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VTS(ECC) Preparation > Environmental & toxicological emergencies > Flashcards

Environmental & toxicological emergencies Flashcards

1
Q

The development of holes in the cellular membrane associated with electrical injury is called:
a. arcing
b. thermal injury
c. electroporation
d. ulceration

A

C

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2
Q

In the feline, what is responsible for noticing the body’s abnormal position during a fall?
a. Central nervous system
b. Vestibular system
c. Limbic system
d. Peripheral nervous system

A

B

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3
Q

What is the most common cause of clinical signs of dry drowning?
a. Diaphragmatic spasm
b. Tachypnea
c. Aspiration
d. Laryngospasm

A

D

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4
Q

The bite from which venomous species leaves a “bullseye” around a central necrotic area?
a. Black widow spider
b. Brown recluse spider
c. Coral snake
d. Water moccasin

A

B

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5
Q

Rewarming shock can occur when a patient experiences which of the following?
a. Decreased metabolism once warmed
b. Too fast an increase in core body temperature
c. Vasodilation due to applied heat
d. Fluid shift to the gastrointestinal tract

A

C

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6
Q

Which of the following is most beneficial when treating a patient with envenomation from a rattlesnake?
a. Glucocorticoids
b. Antibiotics
c. Antihistamines
d. Antivenom

A

D

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7
Q

Hypoxemia associated with salt water drowning occurs as a result of which process?
a. Tachypnea
b. Interference of normal gas exchange
c. Apnea
d. Atelectasis

A

B

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8
Q

Patients that experience electrocution from low voltage currents (A/C) will most likely experience which cardiac conduction disturbance?
a. Asystole
b. Premature ventricular complexes
c. Atrial fibrillation
d. Ventricular fibrillation

A

D

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9
Q

Which of the following is true regarding high rise syndrome?
a. It is not a problem with cats because their PNS helps them land on their feet
b. The injuries occur from vertical deceleration trauma
c. There is less trauma in falls from heights of 7–10 stories
d. It is always fatal, regardless of treatment

A

B

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10
Q

What is the primary method for cooling an awake canine or feline?
a. Evaporation
b. Radiation
c. Conduction
d. Convection

A

A

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11
Q

What drug class is apomorphine?
a. Dopaminergic antagonist
b. Dopaminergic agonist
c. Alpha antagonist
d. Alpha agonist antagonist

A

B

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12
Q

Which of the following drugs would not be used to reduce calcium levels in a patient with cholecalciferol toxicity?
a. Furosemide
b. Pamidronate
c. Calcitonin
d. Calcitriol

A

D

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13
Q

Ethylene glycol toxicity results in which metabolic disturbance?
a. Metabolic acidosis
b. Metabolic alkalosis
c. Respiratory acidosis
d. Respiratory alkalosis

A

A

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14
Q

Which of the following can be helpful when attempting to induce vomiting in a case of toxin ingestion?
a. Feeding the patient a small meal
b. Administering hydrogen peroxide
c. Walking the patient around
d. Administering an antiemetic

A

A

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15
Q

Liver damage, hemolysis, methemoglobinemia, and KCS can all occur as a result of the ingestion of which agent?
a. Ethylene glycol
b. Acetaminophen
c. Organophosphates
d. Amitraz

A

B

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16
Q

Which toxin initially results in gastrointestinal signs, then can progress to neurological signs, and may cause basophilic stippling?
a. Lilies
b. Strychnine
c. Bromethalin
d. Lead

A

D

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17
Q

nducing emesis results in the expulsion of approximately what percentage of stomach contents?
a. 20–40%
b. 40–60%
c. 60–80%
d. 80–100%

A

B

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18
Q

A patient ingesting which toxin would not be expected to benefit from the administration of ILE?
a. Diltiazem
b. Moxidectin
c. Bupivacaine
d. Xylitol

A

D

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19
Q

Which clotting factors are affected when a toxic amount of a vitamin K1 antagonist rodenticide is ingested?
a. II, VII, IX, X
b. I, II, V, VII
c. VIII, IX, X, XI
d. II, VI, X, XII

A

A

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20
Q

Activated charcoal administration after ingestion of which toxin would not be beneficial?
a. Chocolate
b. Bromethalin
c. Xylitol
d. Ibuprofen

A

C

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20
Q

Activated charcoal administration after ingestion of which toxin would not be beneficial?
a. Chocolate
b. Bromethalin
c. Xylitol
d. Ibuprofen

A

C

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21
Q

Primary treatment for toxin exposure

A

Decontamination and detoxification and initiating supportive care: gastroprotectants, hepatoprotectants, neurological support, IVFT, ILE, antidotes

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22
Q

ILE treatment

A

Initial 1.5-4ml/kg over 5min then 0.25ml/kg/min for 1 hour.
If repeat doses are required 0.5ml/kg/hr until improvement of clinical signs

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23
Q

ILE indications

A

Can be used as nutritional support
Lipophilic drug toxicoses (macrolytic lactones, lidocaine, pyrethrums, Ca channel blockers)

