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Acute and Critical Care > Emergency Med > Flashcards

Emergency Med Flashcards

1
Q

What can you use to assess whether a trauma patient needs C spine imaging

A

Canadian C Spine Score

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2
Q

Nice guidance on CT head

A

GCS <13 on initial assessment
GCS <15 at 2hrs after injury
Suspected skull fracture (open or depressed)
Sign of basal skull fracture (e.g. Raccoon eyes/periorbial ecchymosis, CSF rhinorrhea, Battle Sign)
Post-traumatic seizure
Focal neuro deficit (vision, speech, poor power)
>1 vomiting episode since injury

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3
Q

Chart to assess burns surface area

A

Lund and Browder chart

or use rule of 9s.

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4
Q

Rule in burn area

A 
Rule of 9s.
Arm = 9%
Head = 9%
Leg = 18% each
Torso (front) = 18%
Torso (back) = 18%
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5
Q

Investigating a burn patient

A

Bloods - FBC, U+E, group + save + crossmatch, carboxyhemoglobin (CO poisoning), serum glucose.
CXR
Cardiac monitoring
Urine catheter

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6
Q

Antibiotic if blister from burn gets infected

A

7 days of flucloxacillin.

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7
Q

Calculation for fluid requirements in burn

A

Parkland formula.
4 mL/kg/%total body surface are.
Use crystalloid fluid - Hartmann’s 1%

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8
Q

Major thing to rule out in chest injury

A

Flail chest. When part of rib cage becomes broken off.
Will not contribute to rib expansion in breathing.
Pulmonary contusion.
Can puncture lung = pneumothorax.
O/E = in-drawing of chest on inspiration.

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9
Q

Reversible causes of a cardiac arrest

A 
Hypoxia
Hypovolaemia
Hypo/hyper-kalaemia
Hypothermia
H+/acidosis
Thrombosis (PE or in coronaries)
Tamponade
Toxins
Tension pneumothorax
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10
Q

How do you prepare for a patient coming in to resus

A

Assemble team (anaesthetics, nurse, ED doctor) and assign roles.
Prepare bed in resus with suitable anaesthetic machines, monitoring equipment.
Prepare equipment e.g. cannulas, fluids, masks.

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11
Q

Definition of status epilepticus

A

5mins or more of either continuous seizure activity or repetitive seizures without regaining consciousness

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12
Q

Treatment algorythm for status epilepticus

A

1) Buccal midazolam or rectal diazepam.
2) IV lorazepam.
3) IV phenytoin or diazepam infusion in 500ml of detrose if patient is already taking phenytoin.
4) Call for help from CCU/anaesthetics –> likely to RSI with thiopental.

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13
Q

Potential causes of status epilepticus

A 
Vascular - intracerebral haemorrhage
Infection - meningitis, sepsis.
Trauma - head injury
Metabolic - hypoxia
Iatrogenic - non adherence to epilepsy meds.
Neoplasm - cerebral tumour
Congenital - idiopathic epilepsy
Illicit drugs
Ecamplsia
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14
Q

Complications of prolonged fitting

A 
AKI from rhabdomyolysis
Hypoxia
Aspiration of gastric contents
Arrythmia
Cardiac arrest
Death
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15
Q

Management of alcohol withdrawal

A

Delirium tremens - Chlordiazepoxide + Pabrinex

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16
Q

Causes of sudden onset chest pain

A 
ACS/MI
Unstable angina
Aortic dissection
Panic attack
PE
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17
Q

Useful cardiac enzymes

A

Troponin I and T - levels rise in first 3-12hrs, peak at 24-48hrs and decrease by 14days.
Creatinine kinase - CK-MB most useful one in cardiac pts. Levels rise in 2-12hrs and return by 72hrs.

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18
Q

2 drugs for chest PAIN RELIEF

A

GTN

Morphine

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19
Q

Procedure for MI patients and time period to do it

A

Percutaneous coronary intervention + angiography.

Within 120mins of symptoms to prevent cardiac tissue death and improve outcome.

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20
Q

Alternative treatment of MI if ovr 120mins for PCI

A

Thrombolysis with alteplase / reteplase

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21
Q

5 CI for thrombolysis

A 
Pregnancy
Ischaemic stroke in last 6 months
Recent major trauma 
Recent major surgery 
Bleeding disorders
Known AV malformation
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22
Q

3 methods for assessing response to pain in GCS

A

Suprorbital notch pressure
Nailbed squeeze
Mandibular pressure

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23
Q

3 neuro, 3 metabolic, 3 drug causes of decrease consciousness

A 
Neuro = ischaemic stroke, head trauma, meningitis, raised ICP/tumour/abscess 
Metabolic = hypoxia, uraemic encephalopathy, hypoglycaemia, Addison's crisis/myxoedema
Drugs = opioid toxicity, serotonin syndrome, alcohol, benzodiazepines.
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24
Q

Opioid toxicity treatment and cautions to consider once given

A

Naloxone.
If long-acting opioid effects of Naloxone will wear off and pt will deteriorate again.
Opioid withdrawal effects.

