Acute Care Flashcards
What are the causes of airway obstruction
central nervous system depression
swelling - infection or anaphylaxis
foreign body
bronchospasm
What can cause central nervous system depression
head injury intracerebral bleed hypercapnia hypoglycaemia alcohol opioids general anaesthetic
What can cause respiratory arrest
decreased respiratory drive (due to CNS depression)
decreased resp effort
lung disorders
What is the treatment for ACS
IV morphine + antiemetic
15L oxygen via non-rebreathe mask if sats <94%
sublingual glyceryl nitrate (unless hypotensive)
Aspirin 300mg crushed/chewed
How is A assessed
speak to patient
listen to breathing sounds
look at breathing pattern
How is airway obstruction treated
15L oxygen via non-rebreathe mask
airway manoeuvres
suction
Guedel/nasopharyngeal
How is B assessed
resp rate o2 sats pattern of breathing chest deformity trachea chest expansion percussion breath sounds - ?rattle, wheeze, stridor auscultate
How is C assessed
hands - ?cool, warm, pale, pink, mottled CRT peripheral and central pulses HR BP - wide PP = arterial vasodilation, narrow PP = arterial vasoconstriction auscultate ECG
How is D assessed
AVPU
check drug chart for drugs that cause reduced consciousness
pupils
blood glucose
Which cardiac arrest rhythms are shockable?
VF
pulseless VT
Which cardiac arrest rhythms are non-shockable?
asystole
PEA
describe the treatment of shockable cardiac arrest
CPR
secure airway
break CPR every 2 mins to assess rhythm
give shock 150J first
repeat
after third shock give 300mg amiodarone IV and adrenaline 1mg IV
continue CPR and checks every 2mins
repeat 1mg adrenaline IV at alternate shocks
can give 150mg amiodarone IV after five shocks
describe the treatment of non-shockable cardiac arrest
CPR
adrenaline 1mg IV STAT
check rhythm every 2 mins
give 1mg adrenaline IV every other cycle
State the reversible causes of cardiac arrest
Hypoxia
Hyperkalaemia, hypokalaemia, hypoglycaemia
Hypovolaemia
Hypothermia
Thrombosis - MI/PE
Tension pneumothorax
Tamponade
Toxins
State the steps in management of bradycardia
if signs of adverse features, give atropine 500mcg IV
if unsuccessful, arrange senior help and transvenous pacing
if no adverse features, assess for risk of asystole
if risk of asystole, ger senior help and arrange transvenous pacing
What are the adverse features in tachy/bradycardia
shock
heart failure
syncope
MI
What are the steps in management of broad complex tachycardia
are there adverse features present?
no
- correct electrolyte abnormalities
- if most likely monomorphic VT give amiodarone 300mg IV over 20 mins
- if polymorphic VT give 2g magnesium sulfate IV over 10mins
yes - call for senior help, sedate and cardiovert. give 300mg amiodarone IV over 20 mins
900mg amiodarone IV via central line over 24h
What is the difference between monomorphic and polymorphic VT
mono - caused by structural abnormalities. not likely to convert into VF
poly - caused by electrolyte abnormalities, likely to convert into VF
What are the steps in management of narrow complex tachycardia
vagal maneouvres
IV adenosine 6mg, 12mg, 12mg
adverse features?
yes
- sedation and cardioversion
- amiodarone 300mg IV over 20 mins then 900mg amiodarone IV via central line over 24h
no - beta blocker eg. IV metoprolol, amiodarone 300mg IV over 1h or digoxin
How is GCS calculated?
