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MO AED > Stuff > Flashcards

Stuff Flashcards

1
Q

Lisfranc

A

Tarsometatarsal joint (TMTJ) complex injury

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2
Q

Causes of Lisfranc injuries

Classification

A

RTA
Fall from height
Field sports like rugby

Classification: Myerson classification

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3
Q

TMTJ complex contents

A
  • 5 MTs
  • 3 Cuneiforms
  • Cuboid
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4
Q

Lisfranc ligament
x3

A
  1. Dorsal ligament (weakest)
  2. Interosseus ligament (aka Lisfranc ligament; strongest)
  3. Plantar ligament

All run obliquely from medial border of 2nd MT to lateral aspect of medial cuneiform

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5
Q

Lisfranc injury mechanisms

A

axial load on plantar-flexed foot then forcibly rotates / bends / compressed

e.g. miss a step downstairs
lands on heel of a plantar flexed foot

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6
Q

Pathognomonic sign for Lisfranc

A

Plantar ecchymosis
(24-48h after)

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7
Q

Special tests for Lisfranc

A
  1. Pronation-abduction test
  2. TMT squeeze test
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8
Q

Fleck sign for Lisfranc injury

A

Pathognomonic

Avulsion fracture of medial cuneiform or 2nd MT

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9
Q

Cx of Lisfranc injuries

A

Acute
- Vascular compromise
- Nerve injury
- Compartment syndrome

Chronic
- OA
- Chronic midfoot pain

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10
Q

Normal Foot XR findings

A

Normal AP
- medial border of 2nd MT colinear with medial border of middle cuneiform

Normal oblique
- medial border of 4th MT colinear with medial border of cuboid

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11
Q

Carpal bones

A

Trapezium Trapezoid Capitate Hamate
Scaphoid Lunate Triquetral Pisiform

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12
Q

Anatomical snuffbox

A

Medial: EPL
Lateral: EPB, APL
Proximal: Radius styloid Floor: Scaphoid, Trapezium

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13
Q

Jefferson #

A

anterior and posterior arches of C1

from axial load on back of head or hyperextension of neck

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14
Q

Hangman #

A

both pedicles or pars of C2

forcible hyperextension of neck

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15
Q

Jefferson bit off a hangman’s thumb

A
  • Jefferson #
  • Bilateral facet dislocation
  • Odontoid #
  • Atlanto-axial and Atlanto-occipital dislocation
  • Hangman # (hyperextension)
  • Teardrop #
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16
Q

Central cord syndrome

A

Hyperextension injuries
Cervical spondylosis
UL > LL neurological deficit
Bladder dysfunction
Variable sensory loss

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17
Q

Anterior cord syndrome

A

Paralysis
Loss of pain / temp
Preserved propioception / vibration / 2-point

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18
Q

Posterior cord syndrome
(less common)

A

Loss of proprioception / vibration
Ataxic gait
Hypotonia
Loss of deep tendon reflexes
Romberg +ve

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19
Q

NEXUS criteria full name

A

National emergency X-radiography utilization study

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20
Q

NEXUS criteria
(x5)

A
  1. No focal neurology
  2. No midline C-spine tenderness
  3. Conscious
  4. No intoxication
  5. No distracting injury
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21
Q

ABCD2 score for TIA

A

Age >=60

BP >= 140/90

Clinical features of TIA (Unilateral weakness = 2; speech disturbance = 1)

Duration of symptoms (<10 mins = 0; <1h = 1; >- 1h = 2)

DM

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22
Q

Dengue fever symptoms

A

Headache, retro-orbital pain, joint pain
MP rash
Biphasic fever course (saddle back)
Thrombocytopenia
Dengue hemorrhagic fever

WHO 2009 classification
- Dengue without warning signs
- Dengue with warning signs
- Severe dengue

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23
Q

Segond fracture

A

Avulsion # of lateral surface of lateral tibial condyle

Excessive internal rotation + varus stress -> increased tenson on lateral capsular ligament of knee joint

Asso w/ detachment of capsular portion of lateral collateral ligament + ACL tear, +/- medial/lateral meniscal tear

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24
Q

Arcuate sign

A

Avulsion fracture of fibular head (at site of insertion of arcuate ligament complex)
asso w/ cruciate ligament injury

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25
Q

Reverse Segond #

A

Avulsion of deep fibers of MCL
Valgus stress + External rotation

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26
Q

Chauffeur’s # / Hutchinson #

A

Oblique # of radial styloid
FOOSH, compression of scaphoid against radial styloid

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27
Q

Purple glove syndrome

A

IV Dilantin (Phenytoin)

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28
Q

Tillaux fracture

A

occurs when medial aspect of the distal tibial growth plate has started to fuse

from abduction-external rotation mechanism
anterior tibiofibular ligament avulses the anterolateral corner of the distal tibial epiphysis

Vertical fracture through the distal tibial epiphysis (Salter-Harris III) with a horizontal extension through the lateral aspect of the physis.
The lack of a metaphyseal fracture component in the coronal plane (evaluated with lateral x-ray or CT) distinguishes a Tillaux fracture from a triplanar fracture.

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29
Q

Common medical causes of blindness (x4)

A

Cataract
Glaucoma
Age related macular degeneration
Diabetic retinopathy

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30
Q

Takotsubo cardiomyopathy

A

aka stress cardiomyopathy, “broken heart syndrome”

  1. Transient hypokinesis, dyskinesis, or akinesis of the LV midsegments, with or without apical involvement; the regional wall-motion abnormalities extend beyond a single epicardial vascular distribution, and a stressful trigger is often, but not always, present
  2. Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture
  3. New ECG abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in the cardiac troponin level
  4. Absence of pheochromocytoma or myocarditis
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31
Q

SDH chronicity

A

hyperacute <12h - isodense
acute 12h-2d - hyperdense
subacute 2d-1 month - isodense
chronic > 1month - hypodense

anemia / if on NOAC -> will affect density, hyperdensity will become isodense

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32
Q

Fluid level in knee XR
post trauma

A

Lipohemarthrosis
results from an intra-articular fracture with escape of fat and blood from the bone marrow into the joint
asso w/ tibial plateau fracture or distal femoral fracture

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33
Q

Common causes of primary PPH
4Ts

A
  1. Tone
  2. Tissue
  3. Trauma
  4. Thrombin
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34
Q

Common causes of primary PPH
4Ts

A
  1. Tone
    - Uterine atony, tx: Syntocinon infusion, bimanual uterine massage, other: Ergometrine, Prostaglandin F2alpha analog (Hemabate)
  2. Tissue
    - Retained tissue of conception, may need surgical removal
  3. Trauma
    - Perineal, vulva, vaginal or lower uterine segment laceration
  4. Thrombin
    - Clotting abnormality - primary or secondary due to DIC
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35
Q

Cord prolapse initial Mx

A
  1. O2 by mask
  2. Head down position (Sims or Knee-chest) to avoid compression of cord by presenting part
  3. Do not handle cord excessively to avoid vasospasm
  4. Elevate presenting part to ensure umbilical flow until delivery
  5. If prolonged transfer -> Instillation of bladder by Foley (500-750ml NS), may help pushing the present part up and ease pressure on prolapsed cord
  6. Monitor fetal HR
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36
Q

Bells palsy description
x4

A

Lack of wrinkling of forehead
Impaired closure of eye
Flattened nasolabial fold
Drooping of mouth corner

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37
Q

Other symptoms of facial nerve palsy

A

Postauricular pain
Eye pain / tearing
Hyperacusis (n. to stapedius)
Loss of sensation of anterior 2/3 of tongue

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38
Q

Causes of facial n. palsy
x6

A
  1. Bell’s palsy
  2. Ramsay Hunt syndrome aka Herpes zoster oticus (Herpes zoster infection of geniculate ganglion)
  3. Middle ear infection / pathology (OM, cholesteatoma)
  4. Temporal bone #
  5. Parotid tumor
  6. Cerebellopontine angle tumor - Acoustic neuroma
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39
Q

Ramsay Hunt syndrome triad

A

Ipsilateral facial paralysis
Otalgia
Vesicles in auditory canal / on auricle

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40
Q

Acyclovir renal adjustment

A

Increase interval but keep same dose (poor oral bioavailability)
CrCl 10-50: 800mg BD-TDS
CrCl <10: 200mg BD

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41
Q

Life threatening cause of chest pain
x5

A
  1. ACS
  2. PE
  3. Aortic dissection
  4. Cardiac tamponade
  5. Esophageal rupture
    Tension PTX
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42
Q

Boerhaave syndrome

A

aka Effort rupture of esophagus

Spontaneous perforation of eso caused by sudden increase in intraeso pressure + negative intrathoracic pressure (vomit, severe straining)

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43
Q

Mackler’s triad

A

of Boerhaave syndrome
1. vomiting
2. chest pain
3. subcutaneous emphysema

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44
Q

Hamman’s sign / crunch

A

pneumomediastinum
heard over precordium in spontaneous mediastinal emphysema

Mediastinal crackling sound synchronus with heart beat

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45
Q

Cx of Boerhaave syndrome
x6

A
  1. Pneumomediastinum
  2. Mediastinitis
  3. Hydropneumothorax
  4. Empyema
  5. Sepsis
  6. Multiorgan dysfunction syndrome
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46
Q

Ix for Boerhaave syndrome

A

Gastrografin swallow
(cannot use barium as perforation, will cause mediastinitis)

CT thorax

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47
Q

RV STEMI ECG features
(when have inferior STEMI)

A
  1. STE in V1
  2. STE in V1 and STD in V2 (highly specific for RV infarction)
  3. Isoelectric ST segment in V1 with marked STD in V2
  4. STE in III > II
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48
Q

Clinical significance of RV infarction

A

Isolated RV infarction is rare
Most with inferior STEMI
Most useful V4R (5th ICS, Rt MCL)

  • Nitrates contraindicated
  • treat with IVF when hypotension

Very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents

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49
Q

STEMI meds

A

Aspirin
Clopidogrel
Fibrinolytics
- Tenecteplase (TNK) - IV bolus x1
- Alteplase (rt-PA) - IV bolus then 2 infusions
- Reteplase (r-PA) - IV bolus x2
similar effect, TNK easier as one dose no need infusion

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50
Q

CI of Fibrinolytic for STEMI

A

Absolute
1 Any prior ICH
2 Known structural cerebral vascular lesion (e.g. AVM)
3. Known malignant intracranial neoplasm (primary or met)
4. Ischemic stroke within 3 months (except within 4.5h)
5. Suspected aortic dissection
6. Active bleeding (excluse menses) or bleeding diathesis
7. Significant closed-head or facial trauma within 3 months

