Disability Flashcards
what is AVPU?
alert
voice - responds to voice
pain - responds to pain e.g. sternal rub/ trapezius squeeze
Unresponsive
what is the GCS scoring system?
Eyes response
- eyes open spontaneously (4 points)
- eyes open to verbal command
- eyes open to pain
- no eyes opening (1 point)
Voice response
- orientated - 5 points
- confused conversation but able to answer Qs
- inappropriate responses
- incomprehensible sounds/ speech
- no verbal response - 1 point
Motor response:
- obeys commands for movement - 6 points
- purposeful movement to painful stimulus
- withdraws from pain
- abnormal flexion (decorticate)
- abnormal extension (decerebrate)
- no motor response - 1 point
score from 3- 15
describe the causes of reduced GCS
head injury - basal skull fracture, epidural haemorrhage, subarachnoid haemorrhage, subdural haemorrhage, concussion and contusion
neoplasm - e.g. glioblastoma or mets
infection - meningitis, encephalitis
seizures
metabolic - electrolytes, cerebral oedema, hepatic encephalopathy, wernickes , hypoglycaemia, hypoxia, uraemia, acidosis
drugs - opioids, intoxication.
describe overall presentation of a head injury?
laceration
obvious skull deformity
C spine tenderness deformity
signs of basal skull fracture
- racoon eyes, battle sign, rhinorrhoea/ottorrhoea, haemotypanum (blood on tympanic membrane)
signs of raised ICP - headache, papilloedema, vomiting, focal neurological signs (cranial nerves, weakness in certain area)
hearing and visual problems
confusion/ drowsiness/ low GCS , amnesia
seizures
decorticate/ decerebrate positioning
cushings triad - high BP, low HR, irregular breathing (late sign)
unequal pupils
what is coup and contra coup injury?
coup injury is bruising at the site of head trauma
contra coup is injury on the opposite site due to transmission of forces.
what is an epidural haemorrhage ?
between skull and dura
often caused by blow to side of head (at pterion) where the skull fracture can rupture middle meningeal artery.
presents with immediate unconsciousness, lucid interval and then slow loss of consciousness. features of raised ICP too.
what is a subdural haemorrhage ?
between dura and arachnoid
caused by lacerations of bridging veins.
most commonly at frontal and parietal lobes.
risk factors include old age, alcoholism, anticoagulation
what is a subarachnoid haemorrhage?
between pia and arachnoid
sudden occipital headache (thunderclap), worst headache ever, neck pain, photophobia, vomiting
can be caused by ruptured cerebral aneurysm
what is monro kellie Doctrine hypothesis?
volume in the brain is fixed and made up of 3 components: brain, blood and CSF. so if any of these increases the others will reduce to compensate until the displacement has reached its maximum and there will be a sharp rise in ICP and brain can herniate.
for example increased brain tissue will result in raise in ICP which will reduce cerebral perfusion to lower ICP. however this can cause brain ischaemia.
what is the cerebral perfusion pressure ? and what happens to MAP if ICP rises?
Mean arterial pressure - ICP
if ICP rises, then MAP needs to increase to maintain cerebral perfusion pressure otherwise brain ischaemia.
When ICP is high enough, MAP cant compensate and cerebral perfusion pressure drops and results in brain ischaemia. what is the physiological response after this?
sympathetic NS stimulation - vasoconstriction to increase resistance and thus HTN. also by increased HR and CO initially.
parasympathetic stimulation: baroreceptors in aortic arch detect the rise in BP and trigger parasympathetic response via the vagus nerve. this leads to bradycardia
raised ICP also puts pressure on brainstem and respiratory centre in medulla oblongata. this results in an irregular respiratory pattern.
overall = cushings reflex = hypertension, bradycardia, irregular respiration .
what causes raised ICP (categorise into blood, brain , CSF)?
blood - haematoma
CSF - hydrocephalus, cerebral oedema, infection
brain - tumour, abscess, infarct and resulting oedema.
what are the NICE indications for a CT head scan within 1 hour ? (adults)
GCS <13 initially after injury GCS <15 - 2 hours after injury post traumatic seizure >1 episode of vomiting neurological deficit suspected open skull fracture or depression signs of basal skull fracture
although not indicated by NICE, may emergency departments consider anticoagulation as an absolute indication for CT scan in context of head trauma.