Eye Opening Spontaneous 4 To sound 3 To pressure 2 None 1
Verbal Response Orientated 5 Confused 4 Words 3 Sounds 2 None 1
Motor Response Obeys commands 6 Localise to pain 5 Withdraws from pain 4 Flexor response 3 (decorticate) Extensor response 2 (decerebrate) None 1
What are the common causes of reduced GCS
metabolic: drugs sepsis hypoglycaemia/hyperglycaemia respiratory acidosis hypoxia hypothermia addisonian crisis hepatic or uraemic encephalopathy
neurological: trauma meningitis/encephalitis tumour stroke, SAH epilepsy
What are the key signs and symptoms of anaphylaxis
Onset within minutes Airway and breathing Dyspnoea, respiratory distress, wheeze, stridor Cyanosis Circulation Tachycardia, hypotension Skin Urticaria, angioedema
Describe the pathophysiology of anaphylaxis
Sensitisation phase:
Immune system encounters allergen and makes immunoglobulin E (IgE) against it
No clinical features occur
Effector phase:
Allergen cross-links IgE on surface of mast cells
widespread degranulation and release of histamine
mediates inflammatory bronchospasm, vasodilatation, increased capillary permeability, and tissue oedema
What dose of adrenaline do you give to an adult in anaphylaxis
0.5mg (0.5 ml of 1:1,000) IM
What dose of adrenaline do you give to a child 6-12 years in anaphylaxis
300 micrograms (0.3 ml of 1:1,000) IM
What dose of adrenaline do you give to a child aged 5 and under in anaphylaxis
150 micrograms (0.15 ml of 1:1,000) IM
What drugs apart from adrenaline do you give in anaphylaxis
chlorphenamine 10mg IV
hydrocortisone 200mg IV
can give salbutamol 5mg neb and ipatropium bromide 0.5mg neb if wheeze
What blood test can help in the retrospective diagnosis of anaphylaxis
Mast cell tryptase
Take three samples taken as soon as possible, after 1-2 hours and after 24 hours
Useful in making a retrospective diagnosis but the absence of a rise does not exclude anaphylaxis
What are the steps in management of anaphylaxis
SENIOR HELP secure airway 15L oxygen non rebreate mask adrenaline 0.5mg (0.5ml 1:1000) IM IV access - 2x wide bore cannulae 500ml 0.9% sodium chloride over 15mins 10mg chlorphenamine and 200mg hydrocortisone IV nebs if wheeze referral suing SBAR admit
What is the ongoing management for a patient after anaphylaxis
medicalert bracelet
epipen x2
How is adrenaline administered IM
into anterolateral aspect of middle third of thigh
“blue to sky, orange to thigh”
State the initial management of an NSTEMI
oxygen if sats low
morphine 5-10mg IV and metoclopramide 10mg IV
sublignual GTN
aspirin 300mg + second antiplatelet
Metoprolol or verapamil or diltiazem - rate control
ACEi
Fondaparinux - anticoagulation
calculate GRACE score ?PCI within 72 hours
What investigations should be done in suspected pulmonary oedema?
ECG
U+E, troponin, ABG
CXR
echo
What are the possible causes of pulmonary oedema
heart failure due to MI, valvular heart diseae, arrhythmias
ARDS
fluid overload
neurogenic
What are the signs of heart failure on CXR
alveolar oedema (bat's wings) kerley B lines Cardiomegaly upper lobe diversion pleural effusion
What is the immediate management of severe pulmonary oedema
A
B - 15L oxygen via non-rebreathe, listen to chest
C - ECG, IV access
IV diamorphine 1.35-5mg slowly
IV furosemide 40mg slowly
2 puffs GTN spray if BP >90 systolic
SENIOR HELP
?CPAP, nitrate infusion
What are some causes of cardiogenic shock
MI arrythmias myocarditis valve destruction cardiac tamponade aortic dissection PE tension pneumothorax
What is the immediate management of cardiogenic shock
15L oxygen via non-rebreathe
1.25-5mg diamorphine IV for pain and anxiety
SENIOR HELP
ECG
FBC, U+E. troponin, ABG
CXR, echo
What are the signs of a life-threatening asthma attack?