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51
Q

Cx of fibrinolytics

A
  1. ICH (~1%)
  2. Bleeding risk, most common GIB
  3. Hypersitivity reaction, hypotension, reperfusion arrhythmias
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52
Q

Early Cx of AMI

A
  1. Lethal arrhythmias (VT, VF, heart blocks)
    2.
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53
Q

Steps for transcutaneous pacing

A

Explain procedure, consent
Sedation, analgesics
Electrodes placement (anterolateral or anteroposterior)
Set cardiac monitor to pacing mode / demand mode
Set pacing rate 10-30bpm higher than patient’s HR (~60-70)
Increase current output until electrical capture
Check for mechanical capture by feeling femoral pulse (cuz upper body is twitching)

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54
Q

Causes of 3rd n. palsy

A

DM neuropathy
Demyelineating disease (MS, Miller Fisher)
Brain tumor, Trauma
Cerebral aneurysm (Berry aneurysm)

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55
Q

5 causes of headache

A
  1. Acute SAH
  2. CNS infection
  3. Cerebral venous thrombosis
  4. Temporal arteritis
  5. Acute angle closure glaucoma
  6. Carotid / vertebral artery dissection
  7. Brain tumor
  8. HT encephalopathy
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56
Q

CTB finding of basal cistern SAH

A
  1. Hyperdensity over subarachnoid space and basal cistern
  2. Dilated temporal horn of lateral ventricles, suggestive of obstructive hydrocephalus
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57
Q

Common cause of primary SAH

A

Rupture of berry aneurysm
AVM
Coagulopathy
Brain tumor
Arterial dissection
Arteritis
Cocaine use

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58
Q

2 classifications / grading of SAH

A
  1. Hunt and Hess scale
  2. World Federation of Neurological Surgeons grading system
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59
Q

Immediate Tx of SAH on warfarin (meds)

A
  1. PCC Prothrombin complex concentrate
    (Beriplex: 4-factor PCC)
  2. Vitamin K1
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60
Q

Cx of SAH

A
  1. Cerebral vasospasm
  2. Obstructive hydrocephalus
  3. Seizure
  4. Recurrent SAH
  5. Cerebral salt wasting syndrome
  6. Neurogenic pul edema
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61
Q

Wellens syndrome

A

Critical stenosis of proximal LAD
Recent chest pain now resolved

Do not perform stress test e.g. treadmill

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62
Q

ECG features of Wellens syndrome

A

Type A (25%): Biphasic T waves in V2,3
Type B (75%): Deeply symmetrically TWI in V2,3

Pseudo-normalization when LAD occlude again
(T waves become upright, signifies hyperacute STEMI)

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63
Q

ECG V7-9 placement

A

for posterior MI
same horizontal plane as V6

V7: left posterior axillary line
V8: tip of left scapula
V9: left paraspinal region

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64
Q

Sgarbossa criteria

A
  1. Concordant STE >= 1mm any lead
  2. Concordant STD >= 1mm V1, V2, V3
  3. Discordant STE >= 5mm in leads with negative QRS

Modified:
3. Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave

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65
Q

STEMI equivalents

A
  1. Posterior MI (STD V1-3, do posterior leads)
  2. new LBBB Sgarbossa criteria
  3. De Winter T waves (complete LAD occlusion)
  4. Hyperacute T waves (early anterior STEMI)
  5. Wellens syndrome (proximal LAD critical stenosis)
  6. STE in aVR - Left main coronary artery (LMCA) occlusion, Proximal LAD stenosis, severe TVD
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66
Q

DDx for hyperthermia, tachycarida, agitation

A

CNS
1. CNS infection
2. Stroke, tumor (involve thermoregulatory pathway)
3. Status epilepticus

  1. Sepsis

Endocrine
5. Thyroid storm
6. Pheochromocytoma

  1. Heat stroke

Toxicological
8. Sympathomimetic toxidrome
9. Anticholinergic toxidrome
10. Salicylate poisoning
11. Serotonin syndrome
12. Neuroleptic malignant syndrome
13. Benzodiazepine / alcohol withdrawal
14. Malignant hyperthermia

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67
Q

Tx for sympathomimetic toxidrome

A
  1. Physical restraint followed by chemical restraint
  2. Rapid and aggressive cooling for hyperthermia
  3. Aggressive fluid resuscitation
  4. Benzodiazepine
    - can treat agitation, hyperthermia, HT, tachycardia
    - antidote of cocaine and other stimulants
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68
Q

ECG findings of Na channel blocker overdose (e.g. cocaine)

A

Wide complex tachycardia
Right axis deviation
“R” in aVR

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69
Q

Na channel blockers
TCA-PP-DV

Toxi book

A

T - Tricyclic antidepressants
C - Carbamazepine, Cocaine, Citalopram
A - Antiarrhythmic 1A (Procainamide) / 1C (Flecainide), Amantadine

P - Propranolol
P - Phenothiazine (Thioridazine)

D - Diphenhydramine (Benadryl)
V - Venlafaxine

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70
Q

Mx of Na channel blockers overdose

A

Antidote: NaHCO3 50-100ml IV bolus
Indication
1. QRS >100ms
2. Ventricular arrhythmias
3. Hypotension
CI
1. Serum pH >7.5-7.55
2. Intolerable to fluid / Na overload

Endpoint
- QRS <100ms
- No more ventricular arrhythmias
- BP stabilize

GI decon: gastric lavage, activated charcoal within 1-2h

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71
Q

Mx of hyperthermia (cooling method)

A
  1. Remove clothing
  2. Water mist spray and fanning
  3. Ice packs at neck, axillae, groin
  4. Bladder irrigation with ice water
  5. Peritoneal lavage with cold dialysate

aim: reduce core temp to <40 in 30 mins

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72
Q

Serotonin syndrome
3 As

A

Antidepressants (SSRI)
Analgesics (Tramadol, Pethidine, Fentanyl)
Abusive drugs (cocaine, ectasy, “ice”)

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73
Q

Features of Serotonin syndrome

A

usually clonus over LL

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74
Q

Antidote of Serotonin syndrome

A

Cyproheptadine (antihistamine + antiserotonergic)
8-12mg PO x1
2mg Q2H till symptom resolve
Up to 32mg / day

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75
Q

Cocaine intoxication drug CI

A

Beta blockers - unoppposed alpha effect -> paradoxical HT

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76
Q

Tx of HT in cocaine intoxication

A
  1. Benzodiazepine
  2. Phentolamine
  3. Nitroglycerin, Nitroprusside
  4. CCB
  5. Labetalol (controversial)
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77
Q

Phlegmasia cerulea dolens

A

uncommon DVT
congestion and cyanosis of a limb due to massive venous thrombosis

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78
Q

Massive blood transfusion definition

A

10 units packed red cells within 24h

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79
Q

Beck’s triad

A

Cardiac tamponade

  1. Hypotension, narrow pulse pressure
  2. Distended neck veins (jugular veins)
  3. Muffled heart sounds
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80
Q

Colistin

A

Polymyxin E
Last resort for Gram neg infections
SE: Nephotoxicity, neurotoxicity

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81
Q

HBOT indications currently

A

Life-threatening
1. Severe decompression sickness
2. Cerebral arterial gas embolism

Emergency
3. CO poisoning
4. Necrotizing soft tissue infection
5. CRAO

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82
Q

Absolute CI for HBOT

A
  1. Unresolved PTX
  2. Pneumocephalus
  3. Hollow orbital prosthesis
  4. Currently on Bleomycin / Adriamycin (Doxorubicin)
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83
Q

AACG Glaucoma Mx
STAMP

ATM PBL

A

Supine

Timolol eye drops (Topical BB - decrease production aqueous humor)

Acetazolamide IV (Systemic carbonic anhydrase inhibitor - decrease production aqueous humor)

Mannitol IV (Systemic osmotic diuretic - decrease volume of vitreous humor)

Pilocarpine eye drops (Topical muscarinic agonist - constrict pupil, facilitate drainage from ant chamber)

Latanoprost (Topical prostaglandin)

Brimonidine (Alpha 2 agonist - decrease production aqueous humor)

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84
Q

Osborn wave

A

Positive deflection seen at the J point in precordial and true limb leads.

Most commonly associated with hypothermia

Reciprocal, negative deflection in aVR and V1

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85
Q

Causes of Osborn wave

A

Hypothermia

HyperCa
AMI
Takotsubo cardiomyopathy
LV hypertrophy due to hypertension
Normal variant and early repolarization
Neurological insults such as intracranial hypertension, severe head injury and SAH
Severe myocarditis
Brugada syndrome
Le syndrome d’Haïssaguerre (idiopathic VF)

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86
Q

Brudzinski’s sign

A

Passive neck flexion -> Flexion of hips and knees

specific but not sensitive

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87
Q

Kernig’s sign

A

Supine, hip and knee flex to 90 deg
Resistant / Pain during passive extension of leg

specific but not sensitive

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88
Q

Echo
Parasternal short axis view

A

look for RWMA

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89
Q

PE classification

A
  1. Massive (hemo unstable)
  2. Submassive (RV strain)
  3. Non-massive (no RV strain)
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90
Q

ECG low voltage

A

QRS all limb leads <5mm or all precordial leads <10mm

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91
Q

Posterior MI ECG changes

A

Look at V1-3
Horizontal STD, tall & broad R waves, upright T wave, dominant R wave in V2 (R/S >1)

-> do V7-9 (posterior leads)

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92
Q

Posterior MI
litfl

A
  • usu w/ inferior or lateral STEMI
  • implies a much larger area of myocardial damage, with an increased risk of LV dysfunction and death

Isolated posterior MI is less common (3-11% of infarcts)

-> needs urgent PCI

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93
Q

RV infarction

A

usu with inferior STEMI (in 40% of inferior MI)
-> preload sensitive, nitrates contraindicated

STE in V1
STE in V1 + STD in V2
Isoelectric V1 + marked STD in V2
STE Lead 3 > 2

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94
Q

Right side ECG

A

V1-2 same position
V3-6 to V3R - V6R

Most useful = V4R (R 5th ICS, MCL)

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95
Q

De Winter T waves
STEMI equivalent

A

Tall, prominent, symmetrical T waves in precordial leads
Upsloping STD > 1mm at the J point in precordial leads
Absence of STE in precordial leads
Reciprocal STE (0.5mm – 1mm) in aVR

Signifies LAD occlusion

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96
Q

STE in aVR, diffuse STD in other leads

A

LMCA occlusion
or pLAD stenosis, severe TVD…

cause by diffuse subendocardial ischemia / infarction of basal septum

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97
Q

5 types of MI
(EM book)

A

Type 1: related to atherosclerotic plaque rupture with thrombosis

2: related to ischemia due to imbalance btn oxygen demand and supply

3: cardiac death with S/S of coronary ischemia but death before blood samples taken

