac failure
Vascular – stroke, MI
Intracranial infection – meningitis, encephalitis
Raised ICP – space occupying lesions
Epilepsy – status and post-ictal states
Trauma – head injury, especially subdural haematoma
Nutritional – thiamine, nicotinic acid or B12 deficiency
Also urinary retention and constipation (faecal impaction)

Investigations:
Infection – MSU, CXR, blood and sputum culture, LP if indicated
U&E’s for hyponatraemia
Calcium
Blood sugar
Liver and cardiac enzymes
ECG – for silent MI’s
CT head
If indicated then also therapeutic drug levels (anti-convulsants and lithium), endocrines (TFT’s),
vitamin deficiency and illicit drug screen.

Management:
Identify and treat underlying cause.
Reduce distress and prevent accidents – move to quiet side room, minimum amount of staff, ensure
safety. Keep one staff (same person) in attendance to the patient, moderately lit room. Repeated
assurance and orientation to time and place can help. Minimal visitors (only those patient knows
well). Also important to treat constipation as this may make matters worse for confusion. Feed well
to avoid nutritional deficiency.
Minimize medication if possible.
Haloperidol 0.5-2.0mg IM/PO or chlorpromazine 50-100mg IM/PO (avoid in elderly due to cardiac
effects). Wait 20 mins to judge effect and then give more if necessary.
Benzodiazepines for night time sedation

Delirium tremens:
This is delirium as a result of alcohol withdrawal.
Do BP and TPR (temperature, pulse and respiration counts) every 4 hours. BP may go down.
Give chlordiazepoxide generously for first 3 days. 10-50mg/6h PO. Wean off over 7-14 days.
Diazepam or chlormethiazole (can cause addiction) are alternatives.
Give thiamine 200mg oral and multivitamins. Parenteral thiamine may be needed if there is
Wernicke’s encephalopathy.
HEAD INJURY
(from lecture notes on emergency medicine by Moulton & Yates)
Also, look at neurology objectives.

Statistics:
1.4 million people come to A&E each year with a head injury, half are children. (11% of new
patients).
5000 people die from traumatic head injury each year.
1500 survive with severe brain damage.
Many will require long term nursing care and have reduced employment potential.
Majority in adults are men with a mean age of 30.
Many tragedies are preventable.

Pathophysiology of traumatic brain injury: (from essential neurology by I.M.S Wilkinson)
There are two important phases in the damage to the brain.
There is a primary insult that comes about from the initial trauma itself. The damage from the
primary insult is not reversible. After this there is a potential secondary insult that can occur. This
damage can be preventable by doctors in the hospital.
The brain is a floating, soft organ in a fairly rigid box. When an injury occurs, the brain is forced
around within the box. This sudden acceleration and deceleration (or rotation) causes the brain to
move within the brain. The force of these movements will cause damage. If severe enough, then
there will be tearing of nerve fibres and haemorrhages within the white matter as well as contusion
and lacerations of the cortex. If the trauma is very severe then there will be much more severe
diffuse damage as well as brain swelling. This swelling will cause the brain to become to large for
its cavity and so if the pressure is large enough then the brain will start to herniate through the
tentorium. Sometimes, the initial brain injury is severe enough to cause death due to major
herniation and coning. This will result in brainstem failure and death.

Secondary brain injury is the one that is preventable in the hospital and doctors should take great
care from preventing this from happening. There are many ways the brain can have a secondary
insult but all of them lead to brain swelling. The brain swelling will lead to tentorial herniation and
coning. This would lead to brainstem failure and then ultimately death. The mechanisms of
secondary injury are:
 arterial hypotension – blood loss at time of injury from the head or anywhere else in the body.
this will lead to ischaemic cerebral oedema.
 arterial hypoxia – airway obstruction in chest injury or seizure. This will cause hypoxic cerebral
oedema.
 infection – open wound in the skull, or from the ear or nose. Infection causes inflammatory
oedema.
 intracranial haematoma – haematoma forms from a bleed in the brain or meninges. This causes
further compression on the brain by taking up volume in the cranial cavity.

The secondary brain injury can be observed by watching the GCS, if the patient has a seizure or
from impaired brainstem function.
Reperfusion of the damaged brain after hypoxia is also thought to complicate matters in recovery.

Different types of injury mechanisms:
A direct blow  focal scalp injury, depressed vault fracture, extradural haemorrhage, focal brain
injury, focal brain injury, contra-coup injury, brain laceration and intracerebral haemorrhage and
subdural haemorrhage.
Sudden acceleration and deceleration  this causes a shearing injury to the brain and diffuse axonal
injury (DAI). This may lead to LOC but there may not be any external evidence of injury. This is
more common in restrained passengers in RTA’s.
Cervical spine injury  if a mobile head hits a fixed object rather than a fixed head being with by a
mobile object.

Assessment:
Initially a history may not be relevant as you need to assess the injury.
ABC plus oxygen.
Cervical spine is protected.
CPR initiation and neck protection is more important than assessing the brain injury.
Obtain IV access.
Measure  pulse, BP and RR. Record on a neurological observation chart.
Attach to cardiac monitor and pulse oximeter (note the SaO2)
Assess neurological status with AVPU:
          A – alert
          V – responds to voice
          P – responds to pain
          U – unresponsive
Assess pupils for size, equality and reaction to light. Unilateral papillary dilatation can be due to
orbital injury or raised ICP causing oculomotor nerve compression.
Measure blood glucose using the BM stix.