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25
Q

Criteria for intubation and ventilation in head injury patients according to NICE

A

GCS <8/coma
Loss of protective laryngeal reflexes
Irregular resps
Ventilatory insufficiency on ABGs

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26
Q

Assessment of a major trauma patient

A

CABCDE with first C being:

catastrophic haemorrhage and c-spine immobilisation.

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27
Q

Life-threatening chest injuries

A 
Tension pneumothorax
Traumatic haemothorax
Cardiac tamponade
Flail chest
Aortic injury
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28
Q

Use of fluids in major trauma patients

A

Avoid lots of fluids as will help prevent mass bleeding out and dislodging any clots which may have formed.

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29
Q

Indications for whole body CT

A

Polytrauma with multiple suscpected injuries.

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30
Q

4 sources of bleeding

A

Thorax
Abdomen
Long bones
Pelvis

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31
Q

Lethal triad of trauma

A

Hypothermia
Acidosis
Coagulopathy

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32
Q

Dermatological changes in anaphylaxis

A

Urticaria = diffuse red, raised, blended and itchy rash.
Angio-oedema = lips, tongue, eyelid, hands and feet swelling.
Sweating

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33
Q

Respiratory, circulatory and cardiac changes in anaphylaxis

A 
Resp = wheeze, SOB, hoarse voice from laryngeal obstruction.
Circulatory = hypotensive, cyanotic, clammy, pale, delayed CRT.
Cardiac = tachycardia
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34
Q

Pathophysiology of anaphylaxis

A

Acute, severe and life-threatening type 1 IgE mediated hypersensitivity reaction.
Release of immune and inflammatory mediators causes increased vascular permeability, vasodilation and smooth muscle contraction.

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35
Q

Anaphylactoid reaction

A

Presentation similar to anaphylaxis but no degranulation and not IgE mediated.

36
Q

Treatment algorithm of anaphylaxis

A

1) A-E (oxygen support, IV access, warm crystalloids STAT)
2) IM adrenaline 0.5ml of 1:1000 solution.
3) IM Chlorphenamine (antihistamine)
4) IM Hydrocortisone
5) Nebulised salbutamol

37
Q

Pharmacology of adrenaline and adverse effects

A

Peripheral vasocontrictor but central (cardiac and skeletal muscle) vasodilator.
Positive chronotropic agent.
ADR - anxiety, palpitations, angina, headache, arrhythmia, HTN.

38
Q

Risk of sending an anaphylactic patient home when they are stable and recovered

A

Biphasic reaction
Occur in 20% of anaphylaxis
Symptoms reoccur after 72hrs, despite no exposure to allergen.

39
Q

Clinical findings of a DVT

A 
Calf swelling of >3cm compared to unaffected leg.
Localised pain in calf.
Calf erythema and warmth
Vein distension
Pitting oedema
ALL FINDINGS ARE UNILATERAL.
40
Q

Score to assess risk of VTE

A

Well’s Score
Includes:
Active cancer, immobilised recently, calf swelling >3cm, non-varicose superficial veins, local tenderness, pitting oedema, previous Hx of DVT, alternative diagnosis to DVT likely/unlikely.

41
Q

2 sites of paracetamol toxicity

A

LIVER - necrosis starts by 24hrs

Kidneys - acute tubular necrosis

42
Q

Why are serum paracetamol levels taken at 4hrs

A

Time needed for drug to be ingested and absorbed into circulation to give an accurate level of that in the body.

43
Q

Patients who are particularly at risk of liver damage after a paracetamol OD

A 
Malnourished or fasting patients
Pre-exisiting liver disease
HIV
Alcoholics
Those on hepatic-toxic medications e.g. rifampicin, carbamazepine
44
Q

When would you start n-acetylcysteine before the serum paracetamol level?

A 
Delayed presentation (taken drug 8hrs ago or more)
Staggered overdose
Patient is unconscious
45
Q

Blood tests in a paracetamol overdose

A 
INR + albumin
LFT
FBC
U+E
ABG 
BM
Serum paracetamol level.
46
Q

When do you use activated charcoal in paracetamol overdose

A

If the patient presents within 2-4hrs of the ingestion

47
Q

How do you decide the dose of n-acetylcycsteine

A

Plot the 4hr serum paracetamol level against the time on the relevant nomogram

48
Q

Alternative drug to n-acetylcystine

A

Methylamine

49
Q

Adverse effect of lots of 0.9% NaCl fluid

A

Hyperchloraemic metabolic acidosis

50
Q

What conditions must you inform the UK DVLA about?