PEFR <33% best silent chest, cyanosis, feeble respiratory effort slow HR, low BP exhaustion, confusion, coma ABG - reduced pO2, pH <7.35
What are the signs of a near fatal asthma attack
rise in pCO2
What are the signs of a severe asthma attack
PEFR <50% best
HR >110
RR >25
unable to complete sentences
What are the steps in management of severe or life threatening asthma
salbutamol 5mg NEB over 15mins
ipatropium bromide 0.5mg NEB over 15 mins
hydrocortisone 100mg IV or prednisolone 40mg PO
if life threatening:
SENIOR HELP, ICU
monitor ECG
magnesium sulfate 2g IV over 20mins
What is the ongioing management of a severe asthma attack
admission
nebulised salbutamol every 4 hours
prednisolone 40-50mg PO OD for 5-7days
for discharge;
stable for 24 hours on discharge meds
inhalers x2 prescribed
peak flow >75% best/predicted
see GP within 1 week
resp clinic within 4 weeks
What is the immediate management for IECOPD
salbutamol 5mg NEB over 4h
ipatropium bromide 0.5mg NEB over 6h
CXR, ABG
controlled oxygen therapy
200mg hydrocortisone IV + 30mg prednisolone PO OD for 7 days
Abx if infection - doxycycline
if no respomse: NIPPV, intubation and ventilation,
What investigations should be done in IECOPD
ECG
FBC, CRP, U+E, ABG,
blood cultures, sputum culture
CXR
How do you aspirate a pneumothorax?
16-18G cannula
2nd ICS
mid clavicular line
What are the most common organisms to cause CAP
streptococcus pneumoniae
haemophilus influenzae
mycoplasma pneumoniae
How is the severity of CAP assessed?
CURB-65
confusion urea >7mmol/l RR >30 BP <90/60 >65y
How is the management of CAP changed depending on the CURB-65 score
0-1 = 5 days 1g/8h amoxicillin at home
2 = 7-10days of co-amoxicav 1.2g/8g IV + clarithromycin 500mg/12h IV in hospital
3 or more = ICU referral
Describe the management of PE
15L oxygen via non-rebreathe if hypoxic
IV access
morphine 5-10mg IV + metoclopramide 10mg IV
LMWH or fondaparinux IV
NB: if massive PE, give immediate 50mg alteplase bolus not LMWH
if BP <90 systolic:
IV fluids, then SENIOR HELP for dobutamine, then noradrenaline
if BP >90 systolic, start warfarin
What investigations should be carried out in PE
ECG
FBC, U+E, clotting, ABG, ?d-dimer
CXR, CTPA
What are the causes of upper GI bleed
PUD mallory-weiss tears oesophageal varices oesophagitis malignancy
What is the immediate management of an upper GI bleed
protect airway
NBM
2x cannula
bloods - FBC, LFT, U+E, glucose, clotting, G+S, cross-match
IV fluids
if grade III or IV shock give blood
correct clotting abnormalities - Vit K, FFP
?ICU/HDU
endoscopy- - within 4hrs for varices. 12-24h if unstable on admission
What medications should be given in acute variceal bleeding
terlipressin
omeprazole - prevents stress ulceration
What score can be used to assess prognosis in acute GI bleeds
Rockall score
What medication can be given pre-hospital in suspected meningitis
1.2g benzylpenicillin IM
What is Kernig’s sign
pain and resitance on passive extension of knee with flexed hip
What is the immediate management for meningitis
IV fluids
IV cefotaxime 2g (+amoxicillin if <3m or >55y)
if septicaemic - do not attempt LP, contact ITU if shock
if meningitic - dexamethasone 4-10mg/6h IV, LP if no shock and no raised ICP
contact tracing and prophylaxis
inform public health
What are the most common causitive organisms for meningitis?
6-60y = Neisseria meningitidis, Streptococcus pneumoniae
<3m = Group B strep,, E coli, Listeria monocytogenes
> 60y/immunocompromised = Listeria monocytogenes
What investigations should be done in meningitis
urine dip
FBC, U+E, LFT, clotting, glucose, VBG, ABG
blood cultures
CSF MC&S, gram stain, protein,glucose, virology, lactate
?CT head
What is the typical presentation of encephalitis
odd behaviours
reduced consciousness
focal neurology - aphasia
seizure
preceded by infectious prodrome - raised temp, rash, lymph, conjunctivitis
What is the differential diagnosis for encephalitis
hypoglycaemia uraemic encephalopathy hepatic encephalopathy DKA drugs SLE
What organisms can cause encephalitis
viral - HSV, CMV, EBV, VZV, HIV
bacterial - any bacterial meningitis, TB, malaria
aspergillus
What investigations should be done in encephalitis
FBC, U+E,
blood cultures, serum PCR
CT with contrast/MRI
LP
What is the treatment for encephalitis
IV aciclovir
supportive therapy in ICU/HDU
phenytoin for seizures
define status epilepticus
seizure for >30mins
repeated seizures without regaining consciousness
What is the immediate management of status epilepticus
secure airway - oral/nasal, intubate
recovery position
remove false teeth
15L oxygen via non-rebreathe
IV access slow IV bolus lorazepam 2-4mg thiamine if alcoholism or malnourishment suspected IV dextrose if hypoglycaemic IV fluids if hypotension
if seizure continues, give phenytoin or daizepam. then general anaesthesia
What features are seen in prolonged seizures
raised HR
HTN
raised glucose
lactic acidosis
What investigations are useful in status epilepticus
BM, o2 sats!!! FBC, U+E, LFT, glucose, calcium, toxicology, anticonvulsant levels, ABG/VBG blood cultures CT head LP
How is lactic acidosis treated in status epilepticus
resolves spontaneously!