After this treat reversible conditions then reassess:
Hypoglycaemia – take blood for glucose estimation before giving IV dextrose (0.2-0.5mg/kg).
avoid hyperglycaemia.
Seizures – give IV diazepam slowly (0.2mg/kg) (about 10mg in adults)
Narcosis – give IV naloxone (0.4mg)
Agression and restlessness – 100% oxygen. Check airway and sats. Catheterise the bladder. Give
sedation after senior advice. Take AMPLE history. (allergies, medication, past and present illness of
significance, last food and drink and events leading up to presentation). Try to establish mechanism
of injury and obtain X-rays of C-spine and measure blood gas.

Further assessment and management:
Carry out detailed secondary survey – look for injuries in the scalp, auditory canals and tympanic
membranes, pupils and limbs, face and neck. Do a full neurological assessment.
Seek surgical/neurosurgical advice
Catheterise the bladder.
Neurological assessment:
     Level of consciousness – by doing GCS. It is good to see early depression or progression in
        neurological status. When noting GCS, mention score in each part: eyes, motor, verbal.
     Focal neurological signs – e.g. variation in muscle tone, asymmetrical limb movements and
        reflexes and disconjugate eye movements.
     Pulse↓, BP↑, pupil size↑, papillary response↓  easily measured but late indicators of
        raised ICP.
These observations should be repeated at appropriate intervals and plotted on the neurological
observation chart.
After assessing the neurological status you should check for injuries elsewhere in the body as half
of patients have multiple injuries.

Full history:
History can be taken once the patient is stable or it can be taken from family/friends or ambulance
crew. In the history we are looking for:
Mechanism of injury  nature of forces, subsequent complications, any medical problems
preceding the injury (arrhythmia, epilepsy, diabetes)
Time of injury  can be useful.
LOC/amnesia  length of period is known.
Subsequent symptoms  headache, nausea and vomiting, limb weakness, paraesthesiae, diplolpia,
rhinorrhoea and otorrhoea. Need to ask patients as they may not always mention it.
PMH  MJ THREADS. Specifically cardiac arrhythmias, diabetes and epilepsy and also bleeding
tendency (e.g. bleeding disorders or anticoagulation). Previous head injury.
Drug history  recent alcohol, drug ingestion, anticoagulants (warfarin).
Social history  before discharge need to know if someone is at home to look after the person.
Tetanus status  for wounds.

Imaging:
CT is the investigation of choice for head injuries presenting to the A&E.
A head CT is indicated when:
      GCS <13 on initial assessment or if <15 at 2 hours after injury.
      Focal neurological deficit
      Suspected open or depressed skull fracture.
      Signs of basal skull fracture (haemotympanum, ‘panda eyes’, CSF leak and Battle’s sign.
      Post-traumatic seizure
      >1 episode of vomiting
      If on anticoagualation such as warfarin.
CT is also given if:
      The patient is >65 and has had LOC or amnesia since the injury.
      If the mechanism of injury was dangerous such as RTA or a fall>1m.
If still concerned then discuss with seniors.
Features that may be seen on head CT:
Skull fractures  obvious, fragments or depression of bones.
Intracranial haematoma  may cause midline shift. Several forms:
          Extradural haematoma  high-density (white) lens-shaped lesion.
          Subdural haematoma  high-density crescent shaped lesion.
          Both can co-exist.
Cerebral contusion  patches of low or mixed attenuation.
Cerebral swelling can take time to develop but the ventricles will appear smaller than normal.

X-rays are not really used as much but they are quick and cheap. They are useful for skull fractures
but not for intracranial pathology. Skull X-rays are only suggested if CT scanning resources are
unavailable.

Management of specific problems:
Airways and breathing  if respiration is inadequate then there will be hypoxia, acidosis and
hypercarbia. These all lead to cerebral vasodilatation and a rise in ICP. We need to make sure that
patients with head injury who need to be ventilated have PaO2 of more than 16kPa and a PaCO2 of
4.0kPa. This provides enough oxygen to the brain as well as controls the intracranial pressure. This
is because the patient has a relevant hyperventilation (blowing off CO2) which leads to a cerebral
vasoconstriction and a reduction in ICP. Excessive hyperventilation is bad as it can have a toxic
effect on the brain.
Intubation is required if  coma, decreasing conscious level, loss of airway reflexes, ventilatory
insufficiency, PaO2 <10kPa or air or <13kPa on oxygen, PaCO2 >6kPa, spontaneous
hyperventilation causing a PaCO2 <3.5 kPa, irregular respiration, multiple seizures, facial injuries
or bleeding in the airway and extreme agitation.

Circulation  usually changes in BP from 80-200mmHg have no effect on brain flow but in injury
the autoregulation is affected. Cushing’s response is a late sign (bradycardia and hypertension) and
indicates rising intracranial pressure.

Raised ICP  hyperglycaemia should be avoided as it leads to brain swelling. Frusemide can help
reduce brain swelling before clot excavation. Steroid use is controversial.

Seizures  ICP and metabolic demand rise during a seizure. IV diazepam can reduce fits but
beware of respiratory depression.

Alcohol intoxication  changes in conscious level should never be attributed to drugs and alcohol
as something else may be missed.

Urine output  catheterisation of bladder is mandatory as it reduces restlessness and gives a good
indication of tissue perfusion.

Neurosurgical referral:
GCS = or <13 after resuscitation
Deterioration of conscious level or of neurological signs
Seizures with skull fractures or without complete recovery
Skull fracture with any depression of conscious level or with severe headache, repeated vomiting or
acute focal neurological signs
Penetrating injury
Confusion ort other neurological disturbance persisting after 8 hours
Depressed skull fracture
Basal skull fracture
Positive findings on CT.

