Clinical Emergencies Flashcards
what conditions come under acute coronary syndrome
STEMI
NSTEMI
Unstable angina
Initial investigations for someone with suspected STEMI/NSTEMI
ECG
Bloods: FBC, U+E, Troponin, (glucose + lipids)
CXR - but don’t delay management
BP on both arms
Initial management of STEMI
300mg of aspirin if not already given
180mg ticagrelor
5 - 10mg IV morphine + 10mg IV metoclopramide (can repeat morphine after 5 mins if necessary)
Can give oxygen if breathless or sats <95%
Can give bisoprolol if no heart failure, asthma/COPD or cardiogenic shock
Reperfusion therapy in STEMI
- Primary PCI - if less than 12h from symptom start + can be delivered within 2hrs of medical contact; can sometimes be given in 24h if evidence of ongoing ischaemia; also give injectable anticoagulant e.g. bivalirudin
- Thrombolysis with IV tenecteplase (tissue plasminogen activator) If PCI not available. Ideally within 30mins of admission; can be transferred for rescue PCI
- Fondaparinux if presenting >12h after symptom onset
Contraindications for thrombolysis
previous intracranial haemorrhage known bleeding disorder cerebral malignancy recent major trauma/surgery/head injury (3w) recent ischaemic stroke (6m)
relative CI: anticoagulant therapy, pregnancy, advanced liver disease
ECG STEMI findings
ST Elevation in 2 or more consecutive leads
new left bundle branch block
recipricol changes: deep ST depression
ECG NSTEMI findings
ST depression
Flat or inverted T waves
normal
Management of NSTEMI
Antiplatelets: aspirin - 300mg then 75mg OD + ticagrelor - 180mg then 90mg BD
Anticoagulation: Fondaparinux until discharge: 2.5mg OD
Analgesia: morphine 5-10mg IV + 10mg IV metoclopramide
Nitrates (PO or IV)
Beta-blockers (2.5mg bisoprolol), ACE-i, statins (80mg atorvastatin)
Address modifiable risk factors: smoking, hypertension, hyperlipidaemia, diabetes
How can you stratify patients with acute coronary syndrome and why is this important
GRACE score
- history of unstable angina, >70, general co-morbidities e.g. diabetes, previous MI
High risk patients may need coronary angiography –> coronary stenting or CABG
Causes of pulmonary oedema
Cardiovascular: LV failure post MI, valvular heart disease, arrythmias
Acute respiratory distress syndrome
Fluid overload
differential diagnoses for pulmonary oedema
asthma/COPD
pulmonary fibrosis: bi-basal crepitation
Pneumonia
signs/symptoms of pulmonary oedema
general observation: distressed, pale, sweaty, leaning forward
observations: increased pulse + resp rate (+ low O2 sats)
chest exam: increased JVP, wheeze, triple/gallop rhythm, crepitations
investigations for suspected pulmonary oedema
Bedside: ECG, glucose (SOB could be a sign of DKA)
Bloods: U+E, troponin, BNP, ABG
Imaging: CXR, consider echo
findings on CXR for pulmonary oedema
A - alveolar oedema B - kerley B lines C - cardiomegaly D - dilated upper lobe vessels E - pleural effusions (blunting of costophrenic angles)
findings on ECG for pulmonary oedema
MI, dysarrythmia
initial management of pulmonary oedema
oxygen if sats are low
IV diamorphine: 1.25mg - 5mg
IV Furosemide: 40-80mg
GTN/IV nitrate if BP>90/100
can repeat dose of furosemide
consider CPAP
management of pulmonary oedema once patient is stable
daily weights: -0,5kg/day
oral furosemide
consider addition of a thiazide e.g. bendroflumethiazide
consider ACE-i, beta-blockers and spironolactone
causes of cardiogenic shock
Cardiac: MI, arrythmias, myocarditis, aortic dissection
respiratory: PE, tension pneumothorax
management of cardiogenic shock
oxygen
diamorphine: IV 1.25 - 5MG
close monitoring
treat underlying cause
what is cardiac tamponade
increase in pericardial fluid increases intrapericardial pressure making it hard for the heart to fill –> heart stops pumping
causes of cardiac tamponade
signs of cardiac tamponade
management of cardiac tamponade
trauma, lung/breast cancer, pericarditis, MI
Beck’s triad: low BP, high JVP and muffled heart sounds
Also: pulsus paradoxus - pulse fades on inspiration