4a: related to PCI
4b: related to stent thrombosis

5: related to CABG

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98
Q

ECG mimics of STEMI

A
  1. Acute pericarditis
  2. LV aneurysm
  3. Benign early repolarization (BER)
  4. Prinzmetal’s angina (coronary vasospasm)
  5. Brugada syndrome
  6. LVH
  7. HOCM
  8. SAH (raised ICP)
  9. HyperK
  10. LBBB
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99
Q

BER (Benign early repolarization) vs Pericarditis
ECG

A

ST segment / T wave ratio in V6
>0.25 = Pericarditis
<0.25 = BER

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100
Q

Acute epiglottitis most common microbe

A

Haemophilus influenzae type B (historically)
Now: Streptococcus pneumoniae, Streptococcus pyogenes, Staphylococcus aureus

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101
Q

Chest pain life threatening causes (x6)

EM book

A
  1. Acute coronary syndrome
  2. Acute aortic syndrome
  3. PE
  4. Tension PTX
  5. Cardiac tamponade
  6. Eso rupture (Boerhaave’s syndrome)
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102
Q

Hamman’s sign

A

For pneumo-mediastinum

a crunching, rasping sound, synchronous with the heartbeat, heard over the precordium in spontaneous mediastinal emphysema

result from heart beating against air-filled tissues

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103
Q

Westermark sign

A

PE
sign seen on CXR

  • focal peripheral hyperlucency secondary to oligemia resulting in a collapsed appearance of vessels distal to the occlusion
  • central pulmonary vessels may also be dilated
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104
Q

Echo findings of cardiac tamponade

A
  1. Pericardial effusion
  2. Diastolic RV collapse (highly specific)
  3. Systolic RA collapse (earliest sign)
  4. Dilated IVC w/o insp collapse (highly sensitive)
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105
Q

SVT vs VT features

EM book

A
  1. QRS >0.14s in RBBB / >0.16s in LBBB
  2. AV dissociation
  3. Capture or fusion beats
  4. Precordial QRS complex concordance
  5. Axis -90 to +180
  6. QRS configuration…
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106
Q

Causes of VT

A
  1. Coronary artery disease
  2. Hypertrophic cardiomyopathy
  3. MV prolapse
  4. Drug toxicity
  5. Electrolyte disturbance
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107
Q

Torsades de pointes
Tx

A

MgSO4 1-2g over 60-90 seconds
Isoproterenol 1-8 mcg/min

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108
Q

Score for unsalvageable limb
MESS

A

Mangled Extremity Severity Score

> = 7 amputation!

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109
Q

CXR PE findings

A
  1. Westermark sign (focal oligemia)
  2. Hampton’s hump (peripheral wedge shaped opacity)
  3. Palla’s sign (enlarged right dsc pul a)
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110
Q

Echo findings acute PE

A
  1. RV dilatation
  2. RV hypokinesis (w/ sparing of apex) “McConnell’s sign”
  3. D shaped LV
  4. TR
  5. IV septal flattening

increased insp collapse of IVC
D shaped septum

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111
Q

TCA poisoning clinical features
PIC

A

Toxicity within 6h; 1-2h if sig poisoning (>10-20mg/kg adult / >5mg/kg pedi)
Cardiac toxicity (hypotension, tachyarrhythmia)
CNS toxicity (lethargy, confusion, coma, seizure)
Anticholinergic toxidrome

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112
Q

Radio-opaque meds

COINS
/ CHIPS

A

Chloral hydrate / Cocaine packets
Opiate packets
Iron and heavy metal
Neuroleptic agents (e.g. TCA)
Sustained release medications

C Chlorinated hydrocarbons (eg, chloral hydrate, carbon tetrachloride)
Calcium salts (eg, calcium carbonate)
Crack vials
H Heavy metals (eg, iron, arsenic, mercury, thallium, lead)
I Iodinated compounds (eg, thyroxine)
P Psychotropics (eg, phenothiazines, lithium, cyclic antidepressants)
Packets of drugs (eg, cocaine and heroin “body packers”)
Play-Doh
Potassium salts
E Enteric-coated tablets (eg, aspirin)
S Salicylates
Sodium salts
Sustained-release preparations

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113
Q

Blast injury 1/2/3/4

A

Primary
- caused by the blast wave moving through the body

Secondary
- caused by debris that is displaced by the blast wind of the explosion

Tertiary
- caused when the person in displaced through the air and impacts on another object by the blast wind, or when a structure collapses and causes injury to the person

Quaternary
- comprised of all injuries that are not included in primary, secondary, or tertiary blast injury categories.
- can be caused by exposure to resulting, fire, fumes, radiation, biological agents, smoke, dust, toxins, environmental exposure, and the psychological impact of the event

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114
Q

Pedi BP

A

SBP: (Age x2) + 90
Hypotension SBP: (Age x2) + 70

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115
Q

Pediatric Endotracheal Tube Size / Depth

A

Uncuffed = (age/4) + 4
Cuffed = (age/4) + 3

Depth = ETT size x3

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116
Q

Tibial plateau # classification

A

Schatzker (type 1-6)

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117
Q

Pedi maintenance IVF formula
(4-2-1)

A

First 10kg = 4ml/kg/hr = 40ml/hr
Next 10kg = 2ml/kg/hr = 20ml/hr
Then 1ml/kg/hr

Shock: 20ml/kg bolus

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118
Q

Eclampsia Mx

A

Loading: MgSO4 4-6g IV over 15-20 mins
Maintenance MgSO4 1-3g/hr (for 24h after last seizure)

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119
Q

MgSO4 toxicity monitoring

A
  • Loss of deep tendon reflex (patella reflex)
  • Resp depression (RR >12)
  • Foley to BSB for u/o monitoring (>100ml/4h)

Reverse with Calcium gluconate 10% 10ml over 10 mins

CI of MgSO4: Myasthenia gravis

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120
Q

Radio-opaque meds

COINS

A

Cloral hydrate / Cocaine packets
Opiate packets
Iron and heavy metal
Neuroleptic agents (TCA)
Sustained release medications

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121
Q

Delayed cord clamping pros and cons

A

Pros
1. Increase Hb at birth, improves iron store in first few months
2. Better for preterm
- improved transitional circulation
- better establishment of red blood cell volume
- decreased need for blood transfusion
- lower incidence of necrotizing enterocolitis and intraventricular hemorrhage

Cons
- Increase neonatal jaundice

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122
Q

BRASH syndrome

A

Bradycardia
Renal Failure
AV blockade
Shock
HyperK

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123
Q

SCORTEN score

A
  1. Age (>40)
  2. Associated malignancy
  3. HR (>120)
  4. Detacted or compromised body surface (>10%)
  5. Serum urea (>10)
  6. Serum HCO3 (<20)
  7. Serum glucose (>14)
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124
Q

Etiology of SJS/TEN

A
  1. Drugs (allupurinol, AED carbamazepine, lamotrigine, NSAIDs)
  2. Infection (Mycoplasma pneumoniae)
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125
Q

WPW ECG features

A
  1. Short PR interval < 120ms
  2. Delta wave: slurring slow rise of initial portion of the QRS
  3. Prolong QRS 110ms
  4. Discordant ST/T changes
  5. Pseudo-infarction pattern in up to 70% of patients — due to negatively deflected delta waves in inferior/anterior leads (“pseudo-Q waves”), or prominent R waves in V1-3 (mimicking posterior infarction)
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126
Q

Drug Tx for thyroid storm

A

Antithyroid: Propylthiouracil
Iodide (inhibit rlease of stored thyroid hormone): Lugol’s solution
BB: Propranolol

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127
Q

Risk factor of testicular torsion

A
  1. Bell-clapper deformity
  2. Cryptorchidism
  3. Testicular tumor
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128
Q

NMS Tx

A
  1. Dantrolene (also use in malig hyperthermia)
  2. Bromocriptine (dopamine agonist)
  3. Amantadine
  4. Benzo: Lorazepam, Diazepam
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129
Q

Score for TEN/SJS mortality

A

SCORTEN score

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130
Q

Etiology of SJS/TEN

A
  1. Drugs (allupurinol, AED Lamotrigine, NSAIDs)
  2. Infection (Mycoplasma pneumoniae)
131
Q

WPW ECG features

A
  1. Short PR interval < 120ms
  2. Delta wave: slurring slow rise of initial portion of the QRS
  3. Prolong QRS 110ms
  4. Discordant ST-segment and T-wave changes
  5. Pseudo-infarction pattern in up to 70% of patients — due to negatively deflected delta waves in inferior/anterior leads (“pseudo-Q waves”), or prominent R waves in V1-3 (mimicking posterior infarction)
132
Q

Panadol overdose values

A

Toxic: >7.5g or >150mg/kg
Massive: 0.5-1g/kg

133
Q

Panadol overdose types

A
  1. Acute single overdose
    (single ingestion)
  2. Staggered overdose
    (multiple ingestions in 1-24 hrs; <4h interval treat as acute)
    NAC indicated if >150mg/kg
  3. Chronic supratherapeutic overdose
    (multiple ingestions in >2 days with dose >4g/day adult or 90mg/kg/day pedi)
    NAC indicated if S/S of hepatitis, dLFT, Panadol level suggesting delayed clearance
  4. Massive overdose
    (acute ingestion >1g/kg)
    early onset coma, met (lactic) acidosis, early coagulopathy
    acute tubular necrosis, ARDS, myocardial injury, thrombocytopenia, high amylase, pyroglutamic acidosis
134
Q

GI decontamination for panadol overdose

A

Activated charcoal 1g/kg within 1-2h of ingestion

if significant co-ingestion / massive overdose >1g/kg, consider gastric lavage

135
Q

Panadol nomogram name

A

Rumack-Matthew nomogram

136
Q

Poor prognostic marker for liver/death from panadol overdose

A
  1. pH < 7.30 after fluid and hemodynamic resuscitation.
  2. Coexistence of PT>100s, Cr >300 and grade III/IV hepatic encephalopathy
  3. Serum lactate >3.0 to 3.5
  4. Serum phosphate > 1.2 at 40-92 hr
  5. Serum AFP > 3.9 on day+1 after peak ALT identifies patients with favourable outcome
  6. Coagulation factor VIII/V ratio > 30; factor VIII is produced by endothelial cells while Factor V is
    made by hepatocytes
137
Q

Burn care classification
3 levels

A

Level 1. Gen sur / Ortho

Level 2. Burn facility (KWH/QEH/TMH)
- 5-20% TBSA
- Cosmetic
- Full thickness burn
- Electrical / Chemical burn
- Circumferential burn