Resuscitation should be started before phoning the neurosurgeon.
POISONING/OVERDOSE:
(from lecture notes on emergency medicine by Moulton & Yates and oxford handbook of
emergency medicine)

This may be due to accidents, social drug abuse, deliberate self-harm or attempt to harm others.
Think of poisoning if there are bizarre clinical features or unusual combination of clinical features.

Initial assessment:
ABC and oxygen
If patient unwell or reduced level of consciousness then:
- protect airway
- administer high conc of oxygen
- obtain venous access
- control seizures with IV diazepam
- connect patient to ECG, BP, pulse oximeter, measure core temp.
- measure blood glucose
- seek senior/anaesthetic advice.

Further assessment:
- nature of substance taken?
- Type of preparation? Slow-release will have delayed poisoning
- Other substances also taken (like alcohol)
- Specifically ask about paracetamol and aspirin poisoning
- Route of poisoning
- Time taken
- Intended result of poisoning
- Previous episodes?
Look for:
- dyspnoea, bronchospasm and pulmonary oedema
- tachycardia and hypotension
- dysrhythmias and widening of the QRS complex
- depressed level of consciousness
- agitation, restlessness and hallucinations.
- Papillary changes
- Extensor plantar reflexes
- Lowered or raised core temperature.

Specific actions:
Measure U+E’s and glucose
Measure blood gas
Measure or screen for, plasma aspirin, paracetamol level 4 hours after estimated time of ingestion.
Obtain 12-lead ECG
Seek specific poisons advice
Consider the need for gastric decontamination
Consider the need for specific supportive measures
Consider requesting toxicology levels (e.g. lithium, theophylline, methanol, ethylene glycol,
digoxin, paraquat and carboxyhaemoglobin)
Consider the need for specific therapies.
If reduced level consciousness consider IV saline (10ml per kg) unless contraindicated and
catheterise to measure urine output.
Gastric decontamination:
Controversy over its effectiveness and use. Aim is to reduce absorption of the toxin. After 4 hours
emptying the stomach is of little value unless specific drugs such as salicylates or Tricyclics.
Different methods:
     Gastric lavage – reserve for patients with reduced level of consciousness or specific
       indications. GA may be required, especially in children.
       contraindicated if:
        patient unwilling (record in notes)
        there are not adequate facilities available to protect the airway or deal with any
       complications that might arise.
        the substance taken is relatively safe. E.g. benzodiazepines
        substance ingested is safer in the stomach then anywhere else.
       oily or petroleum based products are relatively harmless in the stomach may cause a life
       threatening pneumonitis in the lungs.
       corrosives and caustics may cause oesophageal perforation, especially with the help of a
       lavage tube.

      Emesis – removes at least as much material from the stomach as gastric lavage. Also has the
       same contraindications as lavage. Sometimes it is easier to vomit up tablets than sucking it
       out with the lavage tube. Ipecacuanha syrup (30ml in adults, half dose in children) is given
       to induce vomiting. This is followed by a reasonable volume of lfuid and can be repeated
       after 20 mins if necessary.
       emesis is preferred is there is a specific request, a low risk amount of the drug given,
       ingestion of a relatively low toxicity drug or no indication of treatment with activated
       charcoal.

      Milk – used if the effects of the ingested substances are irritants, low toxicity and dangerous
       to remove by lavage or emesis.

      Activated charcoal – heating of charcoal with chemical activators increases its surface area
       which enables it to absorb relatively small molecules. It is dangerous if aspirated so protect
       the airway.
       It does not absorb  iron, lithium and metallic compounds; cyanides; strong acids and
       alkali; alcohols and petroleum distillates.
       It is indicated for:
       - Tricyclic antidpressants
       - theophylline and related drugs
       - barbiturates
       - aspirin
       - quinine
       - digoxin and other cardiac glycosides
       - sotalol
       - phenytoin and carbamazepine
       - cyclosporine and dapsone
       - paraquat

       activated charcoal should be given in a dose ten times the ingested poison. Initial dose of 50-
       100g will usually ensure this is met. Paracetamol and aspirin are taken in gram quantities so
       a second dose may be needed after a few hours. Repeated dosing is 50g every 4 hours. A
       patient presenting more than 2-4 hours after ingestion is best treated with activated charcoal
       alone if they are fully conscious with a safe airway; are able and willing to drink (fruit juice
        is needed to disguise taste of charcoal) and the substance taken does not delay gastric
        emptying.

