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Acute and Emergency Flashcards

1
Q

in acute bronchitis when should you prescribe antibiotics

A
  • in patients who:
    • are systemically very unwell
    • have pre-existing co-morbidities
    • have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
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2
Q

what antibiotics should you offer in acute bronchitis

A
  • doxycycline first-line
  • doxycycline cannot be used in children or pregnant women
  • alternatives include amoxicillin
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3
Q

how do you differentiate acute bronchitis from pneumonia on history and examination

A
  • History: Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.
  • Examination: No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze. Moreover, systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.
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4
Q

how do you treat acute pulmonary oedema

A
  • SODON
    • sit patient uo
    • oxygen
    • diuretics
    • opiates
    • nitrates
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5
Q

what are the criteria for diagnosing AKI

A
  • Rise in creatinine of 26µmol/L or more in 48 hours OR
  • >= 50% rise in creatinine over 7 days OR
  • Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) OR
  • >= 25% fall in eGFR in children / young adults in 7 days.
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6
Q

what are the different stages of AKI

A
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7
Q

management of AKI

A
  • careful fluid balance
  • review prescriptions
  • diuretics only if clinically overloaded
  • treat complications
    • hyperkalaemia, pulmonary oedema, acidosis or uraemia
  • if secondary to urinary obstruction then → prompt urology referral
  • referral to nephrology if AKI stage 3 or if cause not clear
  • referral for renal replacement therapy if AKI stage 3 or if complications aren’t responding to treatment
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8
Q

6 causes of hyperkalaemia

A
  • acute kidney injury
  • drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
  • metabolic acidosis
  • Addison’s disease
  • rhabdomyolysis
  • massive blood transfusion
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9
Q

ecg findings of hyperkalaemia

A

tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole

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10
Q

5 causes of intrinsic AKI

A
  • glomerulonephritis
  • acute tubular necrosis (ATN)
  • acute interstitial nephritis (AIN), respectively
  • rhabdomyolysis
  • tumour lysis syndrome
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11
Q

5 common drugs that cause hyperkalaemia

A

potassium sparing diuretics,

ACE inhibitors,

angiotensin 2 receptor blockers,

ciclosporin,

heparin

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12
Q

how do you classify hyperkalaemia

A
  • mild: 5.5 - 5.9 mmol/L
  • moderate: 6.0 - 6.4 mmol/L
  • severe: ≥ 6.5 mmol/L
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13
Q

management of hyperkalaemia

A
  • Stabilisation of the cardiac membrane
    • IV calcium gluconate
      • does NOT lower serum potassium levels
  • Short-term shift in potassium from extracellular (ECF) to intracellular fluid (ICF)
    compartment
    • combined insulin/dextrose infusion
    • nebulised salbutamol
  • Removal of potassium from the body
    • calcium resonium (orally or enema)
    • enemas are more effective than oral as potassium is secreted by the rectum
    • loop diuretics
    • dialysis
      • haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia
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14
Q

what are the adrenaline doses in anaphylaxis depending on age

A

REPEAT EVERY 5 MINUTES IF NECESSARY

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15
Q

Where do you inject IM adrenaline in anaphylaxis

A

anterolateral aspect of the middle third of the thigh.

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16
Q

what is refractory anaphylaxis and what should you do

A
  • defined as respiratory and/or cardiovascular problems persist despite 2 doses of IM adrenaline
  • IV fluids should be given for shock
  • expert help should be sought for consideration of an IV adrenaline infusion
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17
Q

management of a patient who had anaphylaxis but is now stabilized

A
  • non-sedating oral antihistamines can be given following stabilisation in patients with persisting skin symptoms (urticaria and/or angioedema)
  • sometimes it can be difficult to establish whether a patient had a true episode of anaphylaxis. Serum tryptase levels are sometimes taken in such patients as they remain elevated for up to 12 hours following an acute episode of anaphylaxis
  • all patients with a new diagnosis of anaphylaxis should be referred to a specialist allergy clinic
  • an adrenaline auto-injector should be givens an interim measure before the specialist allergy assessment (unless the reaction was drug-induced)
  • patients should be prescribed 2 adrenaline auto-injectors
  • training should be provided on how to use it
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18
Q