what are the NICE indications for CT head scan within 8 hours?
loss of conscious/ amnesia + one of following:
- age >65
- dangerous mechanism of injury e.g. motorcyclist
- amnesia retrograde >30 mins
what are the indication for CT scanning of head in under 16s?
known loss of consciousness >5 mins amnesia >5 mins GCS <14 in >1yrs GCS <15 in <1yrs drowsiness
suspected open fracture
signs of basal skull fracture
<1yrs and laceration of >5cm on head or bruising/ swelling
seizure (in non epileptics)
3 or more episodes of vomiting
focal neurological deficit
dangerous mechanism of injury
suspicion of non accidental injury
how is a head injury managed?
A to E
- C spine immobilisation if head injury and GCS <15, neck pain/ tenderness or focal neurology
- intubate if GCS = 8
- avoid hypoxia, low BP (can maintain cerebral perfusion pressure), hypothermia/hyperthermia and hypoglycaemia
treat seizure
treat raised ICP
analgesia (to avoid rise in ICP)
contact neurosurgery if required
wound management
may need Abx and tetanus
frequent neurological observations
discharge advice for patient.
how is raised ICP treated?
elevate head of bed to 30 degrees to promote venous drainage
hyperventilate to keep CO2 low and promote vasoconstriction of cerebral vessels. (not used anymore)
mannitol - 0.5-1mg/kg over 10-15mins
fluid resus - maintain systemic pressure to help MAP and cerebral perfusion.
treat the cause
last resort - Burr holes to relieve pressure.
how often should GCS be recorded post head trauma?
half hourly GCS until GCS is 15, then half hourly for 2 hours, then hourly for 4 hours and then 2 hourly.
what discharge advice would you give someone post head injury?
advised to return if any of the following develop:
- unconsciousness, confusion, drowsiness
- problems with understanding, speaking, balance, weakness
- blurred vision, headache, vomiting
- seizures
- clear straw coloured fluid from nose/ ears
- bleeding from ears.
written and verbal advice should be given
what is the outcome after a head trauma?
death
complete heal after 2 years
ataxia
seizures
speech disorder
tinnitus
CN palsies
personality change - emotional disturbance, irritable
headaches
dizziness, fatigue, depression
poor memory/ concentration
what are the causes of seizures?
genetic - abnormalities in ion channels metabolic space occupying lesion - tumour drugs/ ilicit substance use withdrawal from: Alcohol, benzodiazepine, barbiturates, anti epileptics (ABBA) trauma stroke
what is meant by focal neurological deficit?
signs of impaired neurology that affect one region of the body and thus relate to a specific brain location.
what causes focal neurological deficit?
trauma, tumour, strokes, infections/ abscess, haemorrhage
what focal neurological signs would you see in damage to the:
a) temporal lobe
b) frontal lobe
c) parietal lobe
d) occipital lobe
e) cerebellum
a) emotional and behavioural change, dysphasia
b) personality change (disinhibition), dysphasia (brocas area), anosmia, hemiparesis
c) hemisensory loss, decreased 2 point discrimination, inability to recognise familiar objects, sensory inattention (ignore one side of world)
d) visual loss of one side of vision e.g. left eye temporal loss and right eye nasal loss.
e) DANISH - dysdiadokinesia, ataxia, nystagmus, intention tremor, slurred speech and hypotonia.
what are the characteristics of migraines?
recurrent severe headaches: unilateral and throbbing
associated with: aura, nausea and photosensitivity
aggravated by routine activities of daily living. in women it may be aggravated by menstruation
what are the characteristics of a tension headache?
recurrent, non disabling, bilateral headache, described as a tight band
not aggravated by routine activities of daily living.
what are the characteristics of cluster headaches?
pain typically occurs once - twice a day:
- each episode lasts 15mins to 2 hours
- clusters typically last 4-12 weeks
intense pain around one eye and patient is restless during attack (always affects same eye)
accompanied by: redness, lacrimation, lid swelling
more common in men and smokers.
what are the causes of headaches?