Treatment of specific substances:
Substance        Management
Paracetamol      Paracetamol of 150mg/kg or 12g or 24 tablets in an adult is significant ingestion of the drug.
                    Early features are nausea and vomiting and abdo discomfort which usually settles in 24 hours.
                    Late features – malaise, right subcostal pain and tenderness inidicates hepatocellular necrosis.
                    There may also be delayed renal tubular necrosis (loin pain, haematuria and proteinuria). These
                    features usually present 3-4 days after ingestion. Sometimes there may be even later features such
                    as hypoglycaemia, bleeding and encephalopathy and cerebral oedema.
                    Fatal dose of paracetamol can be as low as 10-15g or 20-30 tablets.
                    Patients presenting at 12 hours or longer after ingestion are at serious risk of liver damage.
                    Antidotes  N-acetylcysteine and methionine.
                    Treatment:
                    Depends on how long since ingestion. Always send blood samples with time of ingestion of drug.
                    Within 4 hours of ingestion  activated charcoal if >12g or 150mg/kg paracetamol in the last
                    hour. Take blood at 4 hours after ingestion and look at the paracetamol treatment graph to assess
                    risk of liver damage. If result above the line then give IV N-acetylcysteine or oral methionine.
                    At 4-8 hours after ingestion  measure paracetamol and use the graph to assess risk of liver
                    damage. Give N-acetylcysteine or methionine if above line. Treatment is most effective if started
                    before 8 hours.
                    At 8-15 hours  if more than 12g taken or 150mg/kg then start N-acetylcysteine or methionine
                    immediately. Measure plasma paracetamol and assess on the graph and start N-acetylcysteine or
                    methionine if above the line. If patient is below the line and asymptomatic then stop treatment.
                    continue treatment if above the line. At the end of N-acetylcysteine or methionine treatment check
                    the INR and plasma creatinine, if these are normal and patient fit then you can discharge.
                    At 15-24 hours  if more than 12g taken or 150mg/kg then start N-acetylcysteine or methionine
                    immediately. Measure plasma paracetamol and assess on the graph and start N-acetylcysteine or
                    methionine if above the line. Check INR and plasma creatinine and paracetamol. If at 24 hours
                    patient has normal INR, normal creatinine and plasma paracetamol <10mg/l then they can be
                    discharged.
                    After 24 hours  measure paracetamol. LFT, U+E, creatinine, INR and ABG. Start treatment with
                    IV acetycysteine if than 12g taken or 150mg/kg. seek expert advice from a poisons department or a
                    liver unit.

                    The paracetamol graph has two lines. A normal patient line and a high risk treatment line.
                    High risk treatment line should be used if the patient has chronic alcoholism, malnutrition,
                    anorexia, cachexia, HIV infection, cystic fibrosis or taking anticonvulsants, rifampicin or St.
                    John’s Wort.

                    N-acetylcysteine is given in three steps:
                    150mg/kg in 200ml of 5% glucose over 15 mins
                    50mg/kg in 500ml of 5% glucose over 4 hours
                    100mg/kg in 1000ml of 5% glucose over 16hours.
                    Adverse reactions are nausea, flushin, itching, urticaria, angioedema, bronchospasm and
                    hypotension. Reactions will stop when acetylcysteine is stopped and with IV chlorpheniramine.
Aspirin             Now it is relatively uncommon. Main features of toxicity are:
(salicylates)       - hyperventilation
                    - tinnitus and deafness
                    - vasodilation
                    - sweating
                    - hypoglycaemia (esp. in children)
                    if severe then there may be convulsions and coma as well as complex acid-base disturbances
                    (nearly in all patients).
                    Initially there is stimulation of the respiratory centre leading to hyperventilation and hence a
                    respiratory alkalosis. As more drug is absorbed this turns to a metabolic acidosis. In between these
                    two phases the blood gas appears normal.
                    Treatment:
                    Gastric lavage if the patient has ingested >4.5g (15 standard tablets) in the last hour. However,
                    gastric lavage is recommended up to 8 hours after ingested because the drug delays gastric
                    emptying. (remember it is never too late for a salicylate)
                  Activated charcoal is given if this dose is ingested as well as it reduces absorption and increases
                  elimination.
                  Measure plasma salicylate, U+E, glucose and blood gas. Usually done at 4 hours but may peak at 6
                  hours.
                  Mild poisoning  plasma level less than 450mg/L in adults (<350mg/L in children) usually only
                  need oral fluids.
                  Moderate poisoning  greater than the above levels require IV fluids to correct dehydration and
                  increase elimination of the drug. Sodium bicarbonate 1.26% alkalinises the urine and leads to a
                  massive diuresis clearing the drug.
                  Severe poisoning  CNS features or plasma level >700mg/L. expert advice. Haemodialysis
                  referral. Correct acidosis and repeated activated charcoal via NG tube. IV glucose will be needed.
                  Forced alkaline diuresis does not work in severe cases and can lead to pulmonary oedema.
                  Haemodialysis is best method.
Ibuprofen and     Toxicity causes nausea, vomiting and tinnitus. Mefanamic acid is most dangerous as it can cause
other NSAIDs      convulsion.
                  Emesis is recommended if more then 100mg/kg is taken in the last four hours.
                  Most patients need observation and monitoring or plasma electrolytes.
                  Gastric emptying is worthwhile if mefanamic acid overdose in the last 4 hours.
                  If in doubt give activated charcoal.
Beta blockers     Depends on specific type. Sotalol can cause bizarre dysrhythmias
                  Most beta blockers may cuase:
                  - Severe bronchospasm
                  - Bradycardia and hypotension
                  - Heart failure
                  - Coma and convulsions.
                  Treatment:
                  Apply supportive measures
                  Give nebulized salbutamol for wheezing
                  Administer IV atropine for bradycardia and hypotension
                  Give IV glucagon for hypotension refractory to atropine
                  Give IV isoprenaline or dobutamine for severe cardiac depression.
                  Establish transvenous pacing for intractable bradycardia.
Tricyclic         This will give an anticholinergic poisoning.
antidepressants   It is quite common and can be fatal.
                  Dothiepin is the most common drug involved. Newer variants of TCA are less toxic.
                  Ingested amounts are usually significant, as the patient will usually want to commit suicide.
                  Effects of TCA toxicity are usually due to anticholinergic effects:
                  - blurred vision and dry mouth
                  - dilated pupils
                  - urinary retention
                  - diverse GI symptoms
                  - tachycardia and dysrhythmias
                  - agitation and anxiety
                  - hyperactivity
                  - disorientation and confusion
                  - drowsiness and lethargy
                  - hallucinations
                  - nystagmus, dysarthria, ataxia and movement disorders
                  - hyperreflexia and extensor plantat response
                  - hyperthermia
                  most serious signs are unrelated to anticholinergic effect:
                  coma – GCS less than 8. occurs in 1/3 but unlikely to last more than 24 hours.
                  Convulsions – severe toxicity, hypoxia and metabolic acidosis. Occur in up to 20%.
                  Cardiorespiratory collapse – hypotension or cardiac dysrhythmias. This is the usual causeof death.
                  Tachycardia is worrying especially with ECG change. Prolongation of the QRS complex > 100ms
                  suggests cardiotoxicity. QRS greater than 160ms is associated with a very high risk of death.

