Environmental & toxicological emergencies Flashcards
The development of holes in the cellular membrane associated with electrical injury is called:
a. arcing
b. thermal injury
c. electroporation
d. ulceration
C
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
B
What is the most common cause of clinical signs of dry drowning?
a. Diaphragmatic spasm
b. Tachypnea
c. Aspiration
d. Laryngospasm
D
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
B
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
C
Which of the following is most beneficial when treating a patient with envenomation from a rattlesnake?
a. Glucocorticoids
b. Antibiotics
c. Antihistamines
d. Antivenom
D
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
B
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
D
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
B
What is the primary method for cooling an awake canine or feline?
a. Evaporation
b. Radiation
c. Conduction
d. Convection
A
What drug class is apomorphine?
a. Dopaminergic antagonist
b. Dopaminergic agonist
c. Alpha antagonist
d. Alpha agonist antagonist
B
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
D
Ethylene glycol toxicity results in which metabolic disturbance?
a. Metabolic acidosis
b. Metabolic alkalosis
c. Respiratory acidosis
d. Respiratory alkalosis
A
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
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
B
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
D
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%
B
A patient ingesting which toxin would not be expected to benefit from the administration of ILE?
a. Diltiazem
b. Moxidectin
c. Bupivacaine
d. Xylitol
D
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
Activated charcoal administration after ingestion of which toxin would not be beneficial?
a. Chocolate
b. Bromethalin
c. Xylitol
d. Ibuprofen
C
Activated charcoal administration after ingestion of which toxin would not be beneficial?
a. Chocolate
b. Bromethalin
c. Xylitol
d. Ibuprofen
C
Primary treatment for toxin exposure
Decontamination and detoxification and initiating supportive care: gastroprotectants, hepatoprotectants, neurological support, IVFT, ILE, antidotes
ILE treatment
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
ILE indications
Can be used as nutritional support
Lipophilic drug toxicoses (macrolytic lactones, lidocaine, pyrethrums, Ca channel blockers)
Decontamination options
Emesis
Gastric lavage
Forced dieresis
Toxins warranting gastric lavage
Metaldehyde
Strychnine
Ca blockers
Baclofen
B-blockers
Macrolytic lactones
Organophosphate/carbamate
Activated charcoal doses
- 5g/kg with cathartic I.e. sorbitol
- Repeated doses 1-2g/kg without cathartic q4-6 for 24h (toxins that undergo enterohepatic recirculation)
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
Cathartics
Increase transit time to increase toxin clearance
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.
Clinical signs of serotonin syndrome
Mild; tremors, diarrhoea
Severe; neuromuscular rigidity, delirium & severe hyperthermia
Other: arrhythmias, tachycardia, mydriasis, increased bowel sounds, agitation, DIC, rhabdomyolysis
Therapeutic and toxic ranges for SSRI, MAOIs and TCA
Therapeutic 2-4mg/kg however toxicosis can occur 0.3-50mg/kg
Approach to OD of SSRI, MAOIs, TCA
- Decontamination (emetics, gastric lavage, AC)
- Address ABC’s
- Repeat AC q6
- IVFT but dieresis won’t enhance excretion (highly protein bound)
- Seizure control
- Intensive supportive care
- Chlorpromazine or cyproheptadine
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
Hydrogen cyanide
Burning of wools, silks etc and is a non-irritant gas that induces histotoxic anaemia interfering with the utilisation of O2
Thermal injury distal to the larynx
Mucosal oedema
Ulceration
Erosion
- lead to URT obstruction
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
PaO2 and SpO2 with smoke inhalation
May remain normal <100% but as progresses may drop
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
Types of heat loss
Convection
Conduction
Radiation
Evaporative
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
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
Thermostat of the body
Hypothalamus and also heat senses in skin and deep tissue
Normal body heat production
Mostly through chemical metabolism of energy substrates in cells
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)
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
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
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
How does hypothermia affect haemostasis
Decrease PLT aggregation
Increases thromboxane
Decreased vWF
Decreased activity of clotting factors > delayed clot formation
Increased PT/aPTT
+- DIC
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
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
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
Neuroprotective benefits of therapeutic hypothermia
Prevents apoptosis
Decreases destructive enzymes
Suppresses free radicals
Decreases cerebral O2 demand
Hallmark of heat stroke
CNS abnormalities associated with multiple organ failure
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
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
Findings of work up in heat stroke
Reduced oculocephalic reflexes, cerebral oedema or haemorrhage
AKI
Hepatic encephalopathy
Hypoglycaemia
Coagulopathic
Haemoconcentrated
DIC
Treatment of heat stroke
- Active cooling to 39.4 (avoid alcohols, ice packs)
- Shock fluids +- colloids (avoid excessive fluids)
- Blood products I.e. FFP
- Positive inotropes and vasopressors
- Oxygen
- Monitor CNS signs (TBI strategies)
- Support and monitor UOP
- Split products
- GI protectants
Electrocution
Disturbs electrophysical activity causing muscle spasms, arrhythmias, loss of consciousness, arrest. There is direct cellular injury through electroporation.
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
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
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
Cardiac arrhythmias in electrical shock
Vfib - low voltage
Asystole - high voltage
If survive ventricular arrhythmias noted
Treatment of electrical shock
- Remove safely from electrical source
- Treat clinical manifestations
- +- CPR
- Strictly controlled IVFT
- oxygen +- bronchodilators
- Burn management
- Pain relief
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
Neurological abnormalities in drowning’s
Due to hypoxic brain injury and depends on duration of hypoxia and extent of injury
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
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
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
Air embolism tolerance in patients
0.35ml/kg/min
About 2ml/1kg will have detrimental effects
Which of nitrogen and CO2 is more severe in air embolism
Nitrogen
Signs of air embolism
Rapid drop in CO2
Mill wheel murmur (harsh, churning)
Tachypnoea and hypoxaemia
Physiological shunting
Air embolism in laparoscopy
Avoid inflating above 15mmHg
Occurs when pressure between intravascular pressure and venous collapse
Treatment of air embolism
Prevent further air entrapment
Provide 100% O2
Head down, dorsal recumbency
Manual embolus reduction
+- HBOT
+- heparin