non need for sodium bicarbonate
What are the signs of a basal skull fracture
haemotympanum
panda eyes
CSF leak through ears/nose
Battle’s sign
State the criteria for a CT head in a head injury of an adult
within 1 hour:
Glasgow Coma Scale (GCS) <13 when first assessed or GCS <15 two hours after injury
Suspected open or depressed skull fracture
Signs of base of skull fracture
Post-traumatic seizure
Focal neurological deficit
>1 episode of vomiting
within 8 hours of injury:
coagulopathy or on oral anticoagulant
What investigations should be done in head injury>
GCS,
FBC, U+E, glucose, alcohol, clotting, toxicology
ABG
CT head if indicated
cervical xray if tenderness or deformity posteriorly
State the management of hyperkalaemia
ECG for signs
10ml 10% calcium gluconate IV - stabilise cardiac membrane
10 units actrapid in 50ml 20% glucose
What are the signs of hyperkalaemia on ECG
tall tented T waves
flat p waves
increased PR interval
Which drugs can give dilated pupils
amphetamines
cocaine
TCA
Which drugs can give metabolic acidosis
alcohol
methanol
paracetamol
Carbon monoxide
What effects can salicylate OD cause
hypoglycaemia
renal impairment
Which drugs class as salicylates
aspirin
What are the features of delerium
acute onset
transient and reversible satet of confusion
result of organic process
Describe the CAM diagnostic tool for delerium
1 + 2 + 3/4 = delerium
- acute onset, fluctuation
- 20-1 inattention
- disorganised thinking
- alteration of consciousness
state some causes of acute confusional state
stroke meningitis/encephalitis hepatic/uraemic encephalopathy hypoglycaemia hyponatraemia hypo/hyperthyroid b12/thiamine MI pneumonia constipation UTI medications drugs - alcohol/recreational
What investigations need to be done in acute confusional state
ECG, urine dip, PR
FBC, U+E. CRP, LFTs, TFT, B12, folate, trop, glucose
blood cultures, urine culture, sputum culture
CXR, CT if focal neurology
What drugs can be given to sedate a patient
haloperidol 0.5mg IM/oral
lorazepam 2mg IV/IM
What is seizure like activity during a vasovagal faint called
reflex anoxic convulsion
Describe the layers of the meninges
SKULL extradural/epidural space dura mater subdural space arachnoid mater subarachnoid space pia mater BRAIN
What is an extradural/epidural haematoma and what causes it
collection of blood in the extradural space between the skull and the dura mater
can be due to fractured temporal or parietal bone damaging the middle meningeal artery or vein.