why do you need to risk stratify discharge of anaphylaxis patients

A

20% can have a biphasic reaction

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19
Q

how do you risk stratify the discharge of patients who have had anaphylaxis

A
  • fast-track discharge (after 2 hours of symptom resolution):
    • good response to a single dose of adrenaline
    • complete resolution of symptoms
    • has been given an adrenaline auto-injector and trained how to use it
  • minimum 6 hours after symptom resolution
    • 2 doses of IM adrenaline needed, or
    • previous biphasic reaction
  • minimum 12 hours after symptom resolution
    • severe reaction requiring > 2 doses of IM adrenaline
    • patient has severe asthma
    • possibility of an ongoing reaction (e.g. slow-release medication)
    • patient presents late at night
    • patient in areas where access to emergency access care may be difficult
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20
Q

what are the 4Hs and 4Ts of reversible causes of cardiac arrest

A
  • Hs
    • Hypoxia
    • Hypovolaemia
    • Hypo-/hyperkalaemia/ metabolic
    • Hypo/hyperthermia
  • Ts
    • Thrombosis – coronary or pulmonary
    • Tension pneumothorax
    • Tamponade – cardiac
    • Toxins
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21
Q

when do you give adrenaline in ALS

A
  • adrenaline 1 mg IV/IO as soon as possible for non-shockable rhythms
  • for shockable rhythms, adrenaline 1 mg IV/IO is given once chest compressions have restarted after the third shock
  • repeat adrenaline 1mg IV/IO every 3-5 minutes whilst ALS continues
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22
Q

when should you use thrombolytic drugs in ALS

A
  • should be considered if a pulmonary embolus is suspected
  • if given, CPR should be continued for an extended period of 60-90 minutes
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23
Q

when do you give amiodarone in ALS

A
  • amiodarone 300 IV/IO mg should be given to patients who are shockable after 3 shocks have been administered.
  • a further dose of amiodarone 150 mg IV/IO should be given to patients who are shockable after 5 shocks have been administered
  • don’t give to unshockable patients
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24
Q

what is the most common cause of an infective exacerbation of COPD

A
  • Haemophilus influenzae
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25
Q

management of acute exacerbation of COPD

A
  • increase frequency of bronchodilator use and consider giving via a nebuliser
  • give prednisolone 30 mg daily for 5 days
  • oral antibiotics only if sputum is purulent or there are clinical signs of pneumonia
  • one of the following oral antibiotics first-line:
    • amoxicillin
    • clarithromycin
    • doxycycline.
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26
Q

DVT management if the wells score is >2

A
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27
Q

DVT management if the wells score is 1 or below

A
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28
Q

what’s included in the wells score for DVT

A
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29
Q

what are the maintenance requirements for IV fluids

A
  • 25-30 ml/kg/day of water and
  • approximately 1 mmol/kg/day of potassium, sodium and chloride and
  • approximately 50-100 g/day of glucose to limit starvation ketosis
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30
Q

what are the diagnostic criteria for DKA

A
  • glucose > 11 mmol/l or known diabetes mellitus
  • pH < 7.3
  • bicarbonate < 15 mmol/l
  • ketones > 3 mmol/l or urine ketones ++ on dipstick
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31
Q

what is the insulin and dextrose req for patients in DKA

A
  • an intravenous infusion should be started at 0.1 unit/kg/hour
  • once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started
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32
Q

management of DKA

A
  • fluid replacement
    • most patients with DKA are deplete around 5-8 litres
  • insulin
    • an intravenous infusion should be started at 0.1 unit/kg/hour
    • once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started
  • correction of electrolyte disturbance
    • serum potassium is often high on admission
    • this often falls quickly following treatment with insulin resulting in hypokalaemia
    • potassium may therefore need to be added to the replacement fluids
    • if rate of potassium infusion is >20 mmol/hour then they need cardiac monitoring
  • their long-acting insulin should be continued and short-acting insulin should be stopped
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33
Q

when should you consider adding back potassium in patients being treated for DKA

A
  • 40mmol of K+ should be added to one litre of normal saline and given to patients being treated for DKA whose K+ is in the 3.5-5.5 range
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34
Q

how do you define DKA resolution

A
  • pH >7.3 and
  • blood ketones < 0.6 mmol/L and
  • bicarbonate > 15.0mmol/L
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35
Q

what is the antidote to benzodiazepine overdose

A

Flumazenil

rarely used due to risk of seizures and since benzo overdose can normally be managed with supportive care