Get a senior at the bedside
investigations for suspected asthma
Bedside: PEF (if not too ill), BM (if suspecting DKA)
Bloods: ABG, FBC, U+E
Imaging: rule out pneumothorax, infection
Features of a severe asthma attack
Unable to complete sentences in one breath
RR>25, HR>110
PEF 33-50%
Features of life threatening asthma attack
general observation: exhaustion, confusion, coma
examination: silent chest, feeble respiratory effort, cyanosis
Bedside tests/observations: hypotension, arrythmia, PEF >33%, Sats <92%
ABG: normal/high PCO2 (>4.6); PO2 <8
Immediate management of asthma attack
oxygen
5mg nebulised salbutamol
30mg PO prednisolone (40mg if severe)
Reassess every 15 mins
- Add 0.5mg/6h ipratropium bromide if not responding or severe asthma
- Repeat salbutamol every 15-30m
- monitor ECG
- consider single dose IV magnesium sulfate 1.2 -2g
- ESCALATE
Continued management of asthma attack
If not improving after initial management
- refer to ICU for ventilatory support + aminophylline/ IV salbutamol
If improving
- continue nebulised salbutamol +/- ipratropium bromide every 4-6h
- 40-50mg prednisolone for 5-7 days
- monitor PEF and oxygen sats
- consider discharge if PEF > 75% 1h after initial treatment
otherwise discharge if
- stable on discharge medication for 24hrs
- check inhaler technique + that they’re on right medication (e.g. inhaled and oral steroids)
- written management plan
- GP appt within 2 days; resp clinic appt within 4weeks
investigations for COPD
Bedside: sputum culture, ECG
Bloods: FBC, U+E, CRP, blood cultures
Imaging: CXR
ethics surrounding advanced COPD
autonomy: what does the patient actually want? Speak to patient early
NM: doing harm by invasive ventilation? - difficult to wean off, ventilation associated pneumonia and pneumothoraces
management of acute COPD
nebulised salbutamol/ipratropium bromide (5mg/4h 0.5mg/6h)
Oxygen: venturi mask 24-28% oxygen; 88-92%
Steroids: 200mg IV hydrocortisone + oral 3omg prednisolone (continue for 7 - 14d)
Antibiotics: (evidence of infection) 500mg amoxicillin TD (or clarythromycin)
If no response
- consider IV aminophilline, NIPPV, intubation and ventilation
causes of pneumothorax
can be spontaneous, esp. in young thin men
trauma: inc. iatrogenic e.g. ventilation
chronic lung disease
infection
carcinoma
connective tissue disorders e.g. marfan
signs and symptoms of pneumothorax
pleuritic chest pain + dyspnoea
reduced chest expansion, hyperresonant, diminished breath sounds on affected side,
tension pneumothorax: trachea deviated away from affected side; respiratory distress, tachycardia, hypotension, distended neck veins
management of pneumothorax
Can discharge if its a primary pneumothorax, less than 2cm on CXR and no dyspnoea
Otherwise: Aspiration/insert chest drain
Tension pneumothorax: insert large bore needle + syringe with 0.9% saline into 2nd IC space, mid clavicular line; then request CXR, insert a chest drain
Most common organisms that cause pneumonia
Strep. pneumonia
Also: haemophilus influenzae, mycoplasma influenzae, influenza virus
ICU: staph. aureus
COPD/HAP: gram negative bacilli e.g. psuedomomas
Investigations for pneumonia
The usual plus:
sputum cultures
viral throat swabs (e.g. COVID)
How to calculate severity of pneumonia
CURB-65
- confusion (<8 on AMT)
- urea > 7mmol
- RR > 30
- BP <90/60
- Age >65
0-1: home
2: hospital
3+: severe pneumonia, consider ICU
management of pneumonia
oxygen
treat hypotension with IV fluids if requires
antibiotics: amoxicillin (5 days); co-amoxiclav if severe
analgesia for chest pain
Risk factors for PE
malignancy surgery (esp, pelvic + lower limb) immobility; active inflammation (infection, IBD) pregnancy, COCP, HRT Previous VTE
signs and symptoms of PE
acute dyspnoea, pleuritic chest pain, haemoptysis and syncope
hypotension, tachycardia, gallop rhythm, increased JVP, right ventricular heave, pleural rub, tachypnoea, cyanosis, AF
investigations for PE
Bedside: ECG - might show sinus tachycardia, RBBB, AF, right ventricular strain