can also be due to tear in dural venous sinuses
What are the features of an extradural haematoma
history of head injury leading to LOC lucid interval then deterioration of conscious level headache N+V seizures
skull fracture bradycardia, HTN haematoma over fracture CSF leakage reduced GCS unequal pupils - fixed and dilated due to compression of CNIII focal neurology
Explain Cushing’s reflex
raised ICP
increase in systemic BP to try to maintain perfusion to brain
caroitid baroceptors recognise rise in BP and decrease HR in response
HTN, low HR
What investigations should be done in extradural haematoma
baseline FBC, U+E
xray skull and spine
CT scan - repeat if further deterioration
How does an extradural haematoma appear on CT
biconvex hyperdense abnormality
midline shift
How is an extradural haematoma managed
A-E
if RICP - IV hypertonic saline or mannitol
burr hole
craniotomy and evacuation
What is a subdural haematoma
collection fo blood in the subdural space between dura mater and arachnoid mater
What is the difference between an acute, subacute and chronic subdural haematoma
subacute - 3-7d after injury. clotted blood liquefies
chronic - 2-3 weeks after injury. blood becomes serous fluid
What is the difference between a simple and complicated subdural haematoma
simple = no parenchymal injury
complicated = associated underlying parenchymal injury eg. contusion
Where can the blood causing a subdural haematoma come from
bridging veins - tear
cortical arteries (branches of carotids)
Which groups of people are subdural haematomas more common in and why
infants - immature veins - tear. NAI
elderly - cerebral atrophy. tension on bridging veins
alcoholics - cerebral atrophy and less platelets and increased bleeding time
anticoagulation
What are the features of subdural haematoma
acute: LOC
chronic: gradually progressive anorexia N+V neurological deficit progressive headache reduced GCS bradycardia and HTN papilloedema (raised fontanellesi in infant)
Give some differentials for a subdural haematoma
other intracranial bleed meningitis or encephalitis cerebral tumour stroke metabolic causes of confusion and reduced consciousness - DKA, hepatic encephalopathy decompensation of dementia
What differentials should be done for subdural haematoma
FBC, U+E, VBG, LFT, clotting, G+S, cross match
blood culture
CT head
cervical spine xray/CT if severe trauma
What is seen on CT in subdural haematoma
crescenteric collection
hyperdense - white, acute
hypodense - black, chronic
What is the management of subdural haematoma
A-E
if RICP - IV hypertonic saline or mannitol
burr hole
if acute and asymptomatic - can monotor obs and examination, do serial CTs
if large, focal signs, RICP, midline shift - needs emergency craniotomy and clot evacuation
What causes a subarachnoid haemorrhage
usually due to bleed from berry aneurysm in circle of willis
or trauma
What are the risk factors for developing berry aneurysms
HTN smoking cocaine alcohol genetics Marfan's FH - first degree relative
What are the features of a subarachnoid haemorrhage
sudden explosive headache - diffuse, severe, pulsates towards occiput seizure confusional state neck stiffness photophobia
in past few weeks - headache, dizziness, orbital pain, diploplia
reduced consciousness
intraocular haemorrhage
isolated dilated pupil with loss of light reflex - die to brain herniation
focal neurology
Give some differentials for SAH
stroke meningitis trauma primary sexual headache carotid artery dissection hypertensive emergency
How should SAH be investigated
immediate CT head without contrast
LP if CT inconclusive
angiography to identify origin of bleed
What can be seen on CT in SAH
hyperdense in basal cisterns and sulci
What can be found on LP in SAH
xanthochromia
= yellow discolouration due to presence of bilirubin from RBC breakdown
How is SAH managed
A-E
transfer to neuro unit with ITU
prevention of vasospam - nimodipine
prevent rebleeding - clipping or coiling
What is the difference between clipping and coiling for SAH
clipping - craniotomy, clips placed around neck of aneurysm
coiling - femoral catheterisation, platinum coil to obliterate aneurysm and for clot within it
What is meningitis?
inflammation of the meninges
can be infective or non-infective
What is meningococcal disease
meningococcal meningitis, meningococcal septicaemia, or a combination of both.
caused by Neisseria meningitidis
Which bacteria most commonly cause meningitis in neonates
Streptococcus agalactiae,
Escherichia coli,
S. pneumoniae,
Listeria monocytogenes
Which bacteria most commonly cause meningitis in children and young people
Neisseria meningitidis,
Streptococcus pneumoniae,
Haemophilus influenzae type b (Hib)
Which bacteria most commonly cause meningitis in the elderly and immunocompromised
Streptococcus pneumoniae
Listeria monocytogenes
TB
gram -ve organisms
What are risk factors for meningitis
Young age Winter season An absent or non-functioning spleen. Older age (more than 65 years). Immunocompromised state Organ dysfunction Smoking, including passive smoking. Living in overcrowded households or in military barracks. CSF or dural shunt sickle cell disease
What are risk factors for meningitis in neonates
low birth weight (below 2500 g), premature delivery, premature rupture of membranes, traumatic delivery, fetal hypoxia maternal peripartum infection.