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35
Q

what is the antidote to benzodiazepine overdose

A

Flumazenil

rarely used due to risk of seizures and since benzo overdose can normally be managed with supportive care

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36
Q

management of lithium toxicity

A
  • mild-moderate toxicity may respond to volume resuscitation with normal saline
  • haemodialysis may be needed in severe toxicity
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37
Q

what is the antidote to heparin

A

protamine sulphate

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38
Q

management of carbon monoxide poisoning

A
  • 100% oxygen
  • hyperbaric oxygen
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39
Q

antidote to cyanide

A

Hydroxocobalamin

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40
Q

presentation of tricyclic antidepressant overdose

A
  • Early features relate to anticholinergic properties:
    • dry mouth
    • dilated pupils
    • agitation
    • sinus tachycardia
    • blurred vision
  • Features of severe poisoning include:
    • arrhythmias
    • seizures
    • metabolic acidosis
    • coma
  • ECG changes include:
    • sinus tachycardia
    • widening of QRS
    • prolongation of QT interval
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41
Q

what is the first line management for arrhythmias caused by tricyclic antidepressants

A
  • IV bicarbonate if there’s widening of the QRS interval >100 msec or a ventricular arrhythmia
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42
Q

what acid base abnormality is caused by salicylate overdose

A
  • salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis
  • Early stimulation of the respiratory centre leads to a respiratory alkalosis
  • Later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis.
43
Q

features of salicylate overdose

A
  • hyperventilation (centrally stimulates respiration)
  • tinnitus (one of earliest symptoms)
  • lethargy
  • sweating, pyrexia
  • nausea/vomiting
  • hyperglycaemia and hypoglycaemia
  • seizures
  • coma
44
Q

management of salicylate overdose

A
  • general (ABC, charcoal)
  • urinary alkalinization with intravenous sodium bicarbonate - enhances elimination of aspirin in the urine
  • haemodialysis
45
Q

indications for liver transplant following paracetamol overdose

A
  • Arterial pH < 7.3, 24 hours after ingestion
  • or all of the following:
    • prothrombin time > 100 seconds
    • creatinine > 300 µmol/l
    • grade III or IV encephalopathy
46
Q

management of paracetamol overdose

A
  • if within one hour of ingestion then charcoal
  • N-acetyl cysteine regardless of plasma paracetamol concentration if:
    • staggered overdose
    • ambiguity over time of dose
  • Otherwise plot plasma paracetamol concentration on graph with treatment line and treat with NAC if above this line
  • infuse NAC over one hour (rather than 15 minutes) to avoid (common) anaphylactoid reactions
    • anaphylactoid reactions to NAC are treated by stopping the infusion and starting at a lower dose
47
Q

management of status epilepticus

A
  • ABC
    • airway adjunct
    • oxygen
    • check blood glucose
  • First-line drugs are IV benzodiazepines
    • in the prehospital setting PR diazepam or buccal midazolam may be given
    • in hospital IV lorazepam is generally used. This may be repeated once after 10-20 minutes
  • If ongoing (or ‘established’) status it is appropriate to start a second-line agent such as phenytoin or phenobarbital infusion
  • If no response (‘refractory status’) within 45 minutes from onset, then the best way to achieve rapid control of seizure activity is induction of general anaesthesia.
48
Q

what is the definition of status epilepticus

A
  • a single seizure lasting >5 minutes, or
  • >= 2 seizures within a 5-minute period without the person returning to normal between them
49
Q