primary - tension, migraine, cluster
secondary - medication overuse, meningitis, encephalitis, subarachnoid haemorrhage, head injury, sinusitis, glaucoma, psychological / anxiety. substance missuse/ withdrawal , metabolic (hypoglycaemia, hypoxia, hypercapnia, CO poisoning)
how would you investigate someone who presents to A+E with a headache?
detailed history - how did it start? worst headache ever? associated symptoms?
examination - rashes? Kernigs sign? papilloedema, neurological examination. palpate sinuses for tenderness.
full set of obs
bloods - rule out metabolic cause (electrolytes, LFTs, glucose), FBC and CRP (infection), if pyrexic (blood cultures)
imaging: CT/ MRI brain - once stable CSF analysis (lumbar puncture)
how do you treat someone who presents with headache
after serious causes are ruled out
analgesia, fluids, IV metoclopramide with IV fluids.
what is the emergency management for meningitis?
cefotaxime 2g IV
if >55yrs add ampicillin to cover listeria
IV dexamethasone
fluids and analgesia
what is the management of a subarachnoid haemorrhage?
A to E
Ix: clotting, FBC, U+Es, CT head, ECG, admit for lumbar puncture (carried out >12 hours after headache onset
use hunt and less scale to grade
analgesia and antiemetic
contact neurosurgery
may require mannitol IV if evidence of raised IC
what is the hunt and hess scale?
scale used for subarachnoid haemorrhage
grade 1 - asymptomatic, mild headache, slight nuchal (neck) rigidity
grade 2 - moderate to severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy
grade 3 - drowsiness/confusion, mild focal neurology
grade 4 - stupor, moderate - severe hemiparesis
grade 5 - coma, decerebrate posturing
how is an acute migraine attack managed?
analgesia and antiemetic
may give sumatriptan (contraindicated in ischaemic heart disease)
what does CSF show in:
a) viral meningitis,
b) bacterial meningitis
c) fungal meningitis
d) TB meningitis
a) clear , slightly raised WCC, mainly lymphocytes, pressure slightly raised
b) cloudy/turbid, very high WCC, neutrophils, raised protein, low glucose, high pressure
c) fibrin webs seen, slightly high white cell, mainly lymphocytes , very high pressure.
d) cloudy/viscous, slightly raised WCC, mainly lymphocytes, raised protein, very low glucose, high
note: mumps is unusually associated with low glucose (also herpes too sometimes)
what tests can be done to analyse CSF fluid?
colour, WCC, Red cells, protein, glucose culture and sensitivity PCR for virology acid fast/ zeihl nelson stain xanthochromia - subarachnoid haemorrhage electrophoresis - oligoclonal bands in MS cytology - tumour
what are the clinical features of poisoning?
fast irregular pulse - salbutamol, antimuscarinics, tricyclics, quinine
respiratory depression - opiate, benzos
hypothermia - barbiturates
hyperthermia - amphetamines, MAOIs, cocaine, ecstasy
seizures - recreational drugs, hypoglycaemic agents, tricyclics, theophylline
constricted pupils - opiates, insecticide
dilated pupils - amphetamines, cocaine, quinine, tricyclics
hyperglycaemia - MAOIs, theophylline
hypoglycaemia - insulin, oral hypoglycaemics, alcohol, salicyclates
metabolic acidosis - alcohol, methanol, paracetamol, CO poisoning
renal impairment - salicyclates, paracetamol
high osmolality - alcohol
coma - benzos, alcohol, opiates, tricyclics, barbiturates
how do we manage acute poisoning?
A to E
- consider ventilation if resp rate <8 or GCS <8
- resuscitate any shock / fluids/ catheterise
- if unconscious nurse in semi prone position to protect against aspiration
assess patient to find cause of poisoning:
- history, speak to family
- plasma toxology screen - all unconscious patients should have paracetamol, salicylates and glucose levels checked.