A

Epilepsy (avoid driving for 1yr from date of last attack).
TIA or stroke - can’t drive for 1 month post attack.
Chronic neuro conditions e.g. MS, Parkinson’s, MND.
Severe mental health disorders.
Those with a pacemaker or ICD fitted.
Diabetics
Many more tbh 🙃🙃

51
Q

Name some types of shock and the pathophysiology

A

Hypovolaemia - circulatory volume depletion.
Cardiogenic - pump failure.
Distributive types: Due to inappropriate peripheral vasodilation.
Septic
Anaphylactic
Neurogenic

52
Q

What causes patients with shock to pop their cogs

A

Coagulopathy
Hypothermia
Metabolic acidosis and compensatory tachypnoea.

53
Q

Main organs at risk in shock

A

Kidney (acute tubular necrosis)
Lungs (acute respiratory distress syndrome)
Heart (MI)
Brain (coma/altered level of consciousness)

54
Q

Causes of hypovolaemia shock

A

Bleeding - ruptured AAA, trauma, upper GI bleed.

Fluid Loss - burn, vomiting, 3rd space loss in pancreatitis, cirrhosis.

55
Q

Causes of cardiogenic shock

A

ACS/MI, arrhythmia, aortic dissection, cardiac tamponade, tension pneumothorax, PE

56
Q

Causes of neurogenic shock

A

Spinal cord transection injury, spinal anaesthesia.

57
Q

Causes of endocrine shock

A

Arenal failure/Addisonian crisis

Myxedema.

58
Q

Definitions of sepsis and septic shock

A

Sepsis = life threatening organ dysfunction due to dysregulated host response to an infection. This organ dysfunction can be identified by SOFA greater or equal to 2 points.
Septic shock = sepsis with circulatory, cellular and metabolic abnormalities associated with increased risk of mortality. Identified with use of vasopressor medications to maintain MAP over 64mmHg or lactate >2 despite Rx.

59
Q

Signs of shock (common for all types)

A 
Hypotension
Tachycardia
Tachypnoea
Prolonged CRT and cool. extremities
Oligouria (<0.5ml/kg/hr)
Altered level of consciousness/confusion.
Pallor
60
Q

What is compensated and uncompensated hypovolaemic shock

A

3 stages of hypovolaemai shock =compensated, uncompensated, irreversible.

Compensated = activation of baroreceptors to low BP causes body to try and maintain higher BP --> increase HR, contractility and peripheral vasoconstriction. Release of vasopressin, renin and aldosterone.
Uncompensated = no vasomotor reflex, increased capillary permeability, lactic acidosis.
61
Q

Over-arching management of shock

A

A B C D E RESUSCITATION ‼️‼️

  • IV access - FBC, group + save/crossmatch, LFT, ABG!
  • High flow Oxygen (15L via non re-breathable mask)
  • Fluid bolus - 500ml of 0.9% normal saline STAT
  • Analgesia if in pain (pcm)
  • Catheter
62
Q

Management of cardiogenic shock

A
  • A-E: Oxygen!
    (Ix to include ECG, U+E, cardiac enzymes, NT-proBNP, ABG, CXR, echo, catheter + urine output)
  • Cardiac monitoring.
  • Arterial line.
  • Immediate FY1 Mx = 500mls 0.9% NaCl bolus, analgesia - morphine, GTN.
  • More specialist Rx = vasopressors e.g. phenylephrine, dobutamine.
63
Q

S+S of anaphylactic shock

A 
IgE medicated hypersensitivity reaction.
Itching
Sweating
D+V
Erythema
Urticaria
Angio-oedema of lips, tongue and eye-lids
Wheeze and cyanosis
Tachycardia and hypotension.
64
Q

What is chorphenamine

A

anti-histamine used in anaphylaxis

65
Q

Management of septic shock

A

A to E resus
SEPSIS 6 = ABG, blood cultures, Catheter + urine output, fluids (0.9% normal saline 500ml STAT), oxygen, ABx.

Ix to also do = FBC, CRP, U+E and creatinine, LFT, clotting screen (?DIC), urine dipstick, CXR and find source of infection.

Abx = piperacillin + tazobactam (tazosin).