Level 3. Burn unit (QMH/PWH)
- 20% TBSA for adults / 10% for children <= 12

138
Q

Methods of GI decontamination

Book

A
  1. Single dose Activated Charcoal (AC)
  2. Gastric lavage (GL)
  3. Multiple dose Activated Charcoal (MDAC)
  4. Whole bowel irrigation (WBI)
  5. Surgical intervention
139
Q

AC dose
Book

A

adult 50-100g
children 1g/kg

140
Q

Indication of AC
Book

A

A potential toxic ingestion within 1-2h
up to few hours

141
Q

CI of AC
Book

A
  1. Corrosive
  2. Rapidly absorbed e.g. ethanol
  3. Small molecular size e.g. lithium
  4. Unprotected airway
  5. GIT injury (e.g. corrosive injury)
  6. Non-functioning GIT (e.g. absent gut motility)
    GI endoscopic visualization considered essential
142
Q

MDAC dose
Book

A

Initial single dose AC
then 0.5g/kg Q2-4h x4

143
Q

Cx of MDAC
Book

A
  1. Fatal aspiration
  2. Pneumonitis
  3. SB obstruction
  4. Appendicitis
144
Q

Indication of GL
Book

A
  • A life threatening posion ingestion where poison likely still in stomach
  • Preferred within 1h
145
Q

CI of GL
Book

A
  1. Caustic ingestion
  2. Large FB or sharp objects
  3. Inability to protect airway
146
Q

Cx of GL
Book

A
  1. Aspiration pneumonia
  2. Eso / Gastric perforation
  3. Tension PTX and empyema
  4. Decreased oxygentation during procedure
147
Q

Indication of WBI
Book

A
  1. Potentially toxic ingestions of sustained release / enteric coated drugs, particially >2h
  2. Toxic ingestion of iron, lithium, potassium
  3. Removal of ingested packets of illicit drugs in body packers
148
Q

CI of WBI
Book

A
  1. Absent bowel sound
  2. Bowel obstruction / perforation
149
Q

Hydroxocobalamin indication

A

Cyanide poisoning

150
Q

Hydroxocobalamin SE

A
  1. Reversible pink discoloration of skin, mucous membrane, urine
  2. Muscle spasm and twitching
  3. Hypertension
151
Q

Sodium nitrite indication

A

Cyanide poisoning (prefer to use hydroxocobalamin)

152
Q

Sodium nitrite SE

A
  1. Hypotension
  2. Methemoglobinemia
153
Q

ABCD2 score for TIA

A

A: Age >60

B: BP >= 140/90

C: Clinical features of TIA
Unilateral weakness +2
Speech disturbance +1
Others 0

D (1). Duration of symptoms
<10mins 0
10 mins-1h +1
>=1h +2

D (2). DM

154
Q

High AG acidosis (HAGMA)

CAT MUD PILES

KULT

A

CAT MUD PILES
Cyanide, CO, colchicine
Alcoholic ketoacidosis, acetaminophen (in large doses)
Toluene
Methanol, metformin
Uremia
DKA
Paraldehyde
Isoniazid, iron
Lactic acidosis
Ethylene glycol
Salicylates

KULT
- Ketones (DM/Alcohol/Starvation)
- Uremia
- Lactate (Metformin, Poisons causing convulsion or shock)
- Toxin (methanol, ethylene glycol, salicylate)

155
Q

Substances not binding to AC

PHAILS

A

Pesticides
Heavy metals
Acid / Alkali / Alcohol
Iron
Lithium
Solvents

156
Q

Maisonneuve fracture

A

spiral # of the proximal third of fibula
associated with a tear of the distal tibiofibular syndesmosis and the interosseous membrane

157
Q

Sign of basal skull #

A
  1. Battle’s sign (bruising of mastoid process of temporal bone)
  2. Raccoon eyes (periorbital ecchymosis)
  3. CSF rhinorrhea
  4. Hemotympanum
158
Q

Croup score

A

Westley Croup Severity Score

159
Q

Dog / Cat bite micro-organisms

A

Pasteurella (G-ve coccobacilli)
- canis, multocida, septica

Capnocytophaga canimorsus

160
Q

Rolando #

A

comminuted intra-articular # base of 1st MC

161
Q

Bennett #

A

intra-articular, simple, oblique fracture at base of 1st MC

reverse Bennett #
- fracture-dislocation of base of 5th MC

162
Q

Digoxin toxicity
when to expect

A
  1. Unexplained bradycardia
  2. Non-specific GI/ Neuro complaints
  3. ECG changes
  4. Unexplained hyperK
  5. RF for chronic digoxin toxicity
    - increase sensitivity: hypoK/ hyperCa / hypoMg, hypoxia, underlying cardiomyopathy, ischemia, conduction problems
    - increase serum digoxin levels: CKD, CCB use, recent macrolide, dehydration
163
Q

Digoxin toxicity ECG changes

A

Scooped ST segments (reverse tick appearance)
Prolong PR
ventricular arrhythmias
sinus bradycardia, impaired AVN conduction

164
Q

Digoxin toxicity specific treatment

A

Digoxin-specific antibody fragments (Fab)
K>5.0 = indication for acute single overdose

other
1. GI decontam - AC / MDAC / GL
2. Atropine / pacing for bradyarrhythmias
3. Replace K / Mg, amiodarone, lignocaine when tachyarrhythmias

165
Q

4 types of shock

COHD

A
  1. Cardiogenic (AMI, CHF)
  2. Obstructive (3Ps - Tension PTX, cardiac tamponade, PE)
  3. Hypovolemic
  4. Distributive (septic, anaphylactic, neurogenic)
166
Q

Anion gap calculation

(3 components)

A

Na - (Cl + HCO3)

> 10 = high anion gap

adjust for albumin 0.25 x (40-alb)

167
Q

Osmolar gap calculation

(3 components)

A

Na x2 + Glucose + Urea

168
Q

Score for NF

A

LRINEC Score
Laboratory Risk Indicator for Necrotizing Fasciitis score

169
Q

Hypertropic cardiomyopathy (HCM) ECG features

A

LVH with increased precordial voltages and non-specific ST/T abnormalities
Deep, narrow (“dagger-like”) Q waves in lateral (I, aVL, V5-6) +/- inferior (II, III, aVF) leads

170
Q

Classification of mid face fracture

A

Le Fort

171
Q

Lemierre’s syndrome

A

infectious thrombophlebitis of IJV

172
Q

C1/2 subluxation classification
(atlantoaxial rotatory subluxation)

A

Fielding and Hawkins classification

173
Q

CRITOE (1-11y)

A

Appearance of ossification centers

Capitellum 1y
Radial head 3y
Internal epicondyle 5y
Trochlea 7y
Olecranon 9y
External epicondyle 11y

174
Q

3 common elbow injuries in children

A
  1. Supracondylar fracture
  2. Radial head subluxation
  3. Lateral condyle fracture
175
Q

Human bite micro-organism

A

Eikenella corrodens

176
Q

CRAO management

A
  1. Ocular massage
  2. Breathe into a paper bag
  3. IV Acetazolamide, Timolol eye drops
  4. HBOT
177
Q

ACLS modifications for pregnant women

A
  1. Manual displacement of uterus to left
  2. IV set above diaphragm
  3. Airway / ventilation priority (expect laryngeal edema)
178
Q

6P for Compartment syndrome

A
  1. Pain
  2. Poikilothermia (Perishing cold)
  3. Paresthesia
  4. Paralysis
  5. Pulselessness
  6. Pallor
179
Q

Pott puffy tumor

A

Subperiosteal abscess due to associated frontal skull osteomyelitis

180
Q

MR SOPA for NRP

A

Mask adjustment
Reposition airway

Suction mouth then nose
Open mouth

Pressure increase (up to 40)

Alternate airway

181
Q

Neck zones 1-3

A

Zone 1: Clavicle to Cricoid cartilage

Zone 2: Cricoid cartilage to angle of mandible

Zone 3: Angle of mandible to base of skull

2 most common, easier exploration
1 most dangerous

182
Q

LEMON rule

A

Look externally
- Facial trauma
- Large incisors
- Beard / moustache
- Large tongue

Evaluate 3-3-2 rule
- Inter-incisor distance 3 finger breadths
- Hyoid-mental distance 3 finger breadths
- Hyoid-thyrioid distance 2 finger breadths

Mallampati (>=3 is difficult)

Obstruction (epiglottitis, quinsy, trauma)

Neck mobility

183
Q

Ramp position for obesity intubation

A

head and torso are elevated such that the external auditory meatus and the sternal notch are horizontally aligned
CI if neck injury

184
Q

Lethal triad of trauma

A

Hypothermia
Acidosis
Coagulopathy

185
Q

Cushing triad for raised ICP

A
  1. Widened pulse pressure
  2. Bradycardia
  3. Irregular respiration (Cheyne–Stokes respirations)
186
Q

Quetiapine overdose effects

A

Dose-dependent CNS depression

Peripheral alpha blockade -> parodixcal hypotension if given adrenaline (beta 2 mediated vasodilatation)

Clinical features
-Sedation
-Tachycardia, common to be 120 bpm
-Hypotension
-Mild to moderate anticholinergic syndrome

187
Q

Magnesium sulphate for Asthma dose

A

MgSO4 2g over 20 mins IV

CI: renal failure, hyperMg

188
Q

Chance fracture

A

Unstable
Flexion-distraction injury
Seatbelt sign
typical in TL junction
asso w/ intra-abd injury e.g. duodenum

189
Q

Zopiclone overdose

A

Methemoglobinemia
Hemolytic anemia

190
Q

Tuna Fish for LBP red flags

A

Trauma
Unexplained weight loss
Neurological symptoms / signs
Age > 50
Fever
Intravenous drug use
Steroid use
History of cancer

191
Q

CXR signs for aortic dissection
x7

EM handbook

A
  1. Widened mediastinum
  2. Left pleural effusion
  3. R sided tracheal deviation
  4. Calcium sign (separation of calcification at aortic arch)
  5. Double aortic knob sign
  6. Pericardial effusion
  7. Displacement of NG tube
192
Q

Echo signs for aortic dissection

EM handbook

A
  1. Aortic root dilatation
  2. Aortic regurgitation (AR)
  3. Pericardial effusion
  4. Ventricular wall regional wall abnormalities implying coronary ostial occlusion
193
Q

Echo probe manipulation

POCUS

A
  1. Sliding
  2. Rocking (towards and away indicator)
  3. Tiliting (Fanning)
  4. Rotation
194
Q

McConnell’s sign for PE

A

RV free wall akinesis with sparing of the apex

195
Q

Echo findings of PE

A

RV dilatation
RV free wall hypokinesis
McConnell’s sign
IV septum flattening -> D shaped LV
Tricuspid regurgitation
60/60 sign