Bloods: U+E, ABG, FBC, clotting
Imaging:
- CXR: rule out pneumonia, COVID etc.; may show wedged shaped infarction and small pleural effusions
- CTPA (ventilation perfusion scan if possible)
Management of PE
15L oxygen if hypoxic
IV morphine 5-10mg + antiemetic if distressed/in pain
IV LMWH/fondaparinux
500ml IV fluid bolus if hypotensive
consider thrombolysis with IV alteplase bolus if still haemodynamically unstable
initiate long term anticoagulation: DOAC or warfarin 3 - 6+ months
causes of upper GI bleeds
peptic ulcer disease gastroduodenal erosions oesophagitis MW tear varices
What are PRISMA guidelines
preferred reporting terms for systematic reviews and meta analyses
guidelines systematic reviews should follow such as clearly defining inclusion and exclusion criteria
what is a forest plot
a plot used in meta-analyses that show the effect/outcome of each study and the overall outcome
what do the lines on a forest plot represent
what happens if the mean diamond crosses the line of null effect
confidence interval
no significant difference between the treatment of interest and the control
what is a systematic review
a review of the literature regarding a research question of interest
what are the pros and cons of an RCT
pros: randomisation could reduce systemic bias by distributing confounding factors, prospective design can demonstrate temporality + causality
cons: expensive (may be funded by bodies with vested interest), time consuming, ethical concerns, requires large numbers of people
pros and cons of cohort study
pros: time sequence –> help identify causality, good for rare exposures, can identify multiple outcomes for given exposure
cons: expensive, time, loss of people to follow up can introduce bias
pros and cons of case control studies
pros: quick and inexpensive, good for rare diseases
cons: subject to recall bias, requires good reporting, can be difficult to select suitable control group, not good for rare exposures
pros and cons of cross-sectional studies
pros: quick and inexpensive, good for assessing health needs of a population
cons: not causal, only a snapshot of the time, use health surveys - subject to recall bias, study population must be representative of total population
pros and cons of case reports
pros: quick, can inform about rare/new presentations
cons: plenty of bias, weak evidence
immediate management for suspected upper GI bleed + shock
(contact endoscopist and notify surgeons)
Protect airway and keep NBM
(VBG)
Insert 2 large bore cannulas and request urgent bloods (FBC, U+E, LFTs, clotting, crossmatch 4-6 units)
Rapid IVI up to 1L (Hartmann’s, avoid saline if cirrhotic)
If signs of stage 3/4 shock (e.g. RR>30, HR>120, Low BP) or Hb<70g/L; start major haemorrhage protocol with O- until crossmatch done
Correct clotting abnormalities
If risk of varices: terlipressin (IV 1-2mg/6h) + broad spectrum IV antibiotics
catheterise and monitor urine output
monitor vital signs every 15mins until stable, then hourly
Consider referral to ICU
Urgent endoscopy for diagnosis and control of bleeding once stable
what is the glasgow-blatchford score
stratifies upper GI patients to determine who is low risk and could be potentially managed as an outpatient
What is the rockall score
determines severity of GI bleed and risk of mortality ( + re-bleed risk)
age, shock, co-morbidities (+ diagnosis, stigmata of recent major haemorrhage)
further management of upper GI bleed
PUD: endoclips
Varices: oesophageal banding or injection sclerotherapy
Check for + treat H.pylori using triple therapy (PPI + 2 antibiotics)
IV PPI
main causes of meningitis
meningococcus, pneumococcus
Management of meningitis
C: take blood + blood cultures, then start broad spectrum antibiotics according to local guidelines (ceftriaxone + amoxicillin >65/immunocompromised), IV fluids if shocked,
D: check + correct glucose, consider IV dexamethasone
Escalate early: seniors, ITU, microbiology, public health (urgent if suspected bacterial or septicaemia)