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24
Decontamination options
Emesis Gastric lavage Forced dieresis
25
Toxins warranting gastric lavage
Metaldehyde Strychnine Ca blockers Baclofen B-blockers Macrolytic lactones Organophosphate/carbamate
26
Activated charcoal doses
1. 5g/kg with cathartic I.e. sorbitol 2. Repeated doses 1-2g/kg without cathartic q4-6 for 24h (toxins that undergo enterohepatic recirculation)
27
Contraindications to activated charcoal
Drugs that don’t readily bind to AC Endoscopy GI obstruction/haemorrhage/perforation Recent surgery Late stage presentation with clinical signs Dehydration/hypovolaemic shock Ileus Compromised airway etc
28
Cathartics
Increase transit time to increase toxin clearance
29
Serotonin syndrome
Drug-induced excessive serotonergic agonism resulting in altered mental status, neuromuscular abnormalities and autonomic instability. Usually occurs when two serotonergic drugs given together and is fatal when SSRI + MAOI given together.
30
Clinical signs of serotonin syndrome
Mild; tremors, diarrhoea Severe; neuromuscular rigidity, delirium & severe hyperthermia Other: arrhythmias, tachycardia, mydriasis, increased bowel sounds, agitation, DIC, rhabdomyolysis
31
Therapeutic and toxic ranges for SSRI, MAOIs and TCA
Therapeutic 2-4mg/kg however toxicosis can occur 0.3-50mg/kg
32
Approach to OD of SSRI, MAOIs, TCA
1. Decontamination (emetics, gastric lavage, AC) 2. Address ABC’s 3. Repeat AC q6 4. IVFT but dieresis won’t enhance excretion (highly protein bound) 5. Seizure control 6. Intensive supportive care 7. Chlorpromazine or cyproheptadine
33
Carbon monoxide
Non-irritant gas that has 230-270X affinity for Hg compared to O2 leading to severe anaemic hypoxia from incomplete combustion of carbon containing materials > carbonmonoxide
34
Hydrogen cyanide
Burning of wools, silks etc and is a non-irritant gas that induces histotoxic anaemia interfering with the utilisation of O2
35
Thermal injury distal to the larynx
Mucosal oedema Ulceration Erosion * lead to URT obstruction
36
Airway damage and obstruction in smoke inhalation
Alveolar Atelectasis > reduced lung compliance due surfactant loss and/or pulmonary oedema and occurs within about 24h of injury > ARDS Mucosal sloughing Bronchial disease Bronchoconstriction Bacterial pneumonia
37
PaO2 and SpO2 with smoke inhalation
May remain normal <100% but as progresses may drop
38
Treatment of smoke inhalation
1) oxygen - reduces HL of carbon monoxide to 26-148min (normally 250min) 2) sodium nitrite - if cyanide followed by sodium thiosulfate 3) airway management - tracheostomy, bronchodilator’s, NAC, nebulise 4) opioids/sedatives 5) mechanical ventilation 6) IVFT - higher fluid requirements but avoid overload 7) AB only if indicated
39
Types of heat loss
Convection Conduction Radiation Evaporative
40
Hypothermia
End result of an animals inability to maintain thermoregulatory homeostasis due to excessive heat loss, decreased heat production or disruption of normal thermoregulatory functions
41
Mild, moderate and severe hypothermia
Mild; 32-37 - shivering, ataxia, vasoconstriction Moderate; 28-32 - decreased consciousness, hypotension, +- shivering Severe; <28 - loss of shivering, dysrhythmias, profound CNS deficits
42
Thermostat of the body
Hypothalamus and also heat senses in skin and deep tissue
43
Normal body heat production
Mostly through chemical metabolism of energy substrates in cells
44
Shivering
Involuntary, oscillating skeletal muscle activity that can increase metabolic rate by 4-10X and is fuelled by carbohydrate oxidation (or protein and lipid when glycogenesis depleted)
45
How does hypothermia affect the heart
Vasoconstriction Eventually decreased heart rate and blood pressure Increased CVP Decreased diastolic and increased systolic pressure Lowered action potential > dysrhythmias (vfib if severe) - prolonged PR and wide QRS
46
How does hypothermia affect the respiratory system
Decreased rate and depth due to reduced sensitivity to drops in CO2 > VQ mismatch due to bronchodilation Pulmonary tissue injury O2 dissociation disturbances Loss of protective mechanisms Decreased ciliary clearance > risk of aspiration pneumonia Apnoea NCPO
47
How does hypothermia affect the neurological system
Depressed mental status Reduced CBF (6-10% per 1 degree when temp <30) Increased synovial fluid viscosity Muscle rigidity when severe
48
How does hypothermia affect haemostasis
Decrease PLT aggregation Increases thromboxane Decreased vWF Decreased activity of clotting factors > delayed clot formation Increased PT/aPTT +- DIC
49
How does hypothermia affect the renal system
Initially diuresis but then low GFR and renal tubular dysfunction > loss of electrolytes, increased glucose due to decreased insulin sensitivity, reduced immune function
50
Passive v. Active warming strategies