196
Q

Drug cause of prolonged QTc
5A + CLAM

Toxi book

A

5A + CLAM

  1. Anti-arrhythmic
  2. Anti-depressants
  3. Anti-psychotic
  4. Anti-histamine
  5. Anti-microbial (Macrolide, FQ, Amantadine, Antifungal)
  6. CLAM (Cisapride, Cesium, Lithium, Arsenic, Methadone)
197
Q

HyperK ECG changes

A
  1. Peaked T waves
  2. P wave widening/flattening, PR prolongation
  3. Bradyarrhythmias: sinus bradycardia, high-grade AV block with slow junctional and ventricular escape rhythms, slow AF
  4. Conduction blocks (bundle branch block, fascicular blocks)
  5. QRS widening with bizarre QRS morphology
198
Q

Triad of opioid toxidrome

Tox book

A

CNS depression
Resp depression
Miosis

199
Q

Methadone

Diploma

A

Long acting synthetic opioid
Prolong QTc

200
Q

Na channel blockade toxidrome

SALT
Diploma

A

Shock
Altered mental status
Long QRS
Terminal right axis deviation

201
Q

One tab kill (10kg infant)

NOCT
Diploma FL

A

Narcotic
Oral hypoglycemic, Oil (Methylsalicylate)
CCB, Camphor, Chloroquine/Quinine
TCA, Theophylline, Thioridazine/Chlorpromazine, Toxic alcohol

202
Q

Toxic alcohol
x3
Toxi book

A

Methanol
Ethylene glycol (EG)
Diethylene glycol (DEG)

203
Q

CNS stimulants example

x3
Toxi book

A
  1. Methamphetamine
  2. MDMA (3,4-Methyl​enedioxy​methamphetamine), aka Ecstasy (tablet), Molly (crystal)
  3. Cocaine
204
Q

CNS depressants example

x6
Toxi book

A
  1. Opioids
  2. Benzodiazepines
  3. GHB (gamma-hydroxybutyrate)
  4. Organic solvent
  5. Barbiturates
  6. Ethanol
205
Q

Dissociatives example

x3
Toxi book

A
  1. Ketamine
  2. Dextromethorphan (DXM)
  3. Phencyclidine

Blocks NMDA receptor

206
Q

Hallucinogens example

x2
Toxi book

A
  1. Cannabis
  2. LSD (lysergic acid diethylamide)
207
Q

Urine ABON for cocaine

Toxi book

A

Unlikely false positive
Detects Benzoylecgonine

208
Q

Toxicity of Cocaine

Toxi book

A
  1. Sympathomimetic toxidrome
  2. CNS (psychomotor agitiation, seizure, ICH, TIA, infarct)
  3. CVS (ACS, HT emergency, AAS, arrhythmia, vasospasm)

Cocaine ACS: enhanced platelet aggregation and reduces endogenous thrombolysis

  1. Pulmonary (Pneumothorax, Pneumomediastinum, Pneumopericardium; non-cardiogenic pul edema, asthma exacerbation

“Crack lung”: diffuse alveolar damage and hemorrhagic alveolitis occuring within 48h of smoking crack.
Present w/ fever, dyspnea, hemoptysis, hypoxia, ARDS

209
Q

Cocaine common killer

x3
Toxi book

A
  1. Hyperthermia
  2. Arrhythmia
  3. ICH
210
Q

Tx for cocaine

Toxi book

A

Rapid cooling, use of BZD and supportive measures
Avoid BB in early phase due to unopposed alpha-adrenergic effect
(use Phentolamine)

Treat ACS
Treat HT emergency / seizure
Treat widening QRS and ventricular arrhythmia (NaHCO3)
Treat limb and bowel ischemia

211
Q

Cannabis - major active ingredient

Toxi book

A

THC (Delta-9-tetrahydrocannabinol)

**CBD (Cannabidiol) does not interact with cannabinoid receptors and does not have same psychoactivity as THC

212
Q

Complications of Cannabis use

Toxi book

A
  1. Pneumothorax
  2. Pneumomediastinum
  3. Paroxysmal AF
213
Q

Urine ABON for Cannabis

Toxi book

A

False positive: Naproxen, Ibuprofen, Efavirenz

Look for THC and its metabolites

214
Q

GHB and GBL

Toxi book

A

Gamma-hydroxybutyrate (GHB) - odorless

Gamma-butyrolactone (GBL) is prodrug of GHB - melon aroma

Urine ABON cannot detect
Send blood/urine sample to TRL in 6 hours

215
Q

Organic solvents / Volatile hydrocarbon
3 types

Toxi book

A
  1. Aliphatic HC
    - Butane (Lighter fuel)
  2. Halogenated HC
    - Trichloroethylene (Correction fluid)
    - Trichloroethane
  3. Aromatic HC
    - Toluene (Thinner)
    - Xylene (Glue)
216
Q

Toxicity of volatile hydrocarbon

Toxi book

A

Aliphatic: CNS, chemical pneumonitis from aspiration

Halogenated: also cardiac (sudden sniffing death -sudden surge of endogenous catecholamines + sensitize myocardium causing ventricular arrhythmia) and liver toxicities

Aromatic:
Toluene - renal tubular acidosis + profound hypoK
Benzene - hematotoxicity (hemolysis, aplastic anemia), carcinogenicity

217
Q

Treatment of volatile HC

Toxi book

A
  1. Supportive care, avoid catecholamine surge
  2. BZD to control agitation
  3. Early use of BB (e.g. esmolol) as anti-arrhythmic in resuscitation of sudden sniffing ventricular tachyarrhythmia
218
Q

Ketamine

Toxi book

A

Dissociative anesthetic agent
Mainly act on CNS + CVS
Snorted in white powder

Binds to NMDA receptors, biogenic amine uptake complex, sigma receptor, ACh receptorCl

219
Q

Ketamine - clinical presentation

Toxi book

A

Altered mental status (most common), with mild sympathomimetic

Chronic: ketamine associated urinary tract dysfunction, ketamine associated abdominal pain
reversible dilated CBD

220
Q

Urine ABON for ketamine

Toxi book

A

False positive common

221
Q

Tx for Ketamine

Toxi book

A
  1. Supportive care, prevent secondary injury
  2. BZD to control agitation
  3. Observe 4-6 hours for effect to wean off
222
Q

Poppers

Toxi book

A

Various volatile alkyl nitrites
used in chemsex
relaxes anal sphincter for MSM
May cause MetHb

223
Q

Drugs used in Chemsex

Toxi book

A

Metamphetamine
Mephedrone
GHB, GBL
Alkyl nitrites, ecstasy (MDMA), foxy, ketamine, cocaine, cannabis, sildenafil

224
Q

Body packer

Toxi book

A

Individuals who attempt to smuggle drugs inside their bodies
Drugs well packed and concealed by ingestion or insertion into body orifices (rectum, vagina)

Cocaine is most common in HK

225
Q

Body stuffer

Toxi book

A

Individuals who ingest or insert illegal drugs hastily to evade law enforcement officials
Drugs poorly wrapped, more than one class of drugs can be ingested
Variable patterns of poisoning

Most are asymptomatic / mildly toxic

226
Q

Cardioactive steroids

Toxi book

A
  • A class of naturally occuring compounds, cotains a steroid nucleus
  • Causes positive inotropic effect and decrease HR at therapeutic dose

2 major actions
1. Inhibit myocardial cells Na-K ATPase pump
Toxic dose: excessive increase intracellular Ca -> tachydysrhythmia

  1. Increase vagal tone
    Sinus bradycardia, AV block, bradydysrhythmia

Toxic effects enchaned by hypoK and hypoMg

227
Q

Causes of acute Digoxin / Cardioactive steroids poisoning

Toxi book

A
  1. Intentional overdose
  2. Cardioactive steroids exposure (accidental Chan Su overdose)
228
Q

Causes of chronic Digoxin / Cardioactive steroids poisoning

Toxi book

A
  1. Dosing error
  2. Decreased renal digoxin elimination (dehydration, impaired renal fx, nephrotoxic drug use)
  3. Increased sensitivity to digoxin (decompensated cardiac conditions, concomitant use of negative inotropic or chronotropic agents, hypoK)
229
Q

Presentation of Digoxin / Cardioactive steroids poisoning

Toxi book

A

GI: Nausea, vomiting, anorexia

CNS: headache, confusion, visual disturbance (alteration in color perception: xanthopsia)

Metabolic: HyperK

230
Q

Risk stratification for Digoxin / Cardioactive steroids poisoning

Toxi book

A

HyperK
(>5.5 all dead)

231
Q

ECG change of Digoxin / Cardioactive steroids poisoning

Toxi book

A

Scooped ST segments (reverse tick appearance)
Prolong PR

*Increase automaticity with high degree AV block
Fast AF not compatible, otherwise all arrhythmia can happen

232
Q

Ix for Digoxin / Cardioactive steroids poisoning

Toxi book

A

Urgent serum digoxin level
(normal 1.1-2.6nmol/L)

ng/ml x 1.3 = nmol/L

undectable digoxin level cannot exclude cardioactive steroid poisoning
may be detectable due to cross-reactivitiy

233
Q

Mx for Digoxin / Cardioactive steroids poisoning

Toxi book

A
  1. ABC
  2. GI decon: GL + AC within 1-2h; consider MDAC in severe cases
  3. Digoxin specific Ab fragments (Digoxin-specific Fab)
    - binds and eliminates intravascular free digoxin
    - thus facilitates dissociation of digoxin from its intracellular binding sites (Na-K ATPase)
  4. HyperK to be treated by DigiFab, no DI drip unless marked hyperK
  5. Avoid Calcium - may arrest, give Digifab before IV calciuim if really indicated, e.g. concomittant CCB poisoning
  6. Cardioversion - start with low energy e.g. 10-25J
  7. Hemoperfusion / HD not useful
234
Q

Indications of Digoxin specific Ab fragments

Toxi book

A

Any of
1. Life threatening clinical presentation (ventricular dysrhythmia, bradydysrhythmia not responsive to atropine)

  1. Serum K >5 (attributable to digoxin / cardioactive steroid)
  2. Serum digoxin level >10ng/ml (13nmol/L) at 6h post ingestion or >15 ng/ml (19.5nmol/L) at any time for acute ingestion
  3. Digoxin ingestion of >10mg in adult or >4mg in child
235
Q

How to give Digoxin specific Ab fragments (DigiFab)

Toxi book

A

Empirical :
Acute - 10 vials (same for adult/child)
Chronic - Start with 1-2 vials, titrate with clinical effect

Ingestion amount in mg x 1.6 = x vials
Serum digoxin (nmol/L) x body weight (kg) / 130 = x vials

236
Q

SE of Digoxin specific Ab fragments (DigiFab)

Toxi book

A
  1. HypoK
  2. Exacerbate CHF
  3. Increase ventricular response in AF patients

Renal failure patients may have digoxin re-intoxication
Falsely elevated serum digoxin level after treatment (measures both free and Fab-bound digoxin in serum)

237
Q

Which vitamin acute overdose has toxicity

x3
Toxi book

A

A (>300kIU or >25kIU/kg in children)

B3, i.e. Niacin

Iron

238
Q

Which vitamin chronic overdose has toxicity

x4
Toxi book

A

A

B6, i.e. Pyridoxine

C

D

239
Q

Vit A overdose

Toxi book

A

Acute + Chronic possible

Present with nausea, vomiting, diarrhea, abd pain
severe cases: CNS - headache, visual disturbance, increased ICP
Pruritus, skin peeling

Supportive Mx
Blood vit A level available in TRL

240
Q

Vit B3 (Niacin) overdose

Toxi book

A

Only acute

Present with GI disturbance, DKA like syndrome
Supportive Mx

241
Q

Vit B6 (Pyridoxine) overdose

Toxi book

A

Only chronic
acute non-toxic

Present with sensory peripheral neuropathy

242
Q

Vit C overdose

Toxi book

A

Only chronic
acute non-toxic

Renal failure patients -> graft failure
high dose parenteral -> oxidative hemolysis, MetHb, AKI in G6PD def

243
Q

Vit D

Toxi book

A

Only chronic
acute non-toxic

Present with hyperCa, GI disturbance, dehydration
Supportive Mx, correct hyperCa/rehydration

244
Q

Indications of IV lipid emulsion (ILE)

Toxi book

A
  1. Severe LA poisoning
  2. Life threatening lipophilic drug poisoning, esp TCA, CCB

Dose: Intralipid 20% 1.5ml/kg IV bolus over 1 min, then infusion 0.2ml/kg/min
end point = cumulative 10ml/kg

245
Q

SE of IV lipid emulsion (ILE)

Toxi book

A
  1. lipemic serum, affecting lab tests
  2. elevated amylase
  3. fever
  4. transient dLFT
  5. resp distress
  6. coagulopathy
  7. circuit obstruction of extracorporeal devices, e.g. ECMO, hemofiltration, plasmapheresis
246
Q

When to consider Enchanced elimination

Toxi book

A

Life threatening clinical toxicity
Dose exposed / blood level indicate severe morbidity / likely mortality
Impaired normal route of elimination
Fail to respond to maximal supportive measures

247
Q

Common routes of EE

Toxi book

A
  1. GIT: MDAC
  2. Urine: Urine alkalinization
  3. Blood: ECTR (Extrocorporeal tx): HD, HP, HF

Forced diuresis, urine acidification, PD no longer considered

248
Q

Urine alkalinization indication (which drugs)

x6
Toxi book

A
  1. Aspirin
  2. Phenobarbital
  3. Chlorpropamide
  4. Formate
  5. MTX
  6. 2-4 D (2,4-dichlorophenoxyacetic acid)
249
Q

Mechanism of urine alkalinization

Toxi book

A

Works by ion trapping
Urine pH >7-8 to be effective
Avoid hypoK - will dump H to reabsorb K - less effective

250
Q

How to do urine alkalinization

Toxi book

A

1-2ml/kg 8.4% NaHCO3 bolus
Continuous infusion of 50ml 8.4% NaHCO3 in 500ml D5 and titrate

Avoid serum pH >7.55 (serial monitor)
Avoid hypoK

251
Q

Choice of ECTR (Extracorporeal tx)

Toxi book

A

Poison factor
- HD preferred if not absorbed by charcoal
- HP preferred if high protein binding

Patient factor
- HF more hemodynamically tolerable

Other factors
- facilities, equipment, expertise

252
Q

Antidotes Lvl 1
NAC, Atropine, Bromocriptine, Calcium

Toxi book

A

NAC (N-Acetylcysteine)
Paracetamol poisoning
Also used in Amatoxin, Chloroform, Carbon tetrachloride, Acrylonitrile, Doxorubicin, Cyclophosphamide, Paraquat, Radiographic contrast nephropathy

3-bag regime
- 150mg/kg in 200ml D5 over 1h (15min if no asthma and present >8h)
- 50mg/kg in 500ml D5 over 4h
- 100mg/kg in 1L D5 over 16h (double if massive overdose)

2-bag regime
- 200mg/kg in 500ml D5 over 4h
- 100mg/kg in 1L D5 over 16h (double if massive overdose)

Atropine
- in Cholinergic poisoning (OP, carbamate insecticide)
0.6-1.2mg IV
Endpoint: Drying of secretions, clearing of bronchial/pul rales
- in Poison induced bradycardia
Endpoint: reverse life threatening bradycardia
SE: anticholinergic effects

Bromocriptine
- Dopamine D2 agonist
- used in NMS / L-dopa withdrawal

Calcium
- in CCB poisoning
1g CaCl2 or 3g Ca gluconate slow IV
Up to 3g CaCl2 without serum Ca monitor
Titrated Ca infusion
Tolerable level at serum Ca <2x ULN or ionized Ca <2mmol/L
-in Hydrofluoric acid poisoning
Topical Ca gluconate gel / local infiltration / intra-arterial Ca gluconate for sig hand exoisures
SE: Local irritation, hyperCa

253
Q

Antidotes Lvl 1
Cyproheptadine, Dantrolene, Desferrioxamine, Digoxin Fab

Toxi book

A

Cyproheptadine
used in Serotonin syndrome
PO 8-12mg, then 2mg Q2H; Max 32mg in first 24h

Dantrolene
Postsynaptic muscle relaxant
used in Malignant hyperthermia

Desferrioxamine
- Iron poisoning with systemic toxicity OR
- Serum iron >500ug/dL (88.8umol/L)
Start with 5mg/kg/h titrate up to 15mg/kg/h IV
6-8g over 24h for adults
SE: rate related hypotension, flushing erythemia, urticaria, increased infection (Yersinia), acute lung injury, vine rose urine

Digoxin Fab
- Digoxin and cardioactive steroids poisoning
10 vials empirical

254
Q

Antidotes Lvl 1
Dimercaprol (BAL), DMPS (Injection), Ethanol, Flumazenil

Toxi book

A

Dimercaprol (BAL i.e. British anti-lewisite)
given IMI
Chelation for lead encephalopathy, acute mercury and arsenic poisoning
75mg/m2 IMI Q4H for 3-5 days

DMPS (Injection), aka Dimaval, [RS]- 2,3-Bis(sulfanyl) propane-1-sulfonic acid
given Oral/IV
Chelation in arsenic, lead, mercury poisoning

Ethanol
- used in Toxic alcohol poisoning

Flumazenil
- Competitive BZD receptor antagonist
- used in CNS depression caused by BZD, zopiclone, zolpidem overdose
Risk: precipitate seizure in epileptics, withdrawal seizures in BZD dependent patients, induce arrhythmia in cardiotoxic drugs co-ingestion
CI:
1. Long term use of supratherapeutic dose of BZD, zopiclone or zolpidem
2. TCA poisoning
3. Co-ingestion of pro-seizure or pro-arrhythmic agents (e.g. abusive drugs, tramadol, bupropion)
4. Known epilepsy
SE: seizure, arrhythmia

Start with 0.2mg IV, onset 1-2 mins
Repeated dose of 0.2-0.3mg IV every 1-2 mins up to 1mg total

255
Q

Antidotes Lvl 1
Glucagon, Hydroxocobalamin, Idarucizumab, Intralipid 20%

Toxi book

A

Glucagon
- used in BB or CCB overdose with hypotension and/or bradycardia
Start with IV bolus 2-5mg IVI over 1 min (up to 10mg)
Maintenance: initial response dose/h in D5, titrate clinically
SE: N/V, hyperglycemia, hypoK, hypoglycemia after prolonged infusion

Hydroxocobalamin
- Cyanide poisoning
- indication: cardiac arrest, GCS <=13, hypotension, lactate >10mmol/L
Adult 5g IV, repeat same dose in severe
SE: reversible red discoloration of skin, mucous membrane and urine

Idarucizumab
- Dabigatran reversal
- 5g IV over 5-10 mins or bolus if emergency
SE: thrombotic events, allergic reactions

Intralipid
- Severe LA poisoning with systemic toxicity
- Investigational therapy for lipophilic drug poisoning (TCA, CCB)
1.5ml/kg bolus over 1 min, followed by infusion 0.25ml/kg/min
Repeat bolus if persistent severe
SE: Lipemic serum affecting lab Ix, elevated amylase, fever, transient dLFT, resp distress, coagulopathy, potential circuit obstruction in extracorporeal devices (ECMO, HF)

256
Q

Antidotes Lvl 1
Methylene blue, Naloxone, Penicillamine, Physostigmine

Toxi book

A

Methylene blue
- MetHbemia with sig symptoms of hypoxia
- Consider for asymptomatic patients with MetHb>20%
1-2mg/kg IV over 5 min; may need repeat dose/infusion
SE: blue/green discoloration of urine, transient worsening of apparent pulse oximeter reading, cautious in G6PD def patients, potential drug-drug interaction with serotonergic drugs resulting SS

Naloxone
- Opioid receptor antagonist
- Reversal of CNS/Resp depression in opioid overdose: RR <12, coma, small pupils
Occasionally effective in Clonidine or other alpha2 agonist, VPA, ACEI overdose
0.4 to 2mg IV bolus; up to 2mg (natural e.g. morphine) or 10mg (synthetic, e.g. tramadol)
Start with lower if chronic user at 0.05-0.1mg to avoid withdrawal
Goal is to keep breathing/oxygenating
Infusion: 2/3 of initial effective bolus dose on hourly basis
SE: opioid withdrawal

Penicillamine
Chelating agent, used in Wilson’s disease (copper poisoning), cystinuria, lead poisoning

Physostigmine
used in Central anticholinergic poisoning
Initial dose 1-2mg IV in adult slow IV over 5 mins
Repeat in 10-15 mins if inadequate effect
Put on cardiac monitor, with atropine and resus equipment standby, stop if cholinergic symptom
SE: precipitate seizure / asystole esp if IV too rapid, cholinergic crisis if wrong Dx

257
Q

Antidotes Lvl 1
Pralidoxime, Pyridoxine, Protamine, Sodium bicarbonate

Toxi book

A

Pralidoxime
- used in OP poisoning
30mg/kg up to 2g over 30 mins
Followed by infusion 8-10mg/kg/h in adult, titrate down in 24-48h according to clinical response
SE: headache, dizziness, diplopia, blurred vision, HT, ECG TWI

Pyridoxine (Vit B6)
- used in Isoniazid, Hydrazine, Gyromitra mushroom, Ginkgo seeds poisoning
- adjunct use in tetramine, ethylene glycol poisoning
SE: Neurotoxicity - peripheral neuropathy

Protamine
- used in heparin reversal

Sodium bicarbonate (NaHCO3)
For sodium load / blood alkalinization
Indication: TCA / other Na channel blockers poisoning with QRS >100ms, Salicylate poisoning
1-2ml/kg 8.4% NaHCO3 IV bolus to achieve serum pH 7.45-7.55
CI:
- serum pH >7.55 (consider hypertonic saline as alternative)
- Intolerable Na/fluid load (consider hyperventilation as alternative)
SE: Na/fluid load, hypoK

For urine alkalinization
Indication: Enhance excretion of Salicylate, Phenobarbitone**, MTX, Chlorpropamide, 2,4-dichlorophenoxyacetic acid, Formate
Generally use MDAC for Phenobarbitone as much more effective
1-2ml/kg 8.4% NaHCO3 IV bolus
50ml in 500ml D5 Q4H and titrate
Aim: serum pH 7.45-7.55, urine pH 7-8
Monitor and replace K

258
Q

Antidotes Lvl 1
Sodium nitrite, Sodium thiosulphate, Sucralfate, Vit K1

Toxi book

A

Sodium nitrite / thiosulphate
- used in Cyanide poisoning (but hydroxocobalamin is preferred)
3% sodium nitrite 10ml (300mg)
25% sodium thiosulphate 50ml (12.5g)
SE: hypotension, MetHBemia

Sucralfate
Protect against GIT corrosive injury
For button battery ingestion
Suspension 5ml (containing 1g sucralfate) PO every 10 mins, up to 3 doses, within 12h

Vit K1
For warfarin/superwarfarin poisoning
1mg to 10mg as starting dose, titrate according to INR, clinical bleeding; severe cases may need >100mg/day
PO/SC preferred
SE: rarely Anaphylaxis in IV

259
Q

Antidotes Lvl 2
Calcium EDTA, Folinic acid, L-Carnitine, Octreotide, Phentolamine

Toxi book

A

Calcium disodium EDTA
- for lead poisoning

Folinic acid
- for MTX poisoning

L-Carinitine
- for VPA induced hyperammonemia, encephalopathy, hepatotoxicity
- consider in massive VPA overdose: >400mg/kg or VPA level >450mg/L (3123umol/L)
Loading 100mg/kg, maintenance 50mg/kg Q8H for 24h
SE: minimal in general

Octreotide
- Refractory hypoglycemia with sulphonylurea poisoning
- Consider in quinine, newer insulin secretagogues, insulin overdose
50ug SC or IV Q6H for 24h (dilute in 50ml NS/D5 over 15-30 mins for IV)
Further observe hypogly for 24h after stopping
SE: stinging sensation at injection site, N/D, abd pain, anaphylactoid

Phentolamine
- Non-selective alpha blocker, can treat HT crisis
- Reversal of vasoconstriction and treatment of dermal necrosis and sloughing
following extravasation of peripheral administration of vasoconstrictor e.g. noradrenaline

260
Q

Antidotes Lvl 2
Antiveom x4

Toxi book

A

Bungarus multicinctus antivenin (for many banded krait)
Naja Naja (atra) antivenin (for chinese cobra)
Green pit viper antivenin (for bamboo snake)
Neuro polyvalent snake antivenin (for banded krait, king cobra, naja kaouthia, malayan krait)

261
Q

Antidotes Lvl 3

Acetamide
Botulism antitoxin heptavalent
Fomepizole
DMPS (oral)
Methionine
Prussian blue
Silibinin / Silymarin
Succimer (DMSA)

Toxi book

A

Acetamide
- for rodenticide Sodium monofluoroacetic acid (SMFA) poisoning

Botulism antitoxin heptavalent
- for botulism

Fomepizole
- for toxic alcohol poisoning (methanol, ethylene glycol)

DMPS (oral)
- for arsenic, lead, mercury poisoning

Methionine
- precursor of glutathione
- for paracetamol poisoning, less preferred than NAC
- only use when definite history of life-threatening NAC hypersensitivity reaction

Prussian blue
- works by ion trapping in GIT for Cesium and thallium poisoning

Silibinin (IV) / Silymarin (PO)
- used for Amatoxin mushroom poisoning
Silibinin 5mg/kg IV over 2h Q6H x 24-48h
Silymarin if silibinin not a/v, 700mg TDS x 4 days
SE: N, GI discomfort, urticaria

Succimer (DMSA)
- used for lead, mercury, arsenic poisoning
SE: GI upset, mild dLFT, neutropenia (rare), allergic reactions

262
Q

Antidotes Lvl 3

Antivenom x6

Toxi book

A

Agkistrodon acutus
Russell’s viper
Tr. Muscrosqumatus + Tr. Gramineus

Scorpion
Sea snake
Stonefish

263
Q

4 types of mushroom poisoning syndromes

Monograph / Book

A
  1. Gastroenteritic (Chlorophyllum molybdites, Russula emetic, Porcini) – 80%
  2. Hepatotoxic (Amanita farinose, Amanita exitalis)
  3. Cholinergic (Inocybe rimosa, Mycena pura)
  4. Hallucinogenic (Porcini – VH of micropsia or macropsia)
264
Q

Amatoxin present in which species

Monograph / Book

A

Amanita species (A. Phalloides, A. verna, A. virosa)
Galerina species (G. autumnalis, G. marginata, G. veneta)
Lepiota species (L. helveola, L. josserandi, L. brunneoincarnata)

Fatal cases: Amanita exitialis

265
Q

Toxicokinetic / pathophysiology of Amatoxin mushroom poisoning

Monograph

A

Toxin: Alpha-amanitin
Interferes RNA polymerase, inhibit protein synthesis, causing cell death
Mainly excrete in urine but also significant amount in bile

266
Q

Clinical features of Amatoxin mushroom poisoning

Monograph

A

Delayed onset GI symptoms >= 6 hours after ingestion

Triphasic syndrome
Phase 1: GE start 6-24h; Vomiting, abd pain, cholera-like watery diarrhea
Phase 2: Lucent period with improving symptoms at 12-36h
Phase 3: Liver, renal failure, death after 2-6 days. Presents with jaundice, HE, coagulopathy, hypoglycemia

267
Q

Ix of Amatoxin mushroom poisoning

Monograph

A

CBC, LRFT, Clotting, blood gas
Serial serum lactate Q6H
Hourly urine output
Save mushroom samples, contact HKPIC for urgent mycologist identification
Send blood and urine to TRL

268
Q

Mx of Amatoxin mushroom poisoning

Monograph

A
  1. IVF rehydration (most important): aim >150ml/hr // 2-3ml/kg/hr
  2. Silibinin IV, useful within 120 hours after ingestion, 5mg/kg IV over 2h Q6H
    Silymarin PO if Silibinin not a/v, 700mg TDS for adult or 10mg/kg for children, do not
    give AC at same time, defer if nasobiliary drainage can be arranged within 2h
    MDAC, give for at least 3 days, defer if nasobiliary drainage can be arranged within 2h
    NAC full course + maintenance
  3. Contact QMH LT unit
  4. Urgent ERCP nasobiliary drain placement without sphincterotomy, preferably within 2h
  5. May consider: High dose Pen G, early charcoal HP
    Not useful: PO cimetidine, forced diuresis, HF or HD, steroid, thioctic acid
269
Q

Scombroid food poisoning
Which fish

Book

A

Scombridae: Tuna, Mackerel, Bonito
Non-scombridae: sardine, mahi-mahi, amberjack, albacore
Usually on spoiled fish skin

270
Q

Clinical features of Scombroid food poisoning

Book

A

Symptom onset within minutes to hours after ingestion
Flushing, urticaria, headache, N/V
Bronchospasm, angioedema, hypotension
Self-limiting, resolves within 6-8 hours

271
Q

Mx of Scombroid food poisoning

Book

A
  1. Supportive tx
  2. IVF for hypotension
  3. Antihistamine for symptoms
  4. Bronchodilator for bronchospasm
  5. Adrenaline seldom needed
  6. Normal serum tryptase (taken 1-2h from onset) -> exclude food allergy/anaphylaxis
272
Q

Mad honey poisoning
Which toxin

Book

A

Grayanotoxin
From Rhododendrons flowers, common in Black Sea area of Turkey and Nepal

273
Q

Clinical features of Mad honey poisoning

Book

A

Dose dependent onset, from few mins to 2 hours or more
Bitter / astringent taste of honey

Mild:
GI: N/V/D, burning throat sensation
Neuro: dizziness, weakness, paresthesia, blurred vision, hypersalivation, excessive perspiration

Severe:
Hypotension, bradycardia, AV block, shock, asystole, convulsion
Mimics AMI

274
Q

Biotoxins for food poisoning
x4

Book

A

Ciguatoxin (coral fish)
Tetrodotoxin (pufferfish)
Saxitoxin (paralytic shellfish)
Histamine (scombroid)

Short incubation more likely toxin
Long incubation more likely infective

275
Q

Food type food poisoning of the following
Vibrio parahaemolyticus
Botulism
Clenbuterol
Pesticide

Book

A

Vibrio – undercooked seafood
Botulism – Canned food
Clenbuterol – Pigs’ offal
Pesticide – vegetables

276
Q

Toxin causing GI symptoms within 6h

Book

A

Staph enterotoxin (S. aureus)
Cereulide (Bacillus cereus)
Ca oxalate raphides (Alocasia macrorrhiza)
Colchicine (Fresh Jin Zhen)
Phytohaemagglutinin (undercooked green bean)
Solanine (green/sprouting potato)
Metallic ions (acidic beverages from metal containers, copper/zinc/tin)
GI irritants (GI irritant mushrooms, e.g. Chlorophyllum molybdites)

277
Q

Toxin causing GI symptoms beyond 6 hours

Book

A

Clostridium perfringens (8-16h, toxin production in gut)
Salmonella, Shigella, Vibrio parahaemolyticus (16-72h)
Amatoxin (>6h)

278
Q

Toxin causing Early neuro and systemic symptoms (Within few hrs)

Book

A

Ciguatoxin
Brevetoxin (neurotoxic shellfish poisoning)
Saxitoxin (paralytic shellfish poisoning)
Domoic acid (amnestic shellfish poisoning)
Tetrodotoxin
Nitrites
Organophosphorus insecticide

279
Q

Toxin causing delayed neuro symptoms >6h

Book

A

Botulinum toxin
Methanol
Cyanogenic glycosides
Methoxypyridoxine (Ginkgotoxin)

280
Q

Bongkrekic acid poisoning

Book

A

Produced by Burkholderia gladioli pv. Cocovenenans (BGC); Gram neg, aerobic bacillus
In fermented corn and coconut products, improperly soaked black fungus
Heat stable polypeptide
Mitochondrial toxin by inhibiting adeneine nucleotide translocase (ANT)

281
Q

Clinical features of Bongkrekic acid poisoning

Book

A

Onset 1-10h
Abd pain, V/D
Hyperglycemia initially then hypoglycemia
Hypotension, arrhythmia
Liver + renal derangement
Hematochezia, hematuria, oliguria, coma, death

282
Q

Diagnosis of BA poisoning

Book

A

Epidemiological link
Demo of BGC by either culture or 16S rDNA sequencing
Demo of BA in food residues

283
Q

Mx of BA poisoning

Book

A

Supportive
Dextrose for hypoglycemia
Renal support for renal failure

284
Q

Ciguatera poisoning in which fish

Book

A

Groupers, snappers, moray eel, hump head wrasse

285
Q

Pathophysiology of Ciguatera poisoning

Book

A

Ciguatoxin produced by dinoflagellate Gambierdiscus toxicus
Concentrated in liver, gonads, viscera
Heat and acid stable
Act on Na channels, increasing their permeability

286
Q

Clinical features of Ciguatera poisoning

Book

A

Within 6h
Subside in days, may last for months
Mainly GI, neuro, CVS symptoms
Neuro symptoms typically most troubling and persistent

GI symptoms
Abd pain, D, painful defecation

Neuro symptoms
Paresthesia, dysesthesia
Tingling sensation in extremities or mouth
Cold dysesthesia over extremities (pathognomonic)
Metallic taste in mouth, sensation of itchy/loose teeth
Others: bradycardia, hypotension, altered mental state, resp failure

287
Q

Mx of Ciguatera poisoning

Book

A

Supportive
GI decon if early
IV mannitol 1g/kg over 1h
Gabapentin 400mg TDS

288
Q

Preventing Ciguatera poisoning

Book

A

Avoid eating large coral fish >3 catties, esp head, skin, viscera
Recovered patients should avoid consuming alcohol, peanuts or beans; avoid further coral fish consumption
(Avoid lose weight?)

289
Q

Clenbuterol poisoning

Book

A

Beta-2-adrenergic agonist with anabolic and lipolytic effect
Pig’s meat / offal
Stimulate beta-2 adrenergic receptor -> dilate BV to skeletal muscles inducing muscle hypertrophy

Influx of K into cell -> hypoK, muscle paralysis
Cautious hypoK replacement as shifting rather than deficient

Mild symptoms require no tx, beta blocker if symptomatic

290
Q

Cyanogenic glycoside poisoning

Book

A

Causes cyanide poisoning
Food involved: kernel of fruits of Prunus specieis, e.g. apricot, peaches, pears, apples; bitter almond; cassava; bamboo shorts; young sorghum

291
Q

Clinical features of cyanogenic glycoside poisoning

Book

A

Early may be non-specific: GI disturbance, dizziness, headache, weakness

Chronic: toxic ataxic neuropathy (optic atrophy, sensorineural hearing loss, posterior column involvement, ataxia), Konzo (spastic paraparesis), hypothyroidism

292
Q

Mx for cyanogenic glycoside poisoning

Book

A

Supportive and symptomatic for mild cases
Antidote for cyanide if severe

293
Q

Haff’s disease

Book

A

Syndrome of unexplained rhabdomyolysis onset within 24h after cooked freshwater food consumption
Burbot, pike, buffalo fish, eel
Freshwater crayfish
Postulated to be an unidentifiable heat stable toxin

294
Q

Clinical features of Haff’s disease

Book

A

Pain in trunk / limbs, often severe and disproportional to CK level
Gross myoglobinuria in severe
Chest pain, SOB, diaphoresis
Rarely ARF, multiorgan failure/death
Myalgia subsides in a few days, CK normalize in a week

295
Q

3 forms of Mercury

Book

A

Elemental
Inorganic
Organic

Considered as different toxins

296
Q

Which form of mercury poisoning is most common in HK

Book

A

Inorganic mercury poisoning from adulterated facial whitening cream / Chinese med

297
Q

Source of elemental mercury

Book

A

Sphygmomanometer, thermometer, fluorescent light tube, compact fluorescent light bulb

297
Q

Toxicokinetic/dynamics of elemental mercury

Book

A

Vaporize at room temp
Absorption mainly by inhalation (negligible oral absorption with normal GIT)
To CNS, kidney, crosses placenta
Convert to inorganic ion forms by enzyme catalase

298
Q

Clinical features of elemental mercury poisoning

Book

A

Occupational
Cough, chills, fever, SOB
N/V/D, metallic taste
Interstitial pneumonitis, ARDS if severe

299
Q

Ix of elemental mercury poisoning

Book

A

CXR for acute inhalation / suspected aspiration
AXR for ingestion
X ray of body parts in SC/IV
Whole blood, 24h urine mercury

300
Q

Mx of elemental mercury poisoning

Book

A

Environmental decontam, do not use vacuum cleaner
Supportive care for acute inhalation
Ingestion – FU X ray

301
Q

Sources of Inorganic mercury poisoning

Book

A

Skin whitening cream adulterated with inorganic mercury
Certain Chinese meds, e.g. cinnabar
Ayurvedic medicinal products
Mercurochrome

302
Q

Ix of Inorganic mercury poisoning

Book

A
  1. Whole blood mercury: reflect intense, acute inorganic mercury exposure, less reliable after redistribution to tissues
  2. Spot urine mercury (need to adjust for Cr conc.)
  3. 24h urine mercury (correlate roughly exposure severity and neuropsychiatric symptoms; confirm exposure and monitor chelation therapy)
  4. Renal biopsy (membranous glomerulonephritis and minimal change disease most common for nephrotic syndrome in inorganic mercury poisoning)
  5. CBC, LRFT, AXR
303
Q

Mx of Inorganic mercury poisoning

Book

A

Source identification + exposure termination
GI decon (GL/AC if early; WBI)
Supportive tx, adequate hydration
OGD if significant corrosive effects
Chelation therapy

304
Q

When to start chelation therapy for inorganic mercury poisoning

Book

A

Clinical features + elevated mercury level

Oral succimer (DMSA- Dimercaptosuccinic acid) for subacute/chronic inorganic
Dimercaprol (BAL - British anti-Lewisite) for acute inorganic

305
Q

Sources of organic mercury

Book

A

Seafood

306
Q

Clinical features of organic mercury

Book

A

Neurological toxicity

Chelation therapy not useful in organic mercury poisoning

307
Q

Arsenic poisoning, which one more toxic

Trivalent vs Pentavalent
Inorganic vs Organic

Book

A

Trivalent arsenic more toxic than pentavalent

Inorganic arsenic more toxic than organic

308
Q

Ix for Arsenic poisoning

Book

A

24h urine arsenic
Speciation of arsenic (differentiate organic and inorganic arsenic)

309
Q

Mx of Arsenic poisoning

Book

A

Source identification + exposure termination
Aggressive fluid replacement
Treat prolonged QTc

GI decontamination
Acutely poisoned patients usually had already vomited
Activated charcoal +/- airway protection can be considered although arsenic is poorly
adsorbed by charcoal

310
Q

Chelation for Arsenic poisoning

Book

A

BAL IV for acute who cannot tolerate oral intake

DMPS IV for acute or PO for subacute or chronic

Succimer PO in subacute or chronic

311
Q

Salicylate found in

Book

A

Aspirin
Cortal (aspirin + caffeine)
Methyl salicylate (e.g. Wintergreen oil)
Salicylic acid (keratolytic agent for corn)

312
Q

Pharmacokinetics of salicylate

Book

A

Peak serum conc in 1-2 hours
Bezoar possible in aspirin overdose
Weak acid with poor CNS distribution at physiological pH
If academia, shifts to non-ionized form and penetrate BB and tissues, CNS toxicity
Mainly conjugated in liver, only small portion excreted in urine
Overdose, metabolic enzymes saturated -> become zero order kinetics, serum half life 15-20h
Renal elimination becomes critical when hepatic metabolism saturated

313
Q

Pathophysiology of salicylate

Book

A

Initial direct stimulation of CNS resp center -> hyperventilation + resp alkalosis

Uncouple phosphorylation, increasing tissue oxygen consumption and hyperthermia

Metabolic acidosis resulting from lactate (anaerobic metabolism), ketoacid, and salicylate itself

314
Q

Clinical manifestation of salicylate poisoning

Book

A

Minimal symptoms if early despite lethal dose

Early symptoms: N/V, hyperventilation (resp alkalosis), tinnitus, lethargy

Life threatening symptoms: CNS toxicity (confusion, convulsion, coma, cerebral edema), acute lung injury (non-cardiogenic pul edema), dehydration, hyperthermia, metabolic acidosis, BG disturbance, hepatic/renal failure, coagulopathy, impaired platelets

315
Q

Classical acid-base abnormality for salicylate poisoning

Book

A

Initial resp alkalosis, then metabolic acidosis
Alkalemic in early phase, with mixed resp alkalosis and metabolic acidosis
pH <7.4 = life threatening, poor prognostic marker

316
Q

Toxic/Fatal dose of salicylate

Book

A

Toxicity: >150mg/kg
Fatal: >500mg/kg

317
Q

Serum salicylate limited role

Book

A

Monitor serial salicylate level, check Q2-4h till 2-3 consecutive falling levels
Focus on clinical status, symptoms, acid-base status

318
Q

Electrolyte disturbance of salicylate poisoning

Book

A

Increase AG
Hypergly – increase gluconeogenesis, glycogenolysis
Hypogly – depletion of easily mobilized glucose stores
Relative CNS hypoglycemia
HypoK
Urine alkalinization is impaired if hypoK

319
Q

Tx of salicylate poisoning

Book

A

GI decon
Adequate hydration
Serum and urine alkalinization
Monitor serum salicylate
Consider MDAC (for aspirin) and enhanced elimination
Pretreat with NaHCO3 to prevent resp acidosis before intubation

320
Q

Indication of serum/urine alkalinization for salicylate poisoning

Book

A

Symptomatic patients with supratherapeutic salicylate level
Serum salicylate >40mg/dL (>2.9mmol/L)

321
Q

How to give NaHCO3 for salicylate poisoning

Book

A

Bolus: 1-2ml/kg 8.4% NaHCO3
Maintenance: 50ml NaHCO3 in 500ml D5 Q4H and titrate, monitor and replace K
Aim: serum pH 7.45-7.55, urine pH 7.5-8

322
Q

When to HD / HF for salicylate poisoning

Book

A

Severe end-organ toxicity (convulsion, pul edema, renal failure, altered mental state)
Clinical deterioration despite standard therapy
Serum salicylate >100mg/dL (>7.2mmol/L)
HF as alternative if HD not a/v

MO AED (8 decks)

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