                  Treatment:
                  Clear airway, intubate if necessary, maintain ventilation and give supportive care.
                  Observe continuously to watch for rapid deterioration
                  Monitor ECG and check ABG in unconscious or post-ictal patients
                  Give activated charcoal by mouth or NG tube if more than 4mg/kg taken within 1 hour and if
                  airway is safe.
                     Treat arrhythmias by correcting hypoxia and acidosis. 8.4% sodium bicarbonate may produce a
                     dramatic improvement to the ECG. Aim of therapy is to maintain a pH between 7.45-7.55.
                     Avoid anti-arrhythmic drugs. If sodium bicarbonate does not work then speak to a poisons
                     specialist.
                     Correct hypotension by giving IV fluids and elevate foot of trolley. Glucagon 1mg IV may help in
                     severe hypotension. Dopamine is sometimes indicate if unresponsive to glucagon.
                     Unconscious patients usually improve over approx 12 hours and regain consciousness within 36
                     hours. Delirium and hallucinations may persist for 2-3 days and require sedation with oral
                     diazepam.
Lithium              Symptoms are usually delayed for 12 hours after overdose. Initially there is lethargy and
                     restlessness and later the patient may have:
                     - diarrhoea and vomiting
                     - thirst and polyuria
                     - ataxia and dysarhtria
                     - muscle weakness, twitching and tremor
                     - convulsions and coma
                     - dehydrastion and hypotension
                     - renal failure and electrolyte imbalance.

                     Treatment:
                     Gastric lavage, only if within an hour. Activated charcoal does not absorb lithium.
                     Whole bowel irrigation may be done if slow release preparation.
                     Haemodialysis is the best way to clear lithium from the blood.
                     Forced diuresis should not be done.
                     Monitor renal function and electrolytes.
Other specific antidotes
Carbon monoxide               Oxygen
Cyanide                       Sodium nitrite, sodium thiosulphate, dicobalt edetate
Digoxin                       Digibind (digoxin antibodies)
Ethylene glycol               Ethanol, fomepizole
Iron salts                    Desferrioxamine
Methanol                      Ethanol, fomepizole
Opioids                       Naloxone
                              Look for depressed level of consciousness, respiratory depression and pip-point pupils.
Organophosphtes               Atropine, pralidoxime
Sulphonylureas                Glucose, ocreotide
Warfarin                      Vitamin K, clotting factors, FFP
Snake bites                   Specific antivenoms.
SWALLOWED FOREIGN BODIES
(from lecture notes on emergency medicine by Moulton & Yates and oxford handbook of
emergency medicine)

This usually occurs in patients who have psychiatric problems or in children. Rounded objects such
as coins are most frequently swallowed. Objects can be radio-opaque (e.g. coins, rings) or non
radio-opaque (e,g, pen lids, aluminium ring pulls). Usually if the object reaches the stomach then it
should hopefully traverse the GI tract. Exceptions to this are irregular shaped articles such as safety
pins which may impact on the pylorus or very long, straight objects which will not be able to pass
through the duodenal loop. Another exception to this rule is button batteries. These will stick to the
bowel wall and lead to the release of toxic contents.
Most objects that cause a problem will usually do so in the oesophagus.
Symptoms will be initially a cough and then no symptoms if it is easily passed. If it is stuck in the
oesophagus then there will be dysphagia and retrosternal discomfort.

Imaging – X-rays:
Most objects that are swallowed are radio-opaque and will show on X-ray. X-rays should be taken
of the chest, abdomen and neck (in that order) until it is located. Remember coins may appear side-
on as a slit.

Management:
If in the pharynx or oesophagus refer to an ENT surgeon immediately for removal at
oesophagoscopy. Usually, if the object reaches the stomach or bowel it will pass through. This may
take several weeks. Patients should come back if they develop abdominal pain.
Ingested sharp objects require observation and either removal or tracking with frequent radiographs.

Button batteries (four types: mercury, silver (usually non-toxic), alkaline manganese and lithium):
Obtain X-rays. Batteries can be tracked every 3-4 days. find out which type.
 Mercury is the most toxic causing fever, abdominal pain, vomiting and blood in the stools.
All emergency departments have information from the manufacturers association.
Oral antacids or milk may help reduce corrosion.
Emesis is contraindicated.
Endoscopic or magnetic removal is often possible.
If in the oesophagus must be removed immediately.
Mercury levels in the blood and urine should be measured if leakage suspected.