- urine toxology - good for recreational drugs
- glucose, FBC, INR, UEs, LFTs, ABG
- ECG
- monitor vitals
definitive treatment for toxin e.g. activated charcoal, gastric lavage, haemodialysis, antidote
psychiatric assessment
what is activated charcoal used for
It reduces the absorption of many drugs from the gut
when repeated doses are given it can increase elimination from blood too.
not useful in - petroleum, corrosives, alcohols, clofenotane, malathion, metal salts (lithium, iron)
give lower dose in children
what is gastric levage?
rarely used now
process of cleaning out stomach contents
done in <30 mins of ingestion
don’t use with petroleum/ corrosives
which toxins can haemodialysis be used for in poisoning?
lithium, methanol, salicyclates, sodium valproate, ethylene glycol
how is paracetamol overdose managed?
use paracetamol treatment curve to decide if treatment needed. if unsure when tablets were taken, treat anyway.
activated charcoal if ingested (ideally within 1 hour but can be given up to <4 hour ago)
N-acetylcysteine (NAC)
liver transplantation
monitor INR, UEs, LFTs
how is salicylate poisoning managed?
usually straight to haemodialysis
used to use urinary alkalisation - however rarely used and contraindicated in pulmonary/ cerebral oedema
how is opioid overdose managed?
how is benzodiazepine overdose managed?
naloxone
flumazenil
how are tricyclic antidepressant overdoses managed?
IV bicarbonate may reduce risk of seizures and arrhythmias in severe toxicity. don’t treat arrhythmias with antiarrhythmics
dialysis
how is lithium overdose managed?
mild/moderate toxicity may respond to fluid resus with normal saline
haemodialysis in severe toxicity
how is warfarin toxicity and heparin toxicity treated?
warfarin - stop warfarin, vitamin K, prothrombin complex
heparin: protamine sulphate
how is ethylene glycol/ methanol toxicity treated?
alcohol - competes for alcohol dehydrogenase to reduce production of toxic metabolites.
fomepizole - competitive inhibitor of alcohol dehydrogenase - now first line
haemodialysis
how is digoxin toxicity treated?
digoxin specific antibody fragments
how are insecticide poisoning treated?
atropine
how is carbon monoxide poisoning treated?
100% oxygen in hyperbaric chamber
how is iron and lead poisoning treated?
iron - desferrioxamine (chelating agent)
lead - dimercaprol, calcium edetate
how is cyanide poisoning treated?
hydroxocobalamin
also combination of amyl nitrite, sodium nitrite and sodium thiosulphate
what are the signs of paracetamol poisoning?
RUQ pain vomiting jaundice encephalopathy organ failure
what amount of paracetamol can be fatal?
12g
how is b blockers toxicity treated?
if bradycardic - give atropine
in resistant cases can give glucagon
what are the features of illness in older people?
present differently
cause greater morbidity/ mortality
co-morbidity is common
lack of physiological reserve so deteriorate quickly
polypharmacy
social problems - poor housing, live alone, lack of care
what should be taken into account when assessing the older patient?
be aware of cognitive impairment
clarify what support they have - family, neighbours etc
screen for problems with hearing, vision, gait/ balance, continence
assess their nutrition
assess their mental health - are they lonely/depressed
assess their level of independence/ activity level
ask if they have advancd care directive/ nominated proxy healthcare decision maker
assess their compliance to medication
what are the different specialities that work in MDT for care of old people?
dietician OT physio psychiatrist GP geriatrician carers
elderly have problems in many aspects e.g. health (eye, ears, cardio, resp, arthritis etc), social (live alone), psychological (lonely, dementia) so need MDT approach
how can syncope be classified?
reflex syncope:
- vasovagal: due to reflex bradycardia and peripheral vasodilation provoked by pain, emotion, standing too long. syncope last 2 mins and there may be brief jerking of limbs due to cerebral hypoperfusion
- situational: with coughing, sneezing
- carotid sinus syncope - hypersensitive baroreceptors
orthostatic syncope:
- primary autonomic failure - parkinsons, MSA
- secondary autonomic failure - diabetes, amyloidosis, uraemia
- drug induced - diuretics, alcohol, vasodilators
- volume depletion - dehydration, haemorrhage, addisons
cardiac syncope:
- arrhythmias
- valvular (aortic stenosis), MI, hypertrophic cardiomyopathy (HOCM)
- P.E, tamponade, acute aortic dissection
other: anxiety, panic attack, hyperventilation
what features would indicate a cardiac cause of syncope?
syncope in supine
syncope during/after exercise
syncope without warning
family history of sudden death
how can we investigate syncope?