66
Q

Red flag markers of sepsis

A 
SBP <90mmHg or a drop of 40mmHg from norm.
Heart rate >130bom
RR >25/min
Sats <90%
Urine output <30ml/hr
Lactate >2mmol/L
Altered mental state
Mottled appearance
Cyanosis of skin, lip or tongue
Non-blanching rash
67
Q

Definition of shock

A

Inadequate organ oxygenation due to circulatory failure. Decreased mean arterial pressure which can be caused by poor cardiac output (hypovolaemic/cardiogenic) or poor systemic vascular resistance (septic, anaphylactic, neuro) (MAP = cardiac output x resistance)

68
Q

Name some common triggers for anaphylaxis

A

Peanuts, eggs, sesame, bee sting, penicillin, IV contrast.

69
Q

Name a blood test you would do once you’ve stabilised an anaphylactic patient

A

Serum tryptase.
From mast cells (degranulation). Peak at 1hr after reaction and elevated for 6hrs post reaction.
Take further sample in follow-up appointment.

70
Q

Long-term follow up post anaphylaxis

A

Ensure no risk of biphasic reaction (72hrs).
Refer to allergy clinic.
EpiPen
Medical emergency identification bracelet.

71
Q

Risk factors for sepsis

A 
Indwelling lines or catheters
IVDU
Recent surgery
Elderly or infants
Chemotherapy, long-term steroids or other immunosuppressant medication.
Splenectomy
72
Q

Identifying sepsis

A

qSOFA = quick sepsis related organ failure assessment.
Altered mental state (GCS <15), fast resp rate (RR >22/min) and low BP (SBP <100mmHg).

SOFA = PaO2, GCS, MAP, use of vasopressor to maintain MAP, UOP, bilirubin, platelet count.

73
Q

A treatment for hypovolaemic shock due to haemorrhage

A

Resuscitative end-vascular balloon occlusion of the aorta. Balloon into aorta, inflation cuts blood supply above haemorrhage point. Only temporary measure.

74
Q

S+S of neurogenic shock

A

Injury to spinal cord + autonomic dysregulation. the autonomic changes cause loss of sympathetic tone to the heart and vasculature.
Cord injury = tenderness, weakness, sensory loss.
Autonomic dysfunction = bradyarrythmia, hypotension, flushing, warm skin.

75
Q

Management of neurogenic shock

A

Immobilse C-Spine
A-E resuscitation.
Fluid challenge with crystalloids.
Persistent hypotension = vasopressor/inotrope e.g. phenylephrine.

76
Q

Where can spinal cord injury occur to cause neurogenic shock

A

Heart innervation from T1-T5 (sympathetic) so needs be above T5.

77
Q

Fracture of middle cranial fossa.

A

Battle’s sign

78
Q

Define cyanosis

A

Bluish hue that occurs in the presence of ~60 g/L deoxyhaemoglobin.

79
Q 
Symptoms in
1. temporal lobe
2. frontal lobe
3. parietal lobe
4. occipital lobe
Seizures
A
  1. epigastric rising, lip smoking, grabbing, post-ical dysphasia and deja-vu.
  2. head and leg movements, posturing, post-ical weakness.
  3. paraesthesia
  4. floaters and flashes
80
Q

If there is autonomic disturbance where must the spinal cord lesion be

A

Above T6

81
Q

Differentiating features of a subarachnoid, subdural and extra-dural haemorrhage

A 
SAH = sudden occipital headache, spontaneous due to rupture of aneurysm. CT = star.
Subdural = old age and alcoholics. Slower onset of symptoms. Fluctuating consciousness and confusion. CT = midline shift and concave.
Extradural = acceleration-deceleration trauma. Lucid interval. CT = lemon shape.
82
Q

Mx of a burn

A
  • A-E assessment - gain good IV access, oxygen (esp carbon monoxide poisoning), catheterise.
  • Assess surface area of burn and calculate fluid replacement.
  • Parkland formula = 4 x weight (kg) x % burn. Hartmann’s solution.
  • Urgent bloods - group+save, U+E, clotting, carbosyhaemoglobin.
  • Saline soaked gauze.
  • Good analgesia (morphine).
  • Abx (flucloxacillin).
83
Q

Carbon monoxide poisoning

A

Heachache, dizzy, nausea, hoarse voice, harsh cough, stridor, inflamed oropharynx, MI, coma.
Ix = carboxyhemoglobin
Mx = high-flow oxygen, hyperbaric oxygen, analgesia and support.

84
Q

MI plus feeling of drowning

A

Flash pulmonary oedema - Rx with diuretics (furosemide).

85
Q

Prevent vasospasm in an SAH

A

Nimodipine

86
Q

Critical limb ischaemia in a young person who smokes…?

A

Buerger’s disease.

limb ischaemia + thrombophlebitis + raynaud’s

Acute and Critical Care (2 decks)

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