For inhaled foreign bodies (choking) see later

For small wound management look at lecture.
HAND INJURIES
(from lecture notes on emergency medicine by Moulton & Yates and oxford handbook of
emergency medicine)

Immediate assessment and management:
Check patients general condition
Make a quick local assessment
Stop major bleeding by direct pressure
Remove rings and bracelets  swelling that occurs with soft tissue injuries may cause venous
occlusion under constricting bands such as rings and bracelets. This will eventually lead to an
interruption in arterial supply. Use cutters if needed.
Detect and document sensory loss
Inject local anaesthetic if necessary  this will help reduce pain and anxiety and make wound
cleaning and examination more comfortable for the patient.
Take a history of the injury  extent of the injury, mechanism (crush, direction of wounding,
retained foreign bodies etc.)
Take a brief past and social history ask whether right or left handed, occupation, hobbies and
social situation. These all have treatment implications. Also ask about smoking as it can impair
wound healing.
Begin detailed
examination
Obtain X-rays.

Always record data
with aids of drawings
and refer to the digits
by name not number
(little, ring, middle,
index and thumb).
Signs of hand injury:
Median nerve            Decreased sensation in the palm over the radial 3.5 digits
                        Unable to abduct thumb against resistance
Ulnar nerve             Decreased sensation over palmar and dorsal 1.5 digits
                        Little finger flexed
                        Unable to cross index and middle fingers
                        Decreased abduction/adduction
Radial nerve            Decreased sensation over the dorsum of the first web space
                        No motor branches in the hand. Proximal injuries causes inability to extend
                        wrist.
Digital nerve           These are continuation of the nerves into the fingers. There is one on each
                        side of the finger (radial and ulnar).
                        Decreased sensation along radial or ulnar half of digit distally.
Superficial flexor      Hold other fingers straight (i.e. immobilise all deep flexors).
                        Unable to flex PIP joint
Deep flexor             Unable to flex DIP joint
Extensors               Complete division prevents extension at DIP joint (mallet deformity)
                          Central slip division causes Boutonniere deformity
Deformity                 Small deformities such as rotation of digit can have profound effects on
                          long term hand function. Check carefully to ensure no abnormal
                          overlapping.


(from The emergency department: A survival guide by Whittake, Brickwood and Curran)
Examination: what to look for:
Injury to  skin, nails, bones, joints, tendons, ligaments, nerves and vessels.
Deformity, dislocation and swelling
Bony tenderness and ROM of joints.
Test flexor profundus – flexion of DIP joints with other joints fixed (power grip)
Test flexor digitorum superficialis – flexion at MCP joint with all other fingers extended (fine
movements)
Test flexor pollicis longus – active flexion of IPJ of thumb
Nerves – test sensation.
Look for ligament laxity especially under ulnar collateral ligament of thumb.

Always compare both hands and examine wrist and forearm in hand injuries.

Investigations:
X-ray  lateral and AP for fingers. Oblique and AP for the hand. X-ray crush injuries as well.

Management:
Soft tissue injuries
Paronychia             Digital nerve block, incise and drain, dressing.
                       Paronychia is a bacterial or fungal infection at the base or side of the nailbed.
Subungal               Trephine the nail to release blood underneath the nail
haematomas
Laceration to          May require removal or suturing together.
nailbed
Finger tip injury      Exclude bony injury and discuss with senior
Crush injury           Check for bony injury, clean wound, avoid closure, elevate, pain relief and
                       review.
Tendon
Tendon injuries        Refer to orthopaedic/plastics
Tendon sheath          Severe pain on passive extension. Tenderness over the tendon.
infections             Refer to orthopaedics.
Mallet finger          Inability to fully actively extend DIP joint. If fracture >30% joint surface refer
                       to fracture clinic. If not zimmer or mallet splint followed by 6 week follow up.
Bony injury
Fifth metacarpal       Little finger. Typical punching injury.
head/neck              Neighbour strap, wool and crepe. Follow up. look for tooth wound.
Base of first          Thumb. Refer to orthopaedics.
metacarpal
Rotational             Refer to ortho
deformities

Dislocations  X-ray before and after reduction.
Always ask about tetanus status and consider need for antibiotics.
FOOT AND ANKLE INJURIES
(from lecture notes on emergency medicine by Moulton & Yates and oxford handbook of
emergency medicine and The emergency department: A survival guide by Whittake, Brickwood
and Curran)

ANKLE:
Injuries to the ankle are very common presentations in the emergency department.
Many injuries are simple sprains and we need to avoid unnecessary X-rays.

Assessment:
Mechanism of injury – inversion, eversion etc. most are inversion injuries causing damage around
the lateral malleolus. Eversion injuries are less common and cause damage around the medial
malleolus. Hyper-dorsiflexion and plantarflexion injuries are less common.
Ability to weight bear – initially and currently. Fracture is likely if initially after injury.
Was a crack or snap heard? Not always indicative of a fracture.
Ice, analgesia and elevation may affect the appearance of an injury.

Examination:
Tenderness  check over the proximal fibula, lateral malleolus and ligaments, medial malleolus
and ligaments, navicular, calcaneum, Achilles tendon and base of 5th MT.
Neurological assessment and pulse check if significant deformity or neurological symptoms – get
help.