What can cause aseptic meningitis
partially treated bacterial meningitis. Viral infection - eg, mumps, echovirus, Coxsackievirus, HSV and herpes zoster virus, HIV, measles, influenza, arboviruses Fungal infection Parasites atypical TB, syphilis, Lyme disease, Kawasaki disease.
What can cause non-infective meningitis
Malignant cells (leukaemia, lymphoma, other tumours).
Chemical meningitis (intrathecal drugs, contaminants).
Drugs (non-steroidal anti-inflammatory drugs (NSAIDS), trimethoprim).
Sarcoidosis.
Systemic lupus erythematosus.
Behçet’s disease.
What are the symptoms and signs of meningococcal disease
Non-blanching rash.
Stiff neck.
Capillary refill time of more than 2 seconds, cold hands and feet.
Unusual skin colour.
Shock and hypotension.
Leg pain.
Back rigidity.
Bulging fontanelle.
Photophobia.
Kernig’s sign (person unable to fully extend at the knee when hip is flexed).
Brudzinski’s sign (person’s knees and hips flex when neck is flexed).
Unconsciousness or toxic/moribund state.
Paresis.
Seizures.
Focal neurological deficit including cranial nerve involvement and abnormal pupils.
also: Fever. Vomiting/nausea. Lethargy. Irritability/unsettled behaviour. Ill appearance. Refusing food/drink. Headache. Muscle ache/joint pain. Respiratory symptoms/signs or breathing difficulty.
What is Kernig’s sign
with hips flexed, passive knee extension leads to pain and resistance
sign of meningitis
What is Brudzinski’s sign?
if their head is bent forwards, the hips flex
sign of meningitis
Describe the rash that could be seen in meningococcal meningitis
at first: generalised petechial rash - red/purple non blanching macules <2mm
then: purple purpuric rash, >2mm
What investigations need to be done in suspected meningitis
LP - Gram stain, Ziehl-Neelsen stain (TB), cytology, virology, glucose, protein, culture, rapid antigen screen or polymerase chain reaction (PCR) if available and India ink for cryptococci
FBC, U+E, CRP, coaf, VBG
blood culture
What might contraindicate an LP in meningitis
raised intracranial pressure (reduced consciousness, very bad headache, frequent fits)
or focal neurology.
How is suspected meningitis managed in the communirty
999 for admission
STAT dose of benzylpenicillin
Which antibiotics are used to treat meningitis empiraclly
<3m - IV cefotaxime + amoxicillin or ampicillin
>3m - IV ceftriaxone
Which antibiotics are used to treat meningococcal meningitis
IV ceftriaxone
Which antibiotics are used to treat pneumococcal meningitis
vancomycin + cefotaxime or ceftriaxone
Which antibiotics are used to treat meningitis caused by Hib
ceftriaxone
How is viral meningitis treated
supportive management
corticosteroids - reduces risk of hearing loss and long lasting neuro complications
aciclovir if herpetic
ganciclovir if CMV
When might you suspect viral over bacterial meningitis
features may be more mild and complications (eg, focal neurological deficits) less frequent.
Any person presenting with suspected meningitis should therefore be managed as having bacterial meningitis until proved otherwise!!!
How are close contacts treated in meningitis
if it was meningococcal meningitis, close contacts need ciprofloxacin or rifampicin as prophylaxis
When are people vaccinated against meningitis
2,4,12m - meningitis B
17-18y - meningitis ACWY
Give some complications of meningitis
Immediate:
septic shock,
DIC
coma with loss of protective airway reflexes,
cerebral oedema and raised intracranial pressure,
septic arthritis,
Subdural effusions
Syndrome of inappropriate antidiuretic hormone secretion (SIADH).
Seizures
Delayed: decreased hearing, or deafness; multiple seizures, focal paralysis, subdural effusions, hydrocephalus, intellectual deficits, ataxia, blindness, Waterhouse-Friderichsen syndrome - adrenal gland failure due to bleeding into the adrenal glands peripheral gangrene.