what is the classic presentation of a extradural haemorrhage

A
  • a patient who initially loses, briefly regains and then loses again consciousness after a low-impact head injury.
  • The brief regain in consciousness is termed the ‘lucid interval’ and is lost eventually due to the expanding haematoma and brain herniation.
  • As the haematoma expands the herniation causes the patient to develop a fixed and dilated pupil due to the compression of the parasympathetic fibers of the third cranial nerve.
50
Q

extradural haemorrhage is commonly caused by damage to which artery

A

middle meningeal artery

51
Q

clinical features of hyperosmotic hyperglycaemic state

A
  • General: fatigue, lethargy, nausea and vomiting
  • Neurological: altered level of consciousness, headaches, papilloedema, weakness
  • Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
  • Cardiovascular: dehydration, hypotension, tachycardia
52
Q

how do you diagnose hyperglycaemic hyperosmotic state

A
    1. Hypovolaemia
    1. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
    1. Significantly raised serum osmolarity (> 320 mosmol/kg)
  • Note: A precise definition of HHS does not exist, however the above 3 criteria are helpful in distinguishing between HHS and DKA. It is also important to remember that a mixed HHS / DKA picture can occur.
53
Q

how do you differentiate between hyperosmotic hyperglycaemic state and DKA

A
  • there’s no acidosis in HSS
  • the history is longer in HSS
54
Q

if serum osmolality is not available how can you estimate it

A

2 x Na+ + glucose + urea

55
Q

management of hyperosmotic hyperglycaemic state

A
  • aggressive fluid replacement
  • aim to replace 50% of estimated fluid loss within the first 12 hours (they could be down up to 10-22 litres)
  • use 0.9% saline but if osmolality isn’t coming down with this then use 0.045%
  • glood glucose should come down with fluid replacement
  • DO NOT use insulin unless there is significant ketonaemia as too sudden a reduction in osmolality could cause central pontine myelinolysis as well as cause cardiovascular crash
  • potassium should be replaced or omitted as required
56
Q

what is the BNF recommendation for abx therapy in each of these settings

A
57
Q

what is the site on the body most commonly affected by necrotising fasciitis

A

perineum

58
Q

management of necrotising fasciitis

A
  • urgent surgical referral debridement
  • intravenous antibiotics
59
Q

risk factors for non-accidental injury

A
  • Delayed presentation
  • Delay in attaining milestones
  • Lack of concordance between proposed and actual mechanism of injury
  • Multiple injuries
  • Injuries at sites not commonly exposed to trauma
  • Children on the at risk register
60
Q

in GP how do you decide whether someone with pneumonia should go to hospital or not

A
  • CRB65 gives risk of death
  • 0: low risk (less than 1% mortality risk)
    • treat at home
  • 1 or 2: intermediate risk (1-10% mortality risk)
    • consider hospital assessment
  • 3 or 4: high risk (more than 10% mortality risk)
    • urgent admission to hospital
  • you can also use CRP
    • CRP < 20 mg/L - do not routinely offer antibiotic therapy
    • CRP 20 - 100 mg/L - consider a delayed antibiotic prescription
    • CRP > 100 mg/L - offer antibiotic therapy
61
Q

how do you decide how to treat community acquired pneumonia in hospital

A
  • CURB65 score:
    • 0 or 1 - low risk
      • 5 day course of amoxicillin
        • tetracycline or erythromycin if pen allergic
    • 2 - moderate risk
      • 7 days of amoxicillin.and a macrolide
    • 3 or more - high risk
      • consider ITU admission
      • piperacillin with tazobactam and erythromycin for 7 days
62
Q

how can you advise patients with pneumonia that their symptoms will resolve and what is the follow up

A

All cases of pneumonia should have a repeat chest X-ray at 6 weeks after clinical resolution to ensure that the consolidation has resolved and there is no underlying secondary abnormalities