Indications for X-ray: (Ottawa ankle rules)
Bone tenderness along the distal 6cm of the posterior edge of the tibia or tip of the medial
malleolus.
Bone tenderness along the distal 6cm of the posterior edge of the fibula or the tip of the lateral
malleolus
Bone tenderness at the base of the fifth metatarsal (for foot injuries)
Bone tenderness at the navicular bone (for foot injuries)
An inability to weight bear both initially and in A&E for four steps.
The Ottawa ankle rules have been found to have a very low false negative rate.
Ankle anatomy:
Medial ligaments:
The medial ligament is large, strong and triangular in shape. Its apex is attached above to the medial
malleolus and its broad base is attached below to a line that extends from the tuberosity of the navicular
bone in front to the medial tubercle of the talus behind.
The medial ligament is subdivided into four parts based on the inferior points of attachment:
Tibionavicular part – attaches in front of the navicular tubercle
Tibiocalcaneal part – central in position. Attaches to the sustenaculum tali of the calcaneus.
Posterior tibiotalar part – attaches to the medial side and medial tubercle of talus
Anterior tibiotalar part – deep to the tibionavicular and tibiocalcaneal. Attaches to medial surface of the talus.




Lateral Ligaments:
The lateral ligament of the ankle is composed of three separate ligaments:
Anterior talofibular ligament – short ligament, attaches to the anterior margin of the lateral malleolus and
adjacent region of the talus
Posterior talofibular ligament – runs horizontally backwards and medially from the mallolar fossa on the
medial side of the lateral malleolus to the posterior process of the talus.
Calcaneofibular ligament – attached above to the malleolar fossa on the posteromedial side of the lateral
malleolus and passes posteroinferiorly to attach below to a tubercle on the lateral surface of the calcaneus.
Specific injuries and management:
Ankle fractures:
Around the ankle, fractures commonly involve the medial malleoli, lateral malleoli and the
posterior part of the distal tibia (sometimes known as posterior malleolus). Joints and ligaments in
the region provide very little rotation or angulation of the ankle and as a result force to the ankle can
cause fractures with ligamentous injuries. Look for talar shift.
Small avulsion fractures – treat with rest, elevation, analgesia and early mobilisation (like sprains).
Large avulsion fracture – initial immobilization with POP cast with crutches and orthopaedic
follow-up.
Undisplaced, isolated, medial or lateral malleolar fractures – usually do well with conservative
measures. Immobilize in well padded POP cast. Advise elevation of limb and orthopaedic follow-
up.
Displace fractures of medial or lateral malleolus – require open reduction and internal fixation.
Analgesia, sedation and allow reduction of talar shift. Immobilize in POP cast and orthopaedic
follow-up.
Bimalleolar or trimalleolar fracutures – unstable. Attempt to reduce talar shift with appropriate
sedation. Place in POP cast, obtain fresh X-rays and then refer to orthopaedic team for surgery.

Ankle dislocation:
Orthopaedic emergency.
There is gross deformity of ankle, severe stretching of the skin and often deficits in peripheral
pulses or sensation. Ankle can dislocate in absence of fractures.
Treatment:
Prompt closed reduction (with analgesia) and immobilise in POP cast. This precedes X-ray.
Give Entonox, IV analgesia, or sedation as appropriate with full precautions.
Warn patient about discomfort when ankle is reduced.
With the knee flexed and supported, gently grasp heel with one hand and support calf with other.
Pull smoothly on heel. Success is indicated by return of normal ankle contours, relief of skin
tension and often dramatic relief of pain.
Once reduced re-check pulses and sensation, immobilize in POP slab and arrange X-ray.
Refer to orthopaedic team immediately.

Ankle sprains:
Sprains usually occur on inversion affecting mainly the anterior talofibular ligament but can affect
other ligaments.
Treatment  RICE (evidence for this is lacking).
Rest initially, elevate above hip level. And apply ice for first 2 days for period of 2 days.
Bandages are more traditional. Should not be worn in bed.
Full recovery occurs over a few weeks.
Analagesia should be taken if needed. NSAIDs.
Resume sports gradually, after two weeks.
Long term complications:
Instability – recurrent sprains, refer to physiotherapy.
Peroneal tendon subluxation – reflects torn peroneal retinaculum allowing peroneal tendons to slip
anteriorly. Presentation is with clicking and slipping feeling. Requires surgery.
Peroneal nerve injury – common. Decreased sensation over part of the dorsum of the foot and
decreased proprioception at the ankle joint.
FOOT:
Assessment:
Mechanism of injury – fall from height (consider calcaneus/talar injuries, also examine hip, back
and neck), associated with ankle injury (fifth metatarsal base and navicular fractures common),
repetitive strain (e.g. road running, consider stress fracture of metatarsal)
Ability to weight bear?
Crush? Approximate weight and time involved.

Examination:
Bony tenderness in ankle injuries – fifth metatarsal and navicular bones.
Calcaneal tenderness and bruising
Neurovascular status in crush injuries.

X-rays:
Calcaneal views should be asked for with suspected calcaneal injuries.
Stress fractures do not become evident until 2 weeks after injury.
Toes X-rayed if obvious deformity.

Talar injuries:
Falls onto feet or violent dorsiflexion of the ankle (e.g. against pedals in a car in crash).
Treat with analgesia, immobilisation in a backslab POP, and refer promptly for orthopaedic
treatment.

Upper/midfoot dislocations:
Violent twisting, invering or everting injuries of the foot. Adequate analgesia, orthopaedic referral
and reduction under GA.

Calcaneal fracture:
Fall from height directly on heel. Examine the calcaneum for swelling, bruising, and tenderness,
especially on the sides. On calcaneal X-ray look at Bohler’s angle (see oxford handbook of
emergency medicine p.486). treat by elevation, analgesia and in some cases open reduction and
internal fixation after CT scanning.

