Remote Capture Flashcards
Considerations for Field Anesthesia with Weather
Timing chosen for appropriate time of year when hazards minimized
ex: Ungulates may be captured in late winter
* Decreased risk of hyperthermia
* Snow helps with tracking
Snow and rain–> hypothermia, esp if wind (convective heat)
Summer months: plan for cooler hours of day
Safe helicopter generally not possible in high winds or foggy conditions
Hypoxemia in Wildlife Ax
common complication of wildlife anesthesia (particularly with ruminants)
Oxygen = fundamental supportive care during field anesthesia
* Aluminum E, D cylinder + sturdy regulator, flowmeter
* Portable oxygen concentrators
Nasal insufflation often adequate to resolve hypoxemia
Emergency Kit for Wildlife Field Anesthesia
Basic kit: epinephrine, atropine, lidocaine, reversal agent
Lac Repair Kit
Environmental Hazards
Beware of surrounding environment: other animals may approach
Esp true/important with social carnivores, bears
Need to have a lookout posted to protect the team
Firearm back up with more dangerous species
All capture team members should receive firearm safety training
* Similar training advisable for people using dart
* Rifles or pistols; pepper spray = alternative as a non-lethal firearm
Basic Safety Features of High Potency Opioids
Carfentanil, etorphine, thiafentanil = risk of lethal toxicity in people
Use protective clothing (disposable gloves and face shields when using)
Pharmacological antagonist available to treat human exposure
Everyone on team trained in human first aid
Equipment available to provide respiratory and airway support
Wildlife anesthesia: NEVER be performed by a single person
* Minimum two people available when potent drugs being used/handled, esp during dart loading
Helicopter Capture Techniques
significant hazard, requires very skilled pilot for wildlife capture
Communication with Local Officials
Advised to meet with local medical personal prior to capture to discuss evacuation and treatment plan in case of inadvertent human exposure
Injuries Assoc with Dart Placement
dart impact trauma
high-velocity injection of dart contents
inaccurate dart placement
Dart Impact Trauma
dispersion of energy on dart impact
o Impact kinetic energy = 1/2M x V2 where M = mass of dart, V = velocity
o Use lowest velocity provides accurate trajectory at a given distance
Inaccurate dart placement
Abdominal, thoracic, or other vital structures of head, neck
Aim for well-muscles area away from viscera
High-velocity injection of dart contents
systems that expel drug via explosive charge disrupt tissue, produce trauma
o Used only on large, well-muscled animals
o Minimize volume of injectate to decrease tissue trauma (<3mL)
Two Mechanisms of Dart Discharge
- Explosive Discharge
- Air Activated
Explosive discharge mechanisms
Reserved for large, well-muscled animals
Darts = aluminum or plastic body, small explosive cap between plunger, tail
On impact, firing pin inside cap forced forward against resistance of spring –> detonation, expanding gas pushes plunger forward
Short duration of injection (0.001 s)
Needle should be barbed so stays in animal during injection
Air Activated Discharge Mechanisms
Aluminum or plastic body into which compressed air introduced through one way valve in tail piece
On impact, silicone seal is displaced exposing a port on side of needle –> plunger pushed forward by air pressure
Opioids in Capture
particularly effective in ungulates, produce analgesia and sedation
Lack muscle relaxation, often cause excitement - hyperthermia, exhaustion, lost animals, death, regurgitation
Can be used alone or with a neuroleptic agent
Predictable, relatively fast, can be reversed
Other AEs: hypoxemia, severe resp depression
Risk of renarcanization
Carfentanil
Particularly useful in ungulates, also used in large carnivores
Advantages: high potency, rapid onset, reliability, reversal with appropriate antagonist
Muscle rigidity when used alone
Disadvantages of Carfentanil
Moose: increased chance of aspiration pneumonia
Long effect: should be antagonized
o If antagonists has shorter half life, re-narcotization
Respiratory depression, hypoxemia, hypertension, CNS excitation
Reversal of Carfentanil
Reverse with naltrexone
* Naloxone, diprenorphine, nalmefene re-narcotization
100mg naltrexone:1mg carfentanil
Etorphine
Particularly effective in ungulates, rhino, and elephants
3000-6000x more potent than morphine
Used alone or in combo with a suitable neuroleptic agent
Underdosing = excitement; optimum dose, first effect 3-8 min post IM
* Full effect 20-30 min
Slow recovery (up to 7-8 hr) without antagonist
* Antagonist IV 1-3min, IM = 5-10 min
Most serious adverse effect = respiratory depression
Other SEs: normal opioid things
Reversal: diprenorphine
Thiafentnail
rapid induction, greater therapeutic index, shorter half-life, lower incidence of renarcotization, less respiratory and cardiac depression vs etorphine, carfentnail
Only commercially avail in South Africa
3000-6000x more potent than morph
Thiafentnail
rapid induction, greater therapeutic index, shorter half-life, lower incidence of renarcotization, less respiratory and cardiac depression vs etorphine, carfentnail
Only commercially avail in South Africa
Reversal: naltrexone 30-50mg:1mg TF
Used alone or in combo with a2 +/- ketamine
Butorphanol
Combination with etorphