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Emergency Medicine Flashcards

1
Q

Neuroepileptic Malignant Syndrome

A

Caused by medications that block dopamine transmission, e.g. risperidone. Fever, rigidity, mental status changes, and autonomic instability. Severe rigidity: profound creatine kinase (CK) elevation.

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2
Q

Medication overdose causing wide QRS?

A

Tricyclic antidepressants e.g. amitryptilline

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3
Q

Describe the algorithm for VF/ pulseless VT

A

CPR - shock (4J/kg) - 2 min CPR - shock + adrenaline (after 2nd shock and then every 2nd shock i.e. 2,4,6,8) - 2 min CPR - shock + amiodarone (after 3rd shock) Note: in non-shockable arrest (PEA/asystole), adrenaline is given immediately, and then every 2nd loop i.e. 1,3,5,7,9 Re-commence CPR after every shock, then assess rhythm after next 2 minutes i.e. if revert to sinus rhythm after shock, still need to give further 2 min CPR (as myocardial muscle is in refractory state and can easily revert back to VF) - don’t need to do this is signs of life are present

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4
Q

If the onset of VF/pulseless VT is witnessed on an ECG monitor then what is the next step?

A
  • Defibrillation (asynchronous shock) should be attempted before any other treatment. However, if unmonitored, or unable to get defib within 30 seconds then start CPR - Don’t use precordial thump (usually for sudden VF) in children
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5
Q

When might you use 3 shocks?

A
  • Where a patient with a perfusing rhythm suddenly develops a shockable rhythm in a witnessed and monitored setting, defib is immediately available, and they were previously well perfused and oxygenated pre-arrest. - Should not take >30 seconds to deliver all 3 shocks
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6
Q

What are the CPR ratios for: newborn, child, adult, lay person

A
  • Newborn 3:1 - Child 15:2 - Adult 30:2 - Lay person 30:2
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7
Q

After the initiation of CPR, when do the coronary arteries start perfusing?

A

After the 5th compression (aortic pressure increases, RA pressure stays the same)

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8
Q

What are the 4 Hs + Ts of cardiac arrest?

A
  • Hypoxia, hypovolaemia hypo/hyperkalaemia, hypothermia - Thrombosis, tension pneumothorax, tamponade, toxins
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9
Q

What are the main causes of asystolic arrest?

A

Hypoxia and hypovolaemia

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10
Q

What are the main causes of PEA (rare, usually go into asystole)?

A

Hypovolaemia, hyper/hypokalemia, tamponade, thrombosis

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11
Q

What are the main causes of VF?

A

Hypothermia/hyperthermia, toxins (TCA poisoning), underlying cardiac disease

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12
Q

What is the dose of adrenaline for anaphylaxis?

A

0.01ml/kg of 1:1000 IM adrenaline (IV = 0.1ml/kg of 1:10,000) = 10mcg/kg (always count 5 x zeros)

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13
Q

What is the most common cardiac cause of sudden collapse?

A

Dilated cardiomyopathy

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14
Q

What are the causes of sudden, unexplained cardiac death?

A
  • Congenital - hypertrophic CM, long QT, WPW, Brugada, Marfans, congenital CA abnormalities - Acquired - commotio cordis, drug abuse, myocarditis - Either: dilated CM, restrictive CM
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15
Q

What is commotio cordis?

A

Sudden death due to VF may occur when a projectile strikes the precordium of an individual with no underlying cardiac disease. One of the leading cuases of sudden cardiac death in young athletes (exceeded only by HOCM).

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16
Q

What is the formula for: - ETT size cuffed - ETT size uncuffed - ETT measurement at lip - ETT measurement at nose

A
  • age/4+3 - age/4+4 - ETT size x 3, age/2 + 12 - age/2 +15
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17
Q

What is the formula for estimating weight?

A

(age + 4) x 2

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18
Q

What is the dose for DC shock?

A

4J/kg

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19
Q

What is the management for a scaphoid fracture?

A

Short arm plaster with thumb spica

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20
Q

What injuries would you backslab?

A
  • Non-displaced fractures, minor injuries, swelling, crsuh, open fracture. - Risk of ischaemic contractures with full plasters (Volkmann’s ischaemic contracture) - should only be used for displaced fractures to maintain reduction
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21
Q

What are the clinical signs and managmeent of a scaphoid fracture?

A
  • Pain on dorsiflexion of the wrist, tenderness in snuffbox, pain on gripping. - Can have normal x-rays first few days - treat all with below elbow POP with thumb spica, remove if normal x-ray at 2 weeks - Complications: avascular necrosis (of prox segment) and non-union
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22
Q

Describe the anatomy surrounding a supra-condylar fracture

A
  • Above elbow = brachial artery, below elbow = radial and ulnar artery - Median and radial nerves most likely affected (ulnar nerve runs posterior to elbow joint)
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23
Q

Describe the nerve innervation of the hand

A
  • Radial nerve - posterior thumb, 2 + 3rd finger to level of PIPJ - Ulnar nerve - ant and posterior 1/2 of 4th + 5th finer - Median nerve - ant hand thumb to 1/2 of 4th finger, back of hand top of 2+3rd fingers
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24
Q

What nerve is injured in a wrist drop?

A
  • Radial nerve palsy - supplies triceps + extensor muscles of the forearm - From spooning, crutches, Saturday night palsy
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25
Q

What sign on x-ray is suspcious for a supracondylar fracture?

A

Posterior fat pad on x-ray indicates bleeding into joint capsule - sail sign - lifts fat pad upwards/becomes more visible. Anterior fat pad is normal.

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26
Q

What is a monteggia’s injury, and what is the management?

A
  • Proximal ulnar fracture and radial head dislocation - Refer to ortho - needs reduction
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27
Q

What is a galleazi injury, and what is the management?

A
  • Distal radius fracture (at wrist) and ulnar dislocation - Refer to ortho
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28
Q

What is the order of ossification in the elbow joint?

A

CRITOE - Capitellum - Radial head - Internal (medial) epicondyle (often avulsed in children) - Trochlear - Olecranon -External (lateral) epicondyle

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29
Q

What is the normal retropharyngeal space appearance on lateral neck x-ray?

A
  • At C2 <1/2 AP diameter of vertebral body - At C6 < full width
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30
Q

Describe a hangman’s fracture

A
  • Fracture C2 pedicles, ant subluxation C2 on C3 - Due to hyperextension of neck e.g. hitting face on windscreen in MVA - Unstable fracture, risk of cord injury
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31
Q

What is a Jefferson fracture?

A
  • Compression fracture of the bony ring of C1 - Unstable - Due to diving into pool/blow to vertex head
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32
Q

Describe the Salter Harris Classification

A

1 - physis (through growth plate) 2 - physis + metaphysis (most common) 3 - physis + epiphysis 4 -physis + metaphysis + epiphysis 5 - crush of physis 80% are 1 or 2 3, 4, 5 - may result in growth disturbance as epiphysis is involved Dsipalced 3 + 4 may require ORIF

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33
Q

SUFE appearance on x-ray?

A

Superior border of prox femoral epiphysis will lie on Klein’s line (line along femoral neck), when it should be higher

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34
Q

Describe Osgood-Schlatter’s disease

A
  • Normal radiology - Traction aphophysis - Osteochondritis of tibial tubercle where patellar tendon inserts - Painful, worse with activity and kneeling
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35
Q

Describe perthes disease

A
  • Osteonecrosis of the femoral head due to ischaemia - Abnormal moth-eaten femoral head - Increased risk with thrombophilia, infection, trauma - M>F, increased risk age 4-8y, bilat in 10% - Pain groin, thigh, knee - Tx: cast or surgery, maintain head in acetabulum
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36
Q

Describe osteoid osteoma

A
  • Benign bone tumour - X-ray: new bone formation, occassionally lucent spot
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37
Q

Osteomyelitis vs. septic arthritis

A
  • OM: more vague history, consider if unexplained fever, irritability, assymetrical use of limb. Most commonly tibia and femur. X-ray abnormalities in 7-10 days - Septic arthritis: may be vague history of trauma, surgerical emergency in hip (pus causes AVN), not usually associated with swelling or limb tenderness
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38
Q

What is an eschar and when does it bleed?

A
  • Dead tissue, contains necrotic tissue, not the same as a scab (whcih has exudate) - Seen in burns, gangrene, ulcer, spider bit wounds - Risk of haemorrhage from eschar separation greatest at 2-3 weeks
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39
Q

What are the risks of lightening strike?

A
  • Deafness (ruptured ear drum) - Amnesia - Prolonged QT - Seizure - Peripheral neuropathy (delayed)
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40
Q

What are the causes of fatality in burns?

A
  • Early mortality due to fluid loss/dehydration - Late mortality due to sepsis/infection
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41
Q

Describe the first aid management of burns

A
  • Running water at room temp, around 18 degrees - Effective for up to 3 hours post burn - Cool for 20 min - Don’t use icepack - Stops progression in zone of stasis which leads to necrosis (zone of coagulation is central area, already damaged)
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42
Q

Describe the rule of 9s in paeds burns

A
  • Head 18% - Torso 18% front, 18% back - Arms 9% each - Legs 14% each - Perineum 1%
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43
Q

What are the side effects of ketamine sedation?

A
  • Laryngospasm and bronchodilation - Tachycardia and hypertension - Vomiting - ? inc ICP - Emergent reactions, like waking up from nightmare - Good for analgesia and amnesia
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44
Q

What are the effects of midazolam for sedation?

A
  • Amnesia, sedation, anti-anxiolytic, anticonvulsant - Respiratory depression - May cause paradoxical hyperactivity - Atagonist: flumezanil
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45
Q

What sedative cuases chest wall rigidity?

A

Fentanyl

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46
Q

What are the contraindications to using entonox (nitrous oxide) for sedation?

A
  • Gas-filled space (pneumothorax, bowel obstruction) - Severe head injuries (risk of pneumocranium) - Intoxication/depressed LOC - If requiring >50% FiO2 - 1st trimester pregnancy
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47
Q

Presentation of pericarditis?

A
  • Usually well, chest pain, recent viral illness - Normal CXR heart and lungs - May have friction rub (inflammation) - May have fluid accummulation -> no rub, decr voltages on ECG, inc heart size on CXR - If no fluid: ST segment elevations, T wave inversion
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48
Q

What are the complications of myocarditis?

A
  • Inflammation of heart muscle/myocardium - Cardiomegaly - Increased pressures (LV, LA, PV, arterial) - Pulmonary oedema and congestive heart failure
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49
Q

What are the causes of myocarditis?

A
  • Usually viral: coxsackie A +B, adenovirus, CMV, echovirus, EBV - Drug hypersensitivity - Drug toxicity - Immune-mediated: rheumatic fever, Kawasaki
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50
Q

What are the symptoms and signs of myocarditis?

A
  • Non-specific malaise, fever, anorexia - Dysrhythmias (AV conduction or junctional, tachy) - Chest pain (due to ischaemia or pericarditis) - Tachypnoea - Decr cardiac output: tachycardia, weak pulses, cool periph, mottling - Muffled HS, S3, AV valve regurgitation murmur - Hepatomegaly, oedema, inc JVP - Rash (viral illness)
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51
Q

What are the ECG findings in myocarditis?

A
  • Low voltage QRS - Pseudo-infarction: pathological Q waves, poor progression R waves - TWI or flattening - LVH - Prolonged PR or QTc - Arrythmias
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52
Q

Treatment of SVT?

A
  • Vagal stimulation - ice to face, carotid sinus massage, valsalva - Adenosine - Synchronised DC cardioversion
53
Q

What is the management of a button battery in the stomach?

A

If asymptomatic and in stomach, then can be allowed to pass. Follow up xray in 24-48 hours, if still in stomach then for endoscopic removal. Check for disruption of battery on x-ray (heavy metal poisoning)

54
Q

What are the complications of Kawasaki Disease?

A
  • Urethritis with sterile pyuria - Hepatic dysfunction - Arthritis or arthralgias - Aseptic meningitis - Pericardial effusion or arrythmias - Hydrops of the gallbladder
55
Q

Commonest cause of painless abdominal distension in a neonate?

A

Sepsis (would have vomiting with volvulus)

56
Q

Describe the ligaments in malrotation?

A
  • Ligament of Treitz is absent (by distal end of transverse colon) - Ladd’s bands present (between caecum and duodenum, lead to midgut volvulus)
57
Q

What is the mortality risk of measles encephalopathy?

A

15%

58
Q

Risk factors, symptoms, and treatment for SUFE?

A
  • Obesity, hypothyroidism, hypopituitary, renal osteodystrophy - Vague acute or chronic groin/thigh/knee pain, may have sudden exacerbation, history of small trauma, limp and externally rotate leg - Posterior and inferior displacement head compared to femoral neck - Abnormal Klein’s line - M>F, L>R, 11-16yo - Tx: bed rest and pinning - Risks: osteonecrosis
59
Q

What is the mechanism of a pulled elbow, and how do you treat it?

A
  • The annular ligament becomes trapped between the radius and humerus - Stabilise radial head, supinate or pronate forearm, and flex elbow
60
Q

Overdose with high anion gap metabolic acidosis?

A
  • Methanol - Ethylene glycol - Salicylates
61
Q

Anticholinergic toxidrome

A
  • Tricyclic antidepressants (amitriptyline), antihistamines, atropine - Mad hatter, blind bat, dry bone, hot hell, flushed beet - Dilated pupils (non reactive), tachycardia, hypertension, tachypnoea - Dry skin and mucous membranes - Decr bowel sounds, ileus, urinary retention - Myoclonus, choreoathetosis, picking/plucking at things - Agitation, delirium, hallucinations - ECG: prolonged QRS, arrhythmia - Tx: sodium bicarbonate, physostigmine (acetylcholinesterase inhibitor)
62
Q

Hallucinogenic/sympathomimetic toxidrome

A
  • e.g. amphetamine, MDMA, LSD, ecstasy - Dilated pupils (brisk reactive), tachycardia, hypertension, tachypnoea, sweaty, nystagmus - Hallucination, agitation, depersonalisation, distorted perception - Fear, panic, dysphoria - Tx: calm environment, midazolam or haloperidol for agitation PRN
63
Q

Opioid toxidrome

A
  • Opioids e.g. morphine, methadone, heroin - Miosis (small pupil) - Drowsiness, coma, slurred speech, impaired attention - Respiratory depression and bradycardia - Euphoria, dysphoria, impaired judgement - Can develop pulmonary oedema and dyspnoea - Tx: naloxone
64
Q

Sedative hypnotic toxidrome

A
  • e.g. benzodiazepines, ethylene glycol, methanol, ethanol - Dilated or small pupils - Bradycardia, bradypnoea, hypotension, hyporeflexia - Confusion and stupor - Ethanol - slurred speech, unsteady, inappropriate behaviour - Ethylene glycol - CN palsies and tetany - Tx: flumazenil for benzo (not for chronic abuse as triggers seizures), fomepizole or ethanol for methanol/EG + urgent dialysis if high AN metabolic acidosis - Tx (others): supportive, IVF for hypotension, benzo and haloperidol for sedation
65
Q

Cholinergic toxidrome

A
  • Organophosphates and insecticides, nerve agents, mushrooms - Small pupils (miosis) - SLUDGEBBB - Lacrimation, salivation, urination, defecation, vomiting - Bronchospasm, bradycardia, bronchorrhea - Fasciculations, weakness, paralysis, seizures, coma - Tx: atropine (competes with acetylcholine), pralidoxime (for fasciculations or weakness)
66
Q

Serotonin syndrome

A
  • e.g. SSRIs (fluoxetine), tramadol, amphetamines - Dilated pupils, tachycardia, hypertension - Hyperthermia - Clonus and trismus, hypertonia, hyperreflexia - Sweating, flushing, tremor, rigidity, diarrhoea - Tx: supportive, diazepam if agitated, antidote is cyproheptadine (serotonin antagonist)
67
Q

Salicylate intoxication

A
  • e.g. aspirin - Respiratory alkalosis followed by high anion gap metabolic acidosis - Can be fatal >3g in children - Tinnitus, vertigo, N and V - Tachypnoea, hyperpnea - Agitation, lethargy, hyperthermia >41, coma - Pulmonary oedema or cerebral oedema - Tx: glucose/dextrose (decr CSF glucose), IV sodium bicarbonate for alkalinisation, may need dialysis
68
Q

What are the main effects seen in digoxin toxicity?

A

Hyperkalaemia (blocks Na-K ATPase) and arrhythmias (AV dissociation - 1st to 3rd degree heart block)

69
Q

Carbon monoxide intoxication

A
  • Headaches, confusion, vomiting, seizures, coma - Tx: 100% O2, hyperbaric oxygen - Neuropsych assessment 1-2 months
70
Q

Neuro-epileptic malignant syndrome

A
  • Idiosyncratic reaction to neuroleptic or antipsychotic drugs (4-14 post starting) - highest in haloperidol. Can also happen in olanzapine, quetiapine, metoclopramide - Gradual onset, prolonged course - Hyperthermia, sweating, unstable BP, stupor - Diffuse rigidity (hypertonia) - Reduced reflexes - Normal pupils - Tx: stop meds immediately, supportive, cooling, hydration
71
Q

Management of unidentified ingestion

A
  • Min 12 hrs observation - Check BSL - IV access if toxicity - Monitor LOC, vital signs, BSL +/- cardiac monitoring - Discharge only in daylight
72
Q

What ECG changes do you see in tricyclic antidepressant overdose and how do you treat it?

A
  • Prolonged QRS (normal QRS < 0.12sec) - IV sodium bicarbonate
73
Q

What is the antidote for B-blocker overdose?

A

Glucagon

74
Q

What is the antidote for CCB overdose?

A

Calcium gluconate/chloride or high-dose insulin and glucose (calcium channel blockers block insulin release leading to hyperglycaemia)

75
Q

What is the antidote for sulfonylurea (eg glipizide) overdose?

A

Octreotide (inhibitor of growth hormone, glucagon, and insulin, is like somatostatin)

76
Q

What is the antidote for tricyclic antidepressant overdose?

A

Sodium bicarbonate

77
Q

What is the antidote for isoniazid (anti-TB) overdose?

A

Pyridoxine

78
Q

What is the antidote for iron overdose?

A

Desferroxime

79
Q

What is the antidote for methaemoglobin overdose?

A

Methylene blue

80
Q

What is the antidote for ethylene glycol overdose?

A

Fomepizole or ethanol

81
Q

What is the antidote for benzodiazepine overdose?

A

Flumazenil

82
Q

Beta-blocker or calcium channel-blocker overdose presentation

A
  • Drowsiness, altered mental status - Bradycardia, hypotension - Normokalaemia (c.f. digoxin with hyperkalaemia) - ECG: sinus brady, abnormal AV node conduction, accelerated junctional rhythm - Tx: glucagon (BB) or calcium gluconate (CCB)
83
Q

Discuss colchicine ingestion

A
  • Heart sink ingestion - Rapidly absorbed - Gastro symptoms within 24 hours - >0.8mg/kg associated with 100% mortality - No antidote, give activated charcoal
84
Q

Activated charcoal is not useful (or is contraindicated) in which settings?

A
  • Pesticides, petroleum - Hydrocarbons, heavy metals >1hr since ingestion - Acids, alkali, alcohol - Iron - Lithium - Solvents
85
Q

What are the causes, signs, and symptoms of neurogenic shock?

A
  • Stimulation of parasympathetic, or inhibition or sympathetic - Widespread vasodilation - Bradycardia, hypotension, warm skin - Causes: spinal cord injury above T5, spinal anaesthesia, vasomotor center depression (pain, drugs)
86
Q

Discuss the movements for C4-S1 nerves

A

Shrug shoulders - C4 Flex elbow - C5 Pull wrist back - C6 Straighten arm - C7 Open and close fingers - C8 Spread fingers - T1 Flex hip - L1 and 2 Straighten knee - L3 Flex ankle up - L4 Push ankle down - L5, S1

87
Q

Pulsating proptosis and cannot look down. Injury is…?

A

Superior wall orbital fracture Cannot look away from the injury = superior

88
Q

Treatment of head injury in Haemophilia A?

A

Give factor 8 to bring factor levels to 100%, even if no evidence of bruising or swelling

89
Q

What are the cases of wound infections post human bite?

A

Staph aureus, strep, Eikenella corrodens

90
Q

At what level of paracetamol ingestion would you be concerned?

A

>200mg/kg or >10g total, based on ideal body weight

91
Q

When do you check parecetamol levels

A

2hrs for elixir, will need repeat if equivocal 4hrs for tablets If >8hrs then start NAC while awaiting paracetamol levels

92
Q

Typical vs atypical antipsychotics

A
  • Typical = haloperidol, chlorpromazine - can cause QT prolongation - Atypical = olanzapine, risperidone (can cause acute dystonia)
93
Q

What is the toxic dose for iron?

A

>60mg/kg elemental iron

94
Q

FFP vs cryoprecipitate

A

FFP contains all factors. Cryoprecipitate contains fibrinogen, vWF, F8 + 13

95
Q

What is the timing or primary, mixed, and permanaent dention?

A
  • Primary 6m-6y, lower central are first, then upper central - Mixed 6y - 12y - Permanent >12y
96
Q

What is a Bohn’s nodule?

A

Remnant of salivary gland located on buccal or lingual mucosa, or hard palate. No treatment needed. Epstein’s pearls = keratin nodules on palate

97
Q

Previously well 7yr old child who collapses after emotion/exercise (jumping into cold sea), family history of SCD. ECG shows frequent ventricular ectopics, not responding to adrenaline ; after giving adrenaline VEs progress to bidirectional ventricular tachycardia Diagnosis Cause Management

A

Catecholaminergic polymorphic VT Mean age presentation 6-10years Exercise/emotion induced syncope/seizure (Ddx LQTS) Diagnosis: Stress test - as exercise ventricular ectopics increase (usually decreases) ; may see bidirectional VT ; (ventricular QRS axis alternating with each beat) risk progression to polymorphic VT/V fib. Consider adrenaline challenge 65% due to mutation in RyR2gene (NB calcium release and ventricular depol) ; AD Gain of function mutation leads to Ca leak in diastole Adrenaline CI as can worsen VEs and cause VT ; opiates/general anaesthetic reduce ectopics Rx Avoid triggers Beta blockers Acute Rx: GA, IV opiates, Fleicanide Consider ECMO if issues hypotension May need ICD if survive cardiac arrest

98
Q

BETA BLOCKER Overdose treatment

A

Glucagon High dose insulin euglycemic therapy Adrenaline Consider IV calcium

99
Q

2 tablets can kill 10kg toddler

A

CCBs Beta blockers Sulphonylureas Opiods TCAs Chloroquine

100
Q

Sulphonylureas OD treatment

A

Causes profound hypoglycaemia Treat hypoglycaemia with IV dextrose bolus Octreotide (somatostatin analogue, inhibits endogenous insulin)

101
Q

Iron OD

A

SE dose and time dependent >60mg/kg systemic toxicity Timing 0-6hours GI SE (vomiting, diarrhoea, abdo pain) 6-12hours, symptoms improving 12-48hrs - shock, metabolic acidosis, hepatorenal F 2-5days fulminant hepatic failure 2-6weeks late GI - cirrhosis, strictures/fibrosis Management ● serum ironlevels ○ usually peak at 4 – 6 hours post ingestion ○ peak level > 90 umol/L thought to be predictive or systemic toxicity ● restoration of adequate circulating volume ● abdominal x‐ray ● wholebowelirrigation(WBI) if >60mg/kg ingestion ● surgical or endoscopic removal if WBI fails or isi mpractical ● Desferrioxamine chelation therapy ○ systemic toxicity ○ serum iron level > 90 umol/L at four hours post ingestion

102
Q

CCB overdose

A

Bradycardia - IV atropine, consider IV calcium, pacing Hypotension - Inotropes (Norad); HIET ; ECMO Consider charcoal or WBI if modified release

103
Q

Salicylate OD

A

Toxicity ● acute intoxication presents with vomiting, tinnitus, hyperventilation, respiratory alkalosis and metabolic acidosis (raised anion gap) ● dose‐related toxicity ○ 150 – 300mg/kg – tachypnoea, tinnitus, vomiting ○ > 300mg/kg – metabolic acidosis, altered mental state, seizures ○ > 500mg/kg potentially lethal ● children rarely ingest a dose of aspirin sufficient to cause toxicity; however small ingestions of methyl‐salicylate containing products are sufficient to cause severe toxicity ○ 5mL of oil of wintergreen can cause death in child < 6 years of age Management ● activated charcoal ● urinary alkalinisation ● hemodialysis

104
Q

Beta blocker OD

A

Toxicity ● blunting of metabolic, chronotropic and ionotropic effects of catecholamines due to decreased cAMP leads to life‐threatening cardiovascular toxicity ○ PR prolongation is an early sign of toxicity ○ bradyarrhythmia, hypotension, cardiovascular collapse ● sodium channel blocker causes QRS widening and ventricular arrhythmias ● seizures, hypoglycemia ● onset of effects usually within 1 ‐2 hours Management ● discharged if normal ECG at six hours ● bradycardia / hypotension ○ atropine (temporizing)/adrenaline ○ HIET ○ ECMO ● widened QRS - give sodium bicarbonate

105
Q

NAC for paracetamol OD SE Mechanism action

A

● NAC is 100% effective at preventing hepatotoxicity if started within 8 hours of ingestion ● Toxicity may be reduced if it is started between 8 to 24 hours after ingestion ● Allergic reactions are commonly reported but are rarely severe ○ usually dose dependent ○ more common in rapid first phase ○ symptoms including flushing, urticaria, wheeze, angioedema, hypotension, fever ○ minor symptoms can be managed with hydrocortisone/promethazine and slowing the infusion ○ serious symptoms require the infusion to be stopped and symptoms managed; one hour after symptoms abated the infusion can be restarted at a slower rate Mechanism of action ○ increased glutathione availability ○ direct binding to NAPQI ○ provision of inorganic sulfate ○ reduction of NAPQI back to paracetamol

106
Q

TCA Overdose

A

In overdose, the tricyclics produce rapid onset (within 1-2 hours) of: •Sedation and coma, Seizures •Hypotension, Tachycardia •Broad complex dysrhythmias •Anticholinergic syndrome Tricyclics mediate their cardiotoxic effects via • blockade of myocardial fast Na+ channels (QRS prolongation, tall R wave in aVR) • inhibition of K+ channels (QTc prolongation) and direct myocardial depression. • Other toxic effects from blockade at muscarinic (M1), histamine (H1) and α1-adenergic receptors. The degree of QRS broadening on the ECG is correlated with adverse events: •QRS > 100 ms is predictive of seizures •QRS > 160 ms is predictive of ventricular arrhythmias (e.g. VT) Rx Sodium Bicarb

107
Q

methanol or ethylene glycol ingestion Rx

A

Methanol becomes more toxic as broken down (by alcohol dehydrogenase) Rx Fomepizole (blocks alcohol dehydrogenase)

108
Q

High anion gap acidosis

A

Methanol, metformin Uremia Diabetic ketoacidosis Paraldehyde Isoniazid, iron, inborn errors of metabolism Lactic acidosis (seen with shock, CO, cyanide) Ethanol, ethylene glycol Salicylates

109
Q

Blood gas findings in salicylate poisoning

A

Metabolic acidosis and respiratory alkalosis

110
Q

4 clinical stages of iron toxicity

A

Stage 1 (0.5 to 6 hours): During this stage, iron exhibits a direct corrosive effect on the small bowel. Symptoms include nausea, vomiting, abdominal pain, and/or GI hemorrhage. Stage 2 (6 to 24 hours): Iron accumulates in the mitochondria; the patient is relatively symptom free. Stage 3 (4 to 40 hours): This phase is characterized by systemic toxicity with shock, metabolic acidosis, depressed cardiac function, and hepatic necrosis. Stage 4 (2 to 8 weeks): During this phase, pyloric stenosis and obstruction can develop as a result of earlier local bowel irritation.

111
Q

Difference between alkali and acid damage following ingestion

A

Alkaki - liquefaction necrosis (dissolves proteins and lipids ; penetrates deeper into tissues) Acid - coagulation necrosis ; forms eschar

112
Q

SVT and shocked

A

Synchronous DC shock 1J/kg –>2J/kg, consider amiodarone

113
Q

SVT not shocked

A

Vagal manoeuvres ; Adenosine 100mcg/kg –>200mcg/kg–>300mcg/kg (up to max 500mcg/kg), next consider Amiodarone or SYNCHRONOUS DC SHOCK

114
Q

Haemodynamically starlet VT

A

Amodarone 5mg/kg over 1-4hours or Procainamide

115
Q

VT with pulse and signs of shock

A

Synchronous DC shock 1J/KG, then 2J/kg Consider asynchronous shock if no response If tornadoes de pointes VT, given IV Magnesium sulphate

116
Q

In toeing

A

• Foot: Metatarsus adductus ; Talipes equinovarus (clubfoot) • Leg: Tibial torsion (internal) • Hip: Femoral anteversion (medial femoral torsion) - Paralysis (polio, myelomeningocele) - Spasticity (cerebral palsy) - Maldirected acetabulum

117
Q

Male with poor posture and poor flexibility

A

Scheuermann kyphosis. This is a wedge-shaped deformity of the vertebral bodies of unclear etiology that causes juvenile kyphosis (abnormally large dorsal thoracic or lumber curves). Common in teenagers, it is distinguished from simple poor posture (“postural round-back deformity”) by its sharp angulation and inability to correct by having the patient stand up straight or lie on top of a bolster. X-ray studies reveal anterior vertebral body wedging and irregular erosions of the vertebral end plate. Treatment consists of exercise, bracing, and, rarely, surgical correction (for severe, painful deformities).

118
Q

Scaphoid fracture Signs Treatment Complications

A

Clinical signs: • Pain on dorsi‐flexion of wrist • Tenderness in snuff box • Pain on gripping Can have normal X‐rays for first few days Treat all with scaphoid plaster (complete BEPOP with thumb spica) OR a wrist splint with thumb extension • Remove if normal X‐rays after 2 weeks Complications: • Avascular necrosis of proximal fragment (x) • Non‐union

119
Q

Monteggia fracture

A

Proximal ulnar fracture Radial head dislocation Need ortho referral for fixation

120
Q

SALTER HARRIS CLASSIFICATION

A
121
Q

ELBOW Xrays

A
122
Q

Osteoid Ostemoa

A

Osteoid osteoma, a benign bone-forming tumor, is typically seen in older children and adolescents and exhibits a male predominance (male-to-female ratio 2:1).

Most children complain of localized pain, usually in the femur and tibia; however, the arms and vertebrae may also be involved.

Radiographs may demonstrate an osteolytic area surrounded by densely sclerotic reactive bone, and bone scans reveal “hot spots.” Computed tomography (CT) scans will show a “nidus” in the middle of the lesion, which is pathognomonic for this diagnosis

123
Q

salter harris

A

diaphysis is the shaft
metaphysis is end of the shaft
epiphysis is at the very end beyond the growth plate
epiphyseal/metaphyseal growth plate lies between the metaphysis and the epiphysis

Salter-Harris 1: fracture straight through the growth plate
Salter-Harris 2: fracture through metaphysis and growth plate
Salter-Harris 3: fracture through the epiphysis and the growth plate Salter-Harris 4: fracture through the metaphysis, growth plate and epiphysis Salter-Harris 5: crush fracture

Salter-Harris 1 and 2 have good prognosis and need no wires
Salter-Harris 3 and 4 displace the growth plate and need K-wires (Kirschner) Salter-Harris 5 has a very poor prognosis

124
Q

RF for DDH

A

Female

First born

Family Hx

Funny presentation (breech)

Others: Oligohydramnios, MSK, NM disease, CP, spina bifida

Inx;

Ortolani/Barlow, Galleazi clinical signs

Limited hip adbuction

<6mo US ; >6mo XR

125
Q

Scoliosis and Cobbs angle

A
126
Q

Seymour fracture

A

Distal phalanx physeal fracture that has an associated nail bed injury commonly with ungual subluxation.

SALTER Harris 1/2

Mx

Antibiotics
Ortho review - surgical/non surgical

127
Q

Ossification centres elbow

A

The ossification centres appear in a predictable order whichcan be memorised using the mnemonic CRITOE.

The age of appearance is variable but can be remembered as 1,3,5,7,9,11 =

Capitellum at 1 year,

Radial Head at 3,

Internal epicondyle at 5,

Trochlear at 7,

Olecranon at 9 and

External (or lateral) at 11 years

128
Q

Tarsal bones foot

A

The seven tarsal bones can be remembered with the mnemonic “Tiger Cub Needs MILC” Talus, Calcaneus, Navicular, Medial Cuneiform, Intermediate Cuneiform and Lateral Cuneiform and Cuboid.

129
Q

CSF flow

A

CSF produced in choroid plexus of lateral ventricles

Travels from lateral ventricles to 3rd ventricle via the foramen of Monro.

From 3rd ventricle to 4th ventricle via Aqueduct Sylvius

From 4th ventricle to subarachnoid space via foramina of Luschka and Magendie

Paeds (25 decks)

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