Discuss antibiotic therapy with microbiology
Isolate for 1st 24hrs
prophylactic management of meningitis
ciprofloxacin to household contacts in droplet range
encephalitis management
C: IV access, blood cultures, viral PCR of serum
D: Acyclovir within 30mins (14 days or 21 if immunocompromised); LP with viral HSV PCR of CSF + contrast CT to confirm diagnosis
Liaise with microbiology to adjust management
status epilepticus management
open + secure airway
IV access: 4mg lorazepam (or rectal diazepam if IV cannot be obtained); repeat if no response after 15 minutes
- URGENT SENIOR REVIEW
IV phenytoin; monitor ECG and BP
- URGENT ITU/ANAESTHETIST SUPPORT BY THIS POINT
Rapid sequence induction with general anaesthesia
Note: consider whether patient could be pregnant; dexamethasone if tumour a possibility
Once stable, continue oral drugs and try to establish cause
causes of raised ICP
trauma
space occupying lesion (e.g. tumour)
bleeding
infection
signs and symptoms of raised ICP
headache worse on coughing/straining/in the morning
coma/drowsiness
Cushing’s triad: low RR + HR, high BP
Papilloedema/pupillary dilatation
management of raised ICP
early referral to neurosurgeons (craniotomy) and anaesthetists (intubation)
A: protect airway, consider intubating
B: CXR to check possible source of infection; ABG etc.
C: IV access, bloods (FBC, U+E, blood cultures), maintain MAP>90, elevate head to 30-40 dgrees
D: discuss with senior about IV mannitol (can cause rebound ICP increase); dexamethasone if tumour suspected
E: check for rash - meningitis?
management of head injury
seek support: trauma call, neurosurgeons etc.
exclude catastrophic haemorrhage
Airway: protect c-spine: 3 point immobilisation + jaw thrust, seek anaesthetist support
E: inspect + palpate skull for deformity, bleeding, CSF leak, Battle’s sign, raccoon eyes (basal skull fracture), tetanus status review
CT head criteria
CT head within 1hr if
- GCS<13 on admission or <15 after 2h
- focal neurology
- vomiting > 1ce
- seizures
- suspected basal skull fracture
CT head within 8h if - anti-coagulated patients - amnesia/LOC + > coagulopathy > dangerous mechanism of injury > over 65
CT spine criteria
GCS < 13 on admission intubation required pre-operatively undergoing a head scan suspected c-spine injury + > over 65 > parasthaesia > dangerous mechanism of injury > focal CNS deficit
things to consider for someone with SAH
CT/MRI Brain
LP: xanthochromia
liaise with seniors, neurosurgeons, ICU if GCS is falling
lie flat, appropriate analgesia, consider nimodipine, dexamethasone if increased ICP
things to consider for someone presenting with stroke
CT brain to rule out haemorrhagic stroke
If not haemorrhagic: 300mg aspirin + thrombolysis within 4.5h
Consider AF: start warfarin after 14d; cholesterol: statin
secondary prevention: lifelong clopidogrel; >70% carotid stenosis –> carotid endarterectomy
things to consider for someone with aortic dissection
imaging: USS/CT
immediate referral to vascular surgeons, anaesthetists, CEPOD (emergency theatre)
what is pheochromocytoma and what are the symptoms
catecholamine neuroendocrine producing tumour, usually from adrenal glands
pain (headaches), pallor, palpitations, panic, perspiration, pressure (high BP)
management of pheochromocytoma
ABCDE
get ICU support
C: short acting alpha blocker e.g. phentolamine, then long acting alpha blocker + beta blocker (labetalol)
urinary/plasma metanephrine levels to confirm diagnosis
surgery 4-6w later (adrenalectomy)
what is the modified glasgow score
tool for assessing severity of pancreatitis; if above 3 then consider ITU
P: PaO2
Age, neutrophils, calcium, renal, enzymes (LDH/AST), albumin, sugar
management + complications of pancreatitis
IV fluids
analgesia
necrotising pancreatitis, collections, ARDS, MI
classification of aki
pre renal: hypotension (sepsis, cardiac, hypovolaemia)
renal: drugs, glomerulonephritis, vasculitis
post renal: obstruction
ABCDE consideration for AKI
B: VBG
C: ECG (K+ arrythmia), U+E, urine output (+ urinalysis)