63
Q

what is catamenial pneumothorax and how common is it

A

it is the cause of 3-6% of pneumothorax and only occurs in menstruating women

thought to be caused by endometriosis within the thorax

64
Q

how do you manage primary pneumothorax

A
  • if the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
  • otherwise, aspiration should be attempted
  • if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
65
Q

how do you manage secondary pneumothorax

A
  • if the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.
  • otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours
  • if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours
66
Q

discharge advice following pneumothorax

A
  • stop smoking
    • massively reduces risk of recurrence
  • fitness to fly
    • absolutely contraindicated until one week post check x ray that finds no residual air
  • scuba diving
    • Diving should be permanently avoided
    • unless the patient has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postoperatively
67
Q

draw the adult als algorithm

A
68
Q

what is the bradycardia algorithm

A
69
Q

what is the adult tachycardia algorithm

A
70
Q

what is a two level PE wells score and what is included and what does the score mean

A
71
Q

management of PE if two level wells score is 4 or above

A
  • PE likely
    • arrange an immediate computed tomography pulmonary angiogram (CTPA)
    • If there is a delay in getting the CTPA then interim therapeutic anticoagulation should be given until the scan is performed.
      • this means a direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban
  • if the CTPA is positive then a PE is diagnosed
  • if the CTPA is negative then consider a proximal leg vein ultrasound scan if DVT is suspected
72
Q

what is the management if the two level wells pe score is less than 4

A
  • DVT unlikely
  • arranged a D-dimer test
    • if positive arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give interim therapeutic anticoagulation until the scan is performed
    • if negative then PE is unlikely - stop anticoagulation and consider an alternative diagnosis
73
Q

ecg changes with PE

A
  • the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. However, this change is seen in no more than 20% of patients
  • right bundle branch block and right axis deviation are also associated with PE
  • sinus tachycardia may also be seen
74
Q

when should you initiate sepsis 6

A
  • if any of the following red flags are present
    • Responds only to voice or pain/ unresponsive
    • Acute confusional state
    • Systolic B.P <= 90 mmHg (or drop >40 from normal)
    • Heart rate > 130 per minute
    • Respiratory rate >= 25 per minute
    • Needs oxygen to keep SpO2 >=92%
    • Non-blanching rash, mottled/ ashen/ cyanotic
    • Not passed urine in last 18 h/ UO < 0.5 ml/kg/hr
    • Lactate >=2 mmol/l
    • Recent chemotherapy
75
Q

features of cauda equina syndrome

A
  • low back pain
  • bilateral sciatica
    • present in around 50% of cases
  • reduced sensation/pins-and-needles in the perianal area
  • decreased anal tone
    • it is good practice to check anal tone in patients with new-onset back pain
    • however, studies show this has poor sensitivity and specificity for CES
  • urinary dysfunction
    • e.g. incontinence, reduced awareness of bladder filling, loss of urge to void
    • incontinence is a late sign that may indicate irreversible damage
76
Q

what is the investigation and management of cauda equina

A
  • Investigation
    • urgent MRI
  • Management
    • surgical decompression
77
Q

what is the management of neoplastic spinal cord compression

A
  • high-dose oral dexamethasone
  • urgent oncological assessment for consideration of radiotherapy or surgery
78
Q

what is the presentation of lumbar spinal stenosis

A

a combination of back pain, neuropathic pain and symptoms mimicking claudication.

One of the main features that may help to differentiate it from true claudication in the history is the positional element to the pain. Sitting is better than standing and patients may find it easier to walk uphill rather than downhill.

79
Q

how do you diagnose and treat lumbar spinal stenosis

A
  • MRI
  • laminectomy
80
Q

what causes toxic shock syndrome

A

staphylococcal exotoxins, the TSST-1 superantigen toxin

81
Q

absolute contraindications to thrombolysis in ischaemic stroke

A
  • More than 4.5 hrs since symptom onset
  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Brain tumour
  • Suspected subarachnoid haemorrhage
  • Stroke or traumatic brain injury in preceding 3 months
  • Lumbar puncture in preceding 7 days
  • GI bleed in preceding 3 weeks
  • Active bleeding
  • Pregnancy
  • Oesophageal varices
  • Uncontrolled hypertension >200/120mmHg
82
Q

what are the criteria for the four different classifications of stroke in the bamford stroke classification