What are the gram stain results of Streptococcus pneumoniae
gram positive diplococci/chain
What are the gram stain results of Escherichia coli
gram negative bacilli
What are the gram stain results of Haemophilus influenzae
gram negative coccobacilli
What are the gram stain results of Listeria monocytogenes
gram positive rod
What is a burn
injury caused by exposure to thermal, chemical, electrical or radiation energy
What is a scald? What depth burn does it cause
a burn caused by contact with a hot liquid or steam
superficial or superficial dermal
What is the difference between a complex and a non-complex burn
non-complex:
partial thickness burn affecting <15% TBSA (10 in children, 5 in <1yr)
deep partial thickness <1% TBSA
not affecting critical area
complex:
partial thickness burn affecting >15% TBSA (10 in children, 5 in <1yr)
affects critical area
chemical or electrical
What is a critical body area in a burn
face, hands, feet, perineum, or genitalia; burns crossing joints, and circumferential burns.
Describe a superficial epidermal burn
only affects epidermis, does nto reach dermis
red and painful skin
no blistering
blanching on CR, <2secs
Describe a partial thickness superficial dermal burn
affects epidermis and upper dermis
red/pale pink
painful blistering
blanches on CR, >2secs
Describe a partial thickness deep dermal burn
affects epidermis and upper and deep dermis. NOT subcutaneous tissues dry blotchy red skin blistering CR does not blanch painful
Describe a full thickness burn
through all layers of skin to subcutaenous tissue, can reach muscle or bone
white, brown, black skin. dru, leathery, eaxy
no blisters
does not blanch on CR
painless
How is the total body surface area affected from a burn calculated
Wallace’s rule of Nine’s
Lund and Browder chart - more accurate
How do you calculate TBSA using Wallace’s rule of 9’s
head - 9% anterior trunk - 18% posterior trunk - 18% arm - 9% leg - 9%
What investigations need to be done in a burn
FBC, U+E, G+S, crossmatch, carboxyhaemaglobin,
CXR
cardiac monitoring
How is a minor burn managed
rinse with cold tap water for at least 20 minutes
if blisters >1cm, can be aspirated using aseptic technique
non-adhesive dressing with gauze padding - change every 3-5 days
reassess at 48 hours
? tetanus prophylaxis
How is a major burn managed
A - any inhalation injury? If yes, intubation!!
B - high flow o2 if risk of CO poisioning
C - two large bore cannulae. Fluids (Hartmann’s) if >15% full/partial thickness burns (10% in children)
How is the amount of fluid resuscitation needed for a burn calculated
Parkland’s formula
4ml x weight in kg X %TBSA affected
Half given over 8 hours, rest given over next 16 hours
When might a patient need to be referred to a burns unit?
All complex burn
full thickness burns
Deep dermal burns affecting more than 5% of total body surface area in adults, and all deep dermal burns in children.
All chemical and electrical burns (including lightning injuries).
Any high-pressure steam injury.
NAI
Burns affecting critical area
Circumferential deep dermal burns in any age group.
Burns associated with suspected inhalation injury.
Burns associated with co-morbidities that may affect wound healing or increase the risk of complications.
Burns associated with significant other injuries or trauma (such as crush injuries, fractures, head injury, or penetrating injuries).
Burns associated with sepsis.
Children under 10 years of age, or adults over 49 years of age.
How might a circumferential burn to the torso or limb need to be managed?
Escharotomy
= division of the encasing band of burn tissue will potentially improve ventilation (if the burn involves the torso), or relieve compartment syndrome and oedema (where a limb is involved)
What is the antidote in a benzodiazepine overdose
Flumazenil (for respiratory arrest) 200mcg over 15 IV
then 100mcg at 60s intervals if needed.
What are the features of salicyclate toxicity
Vomiting, dehydration, hyperventilation, tinnitus, vertigo, sweating.
respiratory alkalosis due to a direct stimulation of the central respiratory centres and then develop a metabolic acidosis.
What arethe features of paracetamol overdose
None initially, or vomiting ± ruq pain.
Later: jaundice and encephalopathy from liver damage (the main danger) ± acute kidney injury (aki).
How can you tell the difference between a virus and a bacterial infection on LP
Viral shows:
lymphocytes, normal/high protein, and HIGH glucose
Bacterial shows:
Bacteria, neutrophils, high protein and LOW glucose