management of AKI
urgent FLUIDS
urgent escalation to seniors and nephrologists if: high potassium, pulmonary oedema, severe metabolic acidosis
Fluid bolus if dehydrated
low BP –> fluid bolus
urinalysis
imaging: urgent renal USS if obstructed or unsure of cause
D: stop nephrotoxic drugs - diuretics, metformin, nsaids, ACEi + nephrotoxic antibiotics
sepsis: sepsis 6 if signs of sepsis
general management of clinical station
patient safety + SBAR (admission, complete obs, trend in obs)
See sickest patient
Delegate responsibilities for other patient to nurses/colleagues
Ask to meet nurse at bedside with notes + start jobs if possible (oxygen, IV access, ECG)
Run through A-E
assessment, observation/investigation, management
ask for help if patient is deteriorating
once stable
- full clinical history + focused examination
- order necessary investigations
- document encounter in notes
- discuss plan with senior + handover to the necessary team if required
management of DKA
follow hospital protocol (esp. regarding fluid)
A
B: VBG, oxygen, CXR
C: IV access, BP, HR, fluids (1L/1hr unless shocked then 500ml/15mins), ECG
D: AVPU, pupils, glucose + ketones; insulin 0.1units/kg/hr; continue regular long acting insulin
E: sources of infection
Further management
- monitor glucose + ketones hourly; check VBG at 2h, 4h, 8h etc.
- assess need for potassium
- add 10% dextrose once BM <15
- prescribe LMWH
What is the p-value
the probability that the null hypothesis is true (needs to be less than 0.05 to be significant)
the probability between 0 and 1 with one being the highest that the outcome of the experiment was due to chance rather than an actual difference
what is the 95% confidence interval
the range in which you are 95% sure the real population lies somewhere between
what is power
the likelihood of a study detecting a true difference. i.e. the probability of not making a type 2 error
absolute risk
the probability of an event occurring within a certain group. can only be between 0 and 1.
absolute risk difference
the difference in absolute risk between the intervention group and control
relative risk
the absolute risk of an event occurring in the in the intervention group compared to the control group (AR group 1/ AR group 2)
If the relative risk is 0.8 then there is a 20% reduction in the relative risk
i.e. 20% less likely to have that outcome
number needed to treat
how many people needed to treat to save 1 person
1 divided by absolute risk difference
odds ratio
the odds of an outcome occurring if exposed to something vs the odds of that outcome occurring if unexposed to that same thing
OR: 1.6
In those who had the case (e.g. not understanding treatment), the odds of them having the exposure (e.g being black) was 1.6 times higher than if they were in the control group (e.g. understanding their treatment)
relative risk reduction
absolute risk reduction divided by incidence in control group
hazard ratio
relative risk at a specific time point
kaplan-meier curve
a graph comparing probability of the event (usually death) as time goes on
Blinding
an attempt at controlling bias by making participants (single blind) and observers (double blind) unaware of their treatment status
can also be double dummy if it is difficult to make the intervention and the placebo look similar (e.g. a patch vs. a pill)
confounding factor
a variable that affects the dependent variable/outcome but it is unaccounted for
intention to treat analysis
analysis of trial participants per the group they were allocated to irrespective of whether they completed treatment
per protocol analysis
analysis of trial participants excluding those who didn’t follow protocol
sensitivity
how good is a test at picking out people who have the disease
specificity
how good is a test at ruling out people who don’t have the disease
positive predictive value
following a positive test, what is the probability that the subject has the disease
type 1 error
rejecting the null hypothesis when it is actually true (false positive result)