There are many other injuries in the foot. Including metatarsal fractures and navicular fractures
which require POP and crutches and sometimes internal fixation. You should be careful in crush
injuries for compartmental syndrome.
BURNS

Quick Assessment:
Mechanism of injury – what caused the burn (water, fire, hot fat, radiator, electricity or chemicals)
Associated injuries – e.g. smoke inhalation
First aid measures taken – cold water?
Tetanus status

Examination:
If affects face then get senior help.
Depth:
Superficial – simple erythema
Partial thickness – superficial skin loss with some fluid
exudates and pain
Full thickness – thick leathery areas with no sensation or
capillary refill.
Assess size to determine body surface area (BSA):
Palm of patient’s hand including fingers = just under 1% of
BSA.
Rule of nines:
Head and neck – 9%              Each arm – 9%
Each leg – 18%                  Front of trunk – 18%
Back of trunk – 18%             Perineum – 1%

Do not use in children as they have slightly different surface areas. Use a Lund and Browder chart
for accurate assessment:
Large Burns:
History:
Was there an explosion?
Was the fire in an enclosed space (carbon monoxide, smoke inhalation)?
What was the burning material? Burning plastics release cyanide
When was the patient removed from the fire?
How long was the patient exposed to fire and smoke?
Was there a history of LOC?
Did the patient fall or jump to escape? Assess other injuries.
Patient’s PMH and tetanus status.

Initial assessment:
ABC – important.
There may be airway burns – hoarseness, stridor, dysphagia, facial and mouth burns, singeing of
nasal hair, soot in nostrils or on palate.
Spinal injury – may occur in blasts or from jumping from buildings.
Breathing problems – contracting full thickness circumferential burns of the chest wall may restrict
chest movements.
Circulatory problems – hypovolaemic shock is a feature of severe burns.

Assess the extent of the burns using the Lund and Browder charts. Patient’s age important.

Assessing depth:
Superficial burns:
First degree – minor erythema (only involves epidermis)
Second degree – painful erythema with superficial blistering (involves superficial dermis and
sometimes deep dermis). Pain depends on amount of nerve damage.
Full thickness burns:
Third degree burns – may be white, brown or black and may look leathery. They do not blister and
have no sensation. There may damage to ligaments, tendons and muscles. If very deep then it may
burn bone. High risk of infection. Sometimes difficult to distinguish from second degree burns
initially but will not affect management.

Resuscitation of large burns:
Ensure adequate airway and give high flow oxygen.
Remove source of burn if there still. Cut out collar.
Look for evidence of inhalation injury (direct thermal injury, bronchospasm, delayed pulmonary
oedema and systemic poisoning) – give salbutamol if there is a wheeze. After initially resuscitated
measure ABG and carboxyhaemoglobin (COHb)level.
Obtain IV access with two large peripheral cannulae.
Send blood- X-matching, FBC, COHb, U+E, glucose and coagulation.
Provide analgesia – IV morphine
Provide an antiemetic – IV cyclizine 50mg.
Measure extent of burns.
Give IV fluids – isotonic crystalloid (0.9%saline) at 2-4ml of crystalloid per kg body weight per %
of BSA burned over the first 24 hours following injury. Five half this volume in first 8 hours. Check
local policy as there are variations to the formula used.
Check pulse, BP, RR and SaO2 every 15 mins.
Insert urinary catheter and test the urine. Myoglobinuria will increase risk of acute renal failure.
catheterisation will also indicate urine output and if fluid resuscitation is adequate.
Adjust the IV volume replacement with the urine output. We need to maintain urine output of
>50ml/hr or 1-2ml/kg/hr in children.
Some centres prefer a colloid (gelofusine).
Red cell transfusion may be required if >10% of body has full thickness burns in addition to above
measures.
Check COHb and ABG for breathing.
Escharotomy may be required for circumferential full thickness burns around the chest to help the
breathing. This procedure cuts into the dead skin to expose fatty tissue which prevents a
compartmental syndrome from occurring.
Obtain a CXR for inhalation.

Chemical burns should be irrigated with warmed water.
Cover the burn in cling film or dry sterile sheets.
Involve a burns specialist at an early stage.
Ensure tetanus prophylaxis.


Smaller burns:
Assessment is same as large burns.
Remove any burning agent. Cool affected area with copious amounts of cold water.
Admit patients who have large burns or if NAI is suspected.
Refer patients with the following – airway burns, significant full thickness burns, burns >10% and
burns in special areas (hands, feet, face and perineum).

Leave full thickness burns uncovered and refer to specialist.
Simple aspiration may be needed for partial thickness burns. Clean and cover with appropriate
dressing. (sterile non-adherent and encourages wound healing – ask senior nurses).
Hand burns – cover with soft paraffin inside a polythene bag or glove and seal at wrist. Change at
24 hours. Or instead use paraffin/tulle dressings. Elevate to minimize swelling.
Facial burns – leave uncovered. Consider applying soft paraffin
Eye burns – check visual acuity and refer to specialist.
Perineal and foot burns – refer to burns specialist unit as they require specialist nursing and wound
care.

NSAIDs is sufficient for analgesia in small burns unless contraindicated.
Ensure tetanus prophylaxis.

Children and NAI  suspect if:
Explanation does not fit the burn.
Late presentation
Other suspicious injuries
Stock and gloving scalds + sparing of the buttocks – i.e. forced immersion in water.
Circular full thickness burns (0.75cm diameter) – cigarette burns.

				
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