A
83
Q

what scoring system can you use to assess for stroke and what is included

A
84
Q

what investigation if you suspect stroke and what will it show

A
  • non-contrast CT scan
    • acute ischaemic strokes
      • may show areas of low density in the region of the stroke. These changes may take time to develop
      • other signs include the ‘hyperdense artery’ sign corresponding with the responsible arterial clot - this tends to visible immediately
    • acute haemorrhagic strokes
      • typically show areas of hyperdense material (blood) surrounded by low density (oedema)
85
Q

Management of acute ischaemic stroke

A
  • A→E (exclude hypoglycaemia)
  • CT → exclude haemorrhage
  • 300mg aspirin stat
  • Thrombolysis
    • if haemorrhage excluded
    • if within 4.5 hrs
    • if not contraindicated
  • Thrombectomy
    • as well as thrombolysis
    • depending on location of clot as identified by CTA or MRA
      • Proximal anterior circulation
        • within 6hrs
        • or within 24 if CT perfusion or diffusion weighted MRI reveals that there’s a limited infarct core (i.e lots of brain to save)
      • Proximal posterior circulation (i.e basilar or PCA)
        • within 24hrs
        • consider only if imaging shows a limited infarct core
  • carotid endarterectomy if:
    • patient has suffered stroke or TIA in the carotid territory and are not severely disabled
    • AND stenosis is >70%
86
Q

when should you lower blood pressure following acute ischaemic stroke and how

A
  • patients for thrombectomy need BP of 185/110mmHg or lower
  • otherwise only lower blood pressure if there’s one of the following:
    • Hypertensive encephalopathy
    • Hypertensive nephropathy
    • Hypertensive cardiac failure/myocardial infarction
    • Aortic dissection
    • Pre-eclampsia/eclampsia
  • this is because high blood pressure helps with collateral blood flow to infarcted regions
  • if you’re going to lower it use labetalol and lower it slowly (i.e. 15% over first 24hrs)
87
Q

supportive management following stroke

A
  • Don’t lower BP in acute phase unless there are complications
    • Hypertensive encephalopathy
    • Hypertensive nephropathy
    • Hypertensive cardiac failure/myocardial infarction
    • Aortic dissection
    • Pre-eclampsia/eclampsia
  • swallow assessment within 24hrs
    • unsafe swallow
      • NG tube
      • convert medicine
    • safe swallow
      • oral hydration preferable to IV
88
Q

secondary prevention following acute ischaemic stroke

A
  • clopidogrel
  • aspirin plus MR dipyridamole if clopidogrel is contraindicated or not tolerated
  • MR dipyridamole alone is recommended only if aspirin AND clopidogrel are contraindicated or not tolerated

NO LIMIT FOR TREATMENT DURATION

89
Q

Investigating SAH

A
  • CT head
    • missed 7% SAH
  • Lumbar puncture
    • Used to confirm SAH if CT is negative.
    • performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown).
    • As well as xanthochromia, CSF findings consistent with subarachnoid haemorrhage include a normal or raised opening pressure
  • Referral to neurosurgery to be made as soon as SAH is confirmed
  • after confirmation of SAH do CT intracranial angiogram to identify cause (e.g. aneurysm or AVM)
90
Q

management of SAH

A
  • The treatment in spontaneous SAH depends on cause
  • Intracranial aneurysms require prompt intervention, preferably within 24 hours
  • Most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
  • Until the aneurysm is treated, the patient should be kept on strict bed rest, well-controlled blood pressure and should avoid straining in order to prevent a re-bleed of the aneurysm
  • Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature) and treated with hypervolaemia, induced-hypertension and haemodilution
  • Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt
91
Q

complications of SAH

A
  • Re-bleeding
    • happens in around 10% of cases and most common in the first 12 hours
    • if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged
    • associated with a high mortality (up to 70%)
  • Vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
  • Hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
92
Q