type 2 error
accepting the null hypothesis when it’s actually false (false negative)
bias
systematic error that leads to deviation from the true value
types of bias
selection
publication
attrition bias
measurement (recall, response/non response, observer, Hawthorne)
what is evidence based medicine
the use of current best evidence in making decisions about the care of individual patients
what is shock
circulatory failure resulting in inadequate organ perfusion
- systolic BP < 90
- MAP < 65
- evidence of tissue hypotension (mottled skin, decreased urine output, serum lactate >2)
how to calculate MAP
cardiac output (stroke volume x HR) x systemic vascular resistance
causes of shock
Cardiac output
- hypovolaemia: bleeding, fluid loss e.g. vomiting + burns
- pump failure: cardiogenic shock e.g. ACS, arrythmias
Peripheral circulatory failure
- sepsis
- anaphylaxis
- neurogenic e.g. spinal cord injury
- endocrine: addison’s, hypothyroidsm
- drugs: anaesthetics, anti-hypertensives
BLS for the unconscious patient
Danger Response to voice and pain Shout for help Airway Breathing: 10s look for chest movement, listen for breath, feel for breath (feel carotid pulse) Call 2222 Start chest compressions: 30-2
unconscious patient management
A: stabilise c-spine if traumatic, maintain airway - manouvres, adjuncts
B: 15LO2, RR, ABG
C: bloods (toxins - alcohol, salicylate, paracetamol), cortisol, glucose, troponin etc.
D: glucose, pupils (overdose), GCS, neuro exam - localising lesion
E: temperature for seizure
what is septic shock
sepsis with hypotension despite adequate fluid resuscitation
when to consider ITU referral for septic patients?
BP<90, lactate > 4
when might anaphylactic reactions occur during hospital
blood transfusions
contrast imaging
medication administration
food exposure
how to manage hypovolaemic shock
raise legs
fluid bolus x 2 –> ICU referral
treat underlying cause
how to manage haemorrhagic shock
stop bleeding 2L crystallois crossmatch or request O-ve blood major haemorrhage protocol if >30% blood loss estimated liaise with seniors/haematologists FFP + red cells consider 2g IV tranexamic acid
what is sepsis
life threathening organ dysfunction due to dysregulated host response to infection
management of sepsis
A
B: oxygen, sputum sample, CXR, ABG (lactate)
C: BP, urine output + catheterise, urinalysis (source of infection), IV access, blood cultures, U+E, FBC, clotting, broad spectrum antibiotics, 2x fluid bolus
D: consciousness level, temperature
E: look for source of infection, rash, infected wounds; swab wounds, consider LP, ascitic tap, joint aspirate
what is anaphylaxis
Type 1 IGE mediated hypersensitivity reaction
management of anaphylaxis
Airway: most important, stop offending agent; manouvres, suction, adjuncts, consider intubation + senior help; IM adrenaline 0.5ml 1:1000 in anterolateral 1/3 of thigh; repeat every 5 mins
B: 15LO2
C: IV access 200mg hydrocortisone, fluid bolus over 15, chlorphenamine 10mg
second line: ICU admission –> IV adrenaline
consider nebulised adrenaline if wheezy
serum tryptase 1-6h; monitor ECG on wards, medic alert bracelet, self administered adrenaline (i.e. epipen)
overdose/poisoning
discuss with toxicology/toxbase
A: consider anaesthetist support to maintain airway (esp. if RR<8, PO2<8, GCS<8)
C: toxicology screen - urine and serum
CO:100% oxygen
benzodiazepine: IV flumazenil
warfarin: <8 + no bleed = withold, minor bleed +/or > 8 = stop warfarin + vit K, major bleed = stop warfarin, vitamin K + beriplex
paracetamol: n-acetylceisine
Hyperkalaemia definitions, ecg findings and management
K+> 6 or 5.5 with ECG changes
small p waves, slurred QRS, long PR, tented t
- cardiac protection (calcium chloride/gluconate)
- shift K+ into cells with salbutamol + insulin/dextrose
- remove k from: loop diuretic + calcium resonium
hypokalaemia definitions, ecg findings and management
<3.5
<2.5 is severe
no T waves, long PR, QT and depressed ST
mild: oral - sando K
severe IV potasium