Passive warming involves the patient augmenting there own heat I.e. blankets where active rewarming is via an exogenous source such as hair huggers, fluid warming and lavage. Mild to moderate hypothermia uses passive strategies and +- active warming where severe requires active warming strategies
51
Rewarming rates
1.4 first hour then approx. 2/hr for second hour onwards * remove exogenous cooling sources * safely raise temp 0.5-2 per hour
52
Neuroprotective benefits of therapeutic hypothermia
Prevents apoptosis Decreases destructive enzymes Suppresses free radicals Decreases cerebral O2 demand
53
Hallmark of heat stroke
CNS abnormalities associated with multiple organ failure
54
Basic pathophysiology of heat stroke
Warm, humid environment +- excercise > dissipative heat strategies overwhelmed by heat production > CBT rises driving failure of thermoregulation, exaggerated acute-phase response and altered heat shock proteins > pro inflammatory and anti inflammatory mediators release > activation of leukocytes triggering SIRS and coagulation > severe endothelial injury, MODS, DIC
55
General presentation of a patient suffering heat stroke
Hyperdynamic state: tachycardia, hyperaemia, tachypnoea, weak pulse, vomiting and diarrhoea +- arrhythmias Alert to comatose with CNS abnormalities
56
Findings of work up in heat stroke
Reduced oculocephalic reflexes, cerebral oedema or haemorrhage AKI Hepatic encephalopathy Hypoglycaemia Coagulopathic Haemoconcentrated DIC
57
Treatment of heat stroke
1. Active cooling to 39.4 (avoid alcohols, ice packs) 2. Shock fluids +- colloids (avoid excessive fluids) 3. Blood products I.e. FFP 4. Positive inotropes and vasopressors 5. Oxygen 6. Monitor CNS signs (TBI strategies) 7. Support and monitor UOP 8. Split products 9. GI protectants
58
Electrocution
Disturbs electrophysical activity causing muscle spasms, arrhythmias, loss of consciousness, arrest. There is direct cellular injury through electroporation.
59
Brief pathophysiology of electrical shock
Electrical current > heat > superheated ICF & ECF > coagulation of tissue proteins, small vessel thrombosis and degenerative arterial vessel changes > necrosis to affected tissue and ischaemia to surrounding tissues > clinical manifestations. Clinical manifestations: ventricular arrhythmias, superficial to full thickness burns, respiratory distress (oedema, haemorrhage), sudden death
60
Low energy v. High energy electrical shock
Low energy into high resistance tissue (dry skin) = less shock High energy into low resistance tissue (wet skin) = more shock
61
Worst electrical shock
Alternating currents due to potential increased exposure and shocks of high voltage also * muscle contractions for alternating currents prevent release from source so high exposure
62
Cardiac arrhythmias in electrical shock
Vfib - low voltage Asystole - high voltage If survive ventricular arrhythmias noted
63
Treatment of electrical shock
1. Remove safely from electrical source 2. Treat clinical manifestations 3. +- CPR 4. Strictly controlled IVFT 5. oxygen +- bronchodilators 6. Burn management 7. Pain relief
64
Drowning
Only 10% do not aspirate water; drowning results in hypoxaemia, surfactant loss (Atelectasis, intrapulmonary shunt) and those that aspirate <22ml/kg more likely to survive
65
Neurological abnormalities in drowning’s
Due to hypoxic brain injury and depends on duration of hypoxia and extent of injury
66
What drowning patients have increased chance of survival and why
Those that are submerged in water <5 degrees and this is due to activation of the diving reflex and reduced metabolic demand. * diving reflex = trigeminal nerve signal to the CNS > lowers HR, Increases BP and shunts blood to coronary and cerebral circulation
67
Treatment of drowning
CPR Improve tissue oxygenation Normalise acid-base Stabilise respiratory, cardiovascular and neurological systems Mechanical ventilation commonly needed (ARDS not uncommon) BAL and AB’s IVFT Mannitol Pro gastric tube to remove fluid from stomach
68
Air embolism
Almost always iatrogenic from IV injection and the size, rate and patient status all contribute to the severity Small - may be absorbed by the tissues Massive - lodge in gravity dependent locations such as the R atrium and pulmonary artery and may cause complete obstruction of blood flow
69
Air embolism tolerance in patients
0.35ml/kg/min About 2ml/1kg will have detrimental effects
70
Which of nitrogen and CO2 is more severe in air embolism
Nitrogen
71
Signs of air embolism
Rapid drop in CO2 Mill wheel murmur (harsh, churning) Tachypnoea and hypoxaemia Physiological shunting
72
Air embolism in laparoscopy
Avoid inflating above 15mmHg Occurs when pressure between intravascular pressure and venous collapse
73
Treatment of air embolism
Prevent further air entrapment Provide 100% O2 Head down, dorsal recumbency Manual embolus reduction +- HBOT +- heparin

VTS(ECC) Preparation (21 decks)

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