how do acute subdurals and chronic subdurals differ

A
  • acute subdurals often have a traumatic cause
  • chronic often have several week to month progressive history of either confusion, reduced consciousness or neurological deficit
    • alcoholics and elderly are particularly vulnerable
  • on CT acute will appear hyperdense (bright) in comparison to the brain
  • on CT chronic subdurals are hypodense (dark) compared to the substance of the brain
93
Q

what are the features of toxic shock syndrome

A
  • ever: temperature > 38.9ºC
  • hypotension: systolic blood pressure < 90 mmHg
  • diffuse erythematous rash
  • desquamation of rash, especially of the palms and soles
  • involvement of three or more organ systems: e.g. gastrointestinal (diarrhoea and vomiting), mucous membrane erythema, renal failure, hepatitis, thrombocytopenia, CNS involvement (e.g. confusion)
94
Q

what causes toxic shock syndrome

A

taphylococcal exotoxins, the TSST-1 superantigen toxin

95
Q

what is non-haemolytic febrile reaction to blood products and how do you treat it?

A

Non-haemolytic febrile reaction

Thought to be caused by antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cell during storageFever, chills

Red cell transfusion (1-2%)
Platelet transfusion (10-30%)Slow or stop the transfusion

Paracetamol

Monitor

96
Q

what is acute haemolytic reaction to transfusion products and how do you treat it?

A

Acute haemolytic reaction

ABO-incompatible blood e.g. secondary to human errorFever, abdominal pain, hypotension

Stop transfusion

Confirm diagnosis

  • check the identity of patient/name on blood product
  • send blood for direct Coombs test, repeat typing and cross-matching

Supportive care

  • fluid resuscitation
97
Q

what is transfusion associated circulatory overload and how do you treat it

A

Transfusion-associated circulatory overload (TACO)

Excessive rate of transfusion, pre-existing heart failurePulmonary oedema, hypertensionSlow or stop transfusion

Consider intravenous loop diuretic (e.g. furosemide) and oxygen

98
Q

what is transfusion related acute lung injury and how do you treat it?

A

Transfusion-related acute lung injury (TRALI)

Non-cardiogenic pulmonary oedema thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated bloodHypoxia, pulmonary infiltrates on chest x-ray, fever, hypotensionStop the transfusion

Oxygen and supportive care

99
Q

how can you differentiate TACO from TRALI

A
  • in transfusion related acute lung injury there is hypotension
  • whereas in transfusion related circulatory overload there is hypertension
100
Q

what is the diagnostic criteria for STEMI

A
  • clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
    • ≥ 2.5 small squares ST elevation in leads V2-3 in men under 40 years, or ≥ 2 small squares ST elevation in leads V2-3 in men over 40 years
    • 1.5 mm ST elevation in V2-3 in women
    • 1 mm ST elevation in other leads
    • new LBBB (LBBB should be considered new unless there is evidence otherwise)
101
Q

Once a STEMI has been confirmed the first step is to immediately assess eligibility for coronary reperfusion therapy. what are the two types of coronary reperfusion therapy?

A
  • percutaneous coronary intervention
    • should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
    • if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
    • drug-eluting stents are now used. Previously ‘bare-metal’ stents were sometimes used but have higher rates of restenosis
    • radial access is preferred to femoral access
  • fibrinolysis
    • should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given
    • a practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) that does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. If the patient’s ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI
102
Q

what antiplatelets do patients need before PCI

A
  • this is termed ‘dual antiplatelet therapy’, i.e. aspirin + another drug
  • if the patient is not taking an oral anticoagulant: prasugrel
  • if taking an oral anticoagulant: clopidogrel
103
Q

how do you check effectiveness of stemi managment after fibrinolysis

A

they need en ecg 60-90 minutes after fibrinolysis which should show resolution of ST elevation

if it doesn’t then they’re for PCI

104
Q

management of NSTEMI summary

A
105
Q

which patients with unstable angina/NSTEMI should have coronary angiography/PCI and when should they have it

A
  • immediate: patient who are clinically unstable (e.g. hypotensive)
  • within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk

Finals (19 decks)

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