acutely: A to E, ECG, FBC (anaemia), glucose (hypoglycaemia) , ECHO
history - when was the black out, what happened, loose awareness, vision? movements? injury? incontinence? what were they doing before? what happened after?
later: postural BP reading, tilt table test
how can postural BP readings help us diagnose syncope?
diagnostic if fall in systolic >20mmHg or diasytolic >10mmg
or drop in systolic <90mmHg
what factors increase old persons risk of falling?
poor vision poor balance poor proprioception poor muscle mass poor central processing of sensory and motor info
what defines hypothermia?
core (rectal) body temperature of <35 degrees
what are the causes of hypothermia?
impaired homeostatic mechanisms - age related
low room temperature - poor housing
impaired thermoregulation - pneumonia, MI, heart failure, MS, sepsis, pancreatitis
reduced metabolism - hypothyroidism, DM, hypopituitarism
autonomic neuropathy - Parkinson’s, diabetes
excessive heat loss - psoriasis , burns
reduced cold awareness - dementia
drugs - alcohol
trauma patients are more susceptible to hypothermia
neuromuscular disorder.
what are the risk factors to becoming hypothermic?
very old/ young chronic illness malnourished intoxication cognitive impairment
how does someone with hypothermia present?
low temperature recorded
other signs - shivering, slurred speech, slow breathing rate, cold pale skin, lethargy, low GCS, agitation, bradycardia, hypotension, arrhythmias
if patient is not shivering despite <35 degrees = severe hypothermia
where can core body temperature be recorded from?
axilla
oral
rectal
infra-red ear thermometer
last 2 are the best.
what tests should be done in hypothermic patients?
UEs, plasma glucose, amylase, TFTs, FBC, blood cultures, ABG/VBG, ECG, coagulation studies (DIC may occur)
what ECG changes are seen in hypothermia?
J waves , increased PR and QT
how do we treat hypothermia?
A to E
all patients should receive warm humidified O2
remove any wet clothing and slowly rewarm using blankets
vital signs every 30 mins
warm IV fluids
keep ECG on - arrhythmia can occur during re-warming
give prophylactic Abx for those >65 and T<32
do not warm too quickly - aim for 1-2 degrees / hour (rewarming too quickly can cause peripheral vasodilation and shock)
what are the complications of hypothermia?
arrhythmia, pneumonia, pancreatitis, AKI, DIC
what is pyrexia?
temperature >37 degrees
what are the causes of pyrexia?
infection inflammatory conditions - RA, SLE, AS malignancy drugs - malignant hyperthermia vaccination heat exhaustion tissue destruction - rhabdomyolysis , surgery
what investigations would you do in someone with pyrexia?
look for infection with basic bloods - FBC, CRP/ESR, blood cultures, UEs, LFTs
urine - culture and microscopy
analysis of CSF - lumbar puncture
imaging of suspected source e.g. CXR, CT/MRI head etc
when should Abx be given in infection?
after microbiology samples are taken
then ASAP
what should be considered before Abx are prescribed?
allergies dose renal function medication interaction pregnant/ lactating?
what Abx should be given for:
a) exacerbation of chronic bronchitis
b) community acquired pneumonia
c) atypical pneumonia
d) hospital acquired pneumonia ?
a) amoxicillin or tetracycline or clarithromycin
b) amoxicillin (doxycycline or clarithromycin if pen allergy. add flucoxacillin if staphylococcus suspected)
c) clarithromycin
d) <5 days of admission:Co -Amoxiclav or cefuroxime
> 5 days of admission: piperacillin with tazobactam OR broad spec cephalosporin or quinolone (ciprofloxacin)
what antibiotics are used to treat
a) lower Urinary tract infections
b) acute pyelonephritis
c) Acute prostatitis ?
a) nitrofurantoin or trimethroprim
b) cephalosporin or quinolone
c) quinolone or trimethroprim
what antibiotics are used to treat:
a) gonorrhoea?
b) chlamydia?
c) syphilis?
d) PID?
e) bacterial vaginosis ?
a) IM ceftriaxone and oral azithromycin
b) doxycycline or azithromycin
c) benzathine benzylpenicillin or doxycycline or erythromycin
d) oral ofloxacin and oral metronidazole
OR IM ceftriaxone + oral metronidazole and doxycycline
e) oral or topical metronidazole or topical clindamycin
what antibiotics are used to treat:
a) clostridium difficile
b) campylobacter enteritis?
c) salmonella (non typhi)
d) shigellosis
a) metronidazole or vancomycin
b) clarithromycin
c) ciprofloxacin
d) ciprofloxacin
what Abx are used to treat:
a) impetigo?
b) cellulitis?
c) erysipelas
d) animal/ human bite
e) mastitis during breast feeding?
a) topical fusidic acid/ oral flucoxacillin or erythromycin
b) floxacillin (clarithromycin if pen allergy)
c) phenoxymethylpenicillin (erythromycin if pen allergy)
d) co-amoxiclav (doxy + metronidazole if pen allergy)
e) flucloxacillin
what Abx should be used to treat:
a) throat infections
b) sinusitis
c) otitis media
d) otitis externa
a) phenoxymethylpenicillin (erythromycin if pen allergy)
b) amoxicillin or doxycycline or erythromycin
c) amoxicillin (erythromycin if pen allergy)
d) flucloxacillin (erythromycin if pen allergy)
list the main notifiable disease
brain: acute meningitis, acute encephalitis, meningococcal septicaemia
GIT: cholera, enteric fever, typhus, haemolytic uraemic syndrome, food poisoning, infectious bloody diarrhoea
blood borne: malaria, yellow fever, haemorrhagic fever (e.g caused by virus’s ebola, Marburg, yellow fever),
respiratory/ rashes: TB, whooping cough, SARS
neuro: polio, anthrax, botulism, diphtheria, leprosy, rabies, tetanus
rash: measles, mumps, rubella, scarlet fever, plaque, small pox
other: brucellosis , invasive group A streptococcus and acute infectious hepatitis
what are the different types of burns?
thermal
chemical
electrical
radiation
how can we assess a burn?
history - how it happened, material they were burnt with? any smoke inhalation?
examination: any airway burn? some extensive burns can constrict chest movement? hypovolaemic shock? hypothermia?
assess extent - use lund and browder chart to map out surface area
assess depth
overall assessing severity so we can triage correctly
how can the depth of a burn be categorised?
superficial: minor erythema, painful with blistering (first degree), epidermis only
second degree burns: do not blanch on pressure. epidermis and part of dermis
third degree/ full thickness: white, brown or black and look leathery, no sensation, no blister. through dermis and into subdermal structures.
how are major burns managed?
A to E
- high flow O2 , consider early intubation
- fluid resuscitation - 0.9% saline (calculated based on weight and body surface area burnt) + catheterise and fluid balance monitored.
- may require blood transfusion
take bloods - Xmatch FBC, UEs, glucose, coagulation, COHb levels
irrigate chemical burns with water (for 20-30mins
cool running water (be aware of hypothermia)
cover burns in clean sheets - clingfilm, wet dressings, gel dressings
remove clothes that are burnt
analgesia and anti-emetic
tetanus and Abx prophylaxis
check urine for myoglobinuria (high risk of renal failure)
get a burn specialist
treat specific problems:
- CO poisoning - may need hyperbaric chamber
what is the parkland formula?
used to calculate the amount of volume needed for fluid resuscitation…
volume in ml = body surface area % x weight kg x 4
first half of fluid over 8 hours, second half over 16 hours
how are smaller burns managed?
cool the burn - cool pack but NOT ice
simple saline/ paraffin gauze
analgesia
tetanus/ Abx prophylaxis
what burns are more serious out of acid and alkali?
alkali tend to be deeper and more serious
how long should alkali burns to the eye be irrigated for?
8 hours
what is a complication of an electrical burn?
rhabdomyolysis - resulting in AKI
should increase fluids in this case
how are wounds managed?
assessment:
- history - what caused it ? when? what has been done since?
- examination - site, depth, contamination, test neurology, tendons and vascular injury, look for fractured bones, signs of infection?
- imaging - may need X ray
management:
- cleaning- remove any foreign body and irrigate with saline
- lignocaine may be needed
- closure - sutures, steristrips, skin glue, staples (cant be closed if >12 hours ago
- dressing on top
- document
- tetanus/ Abx
- follow up and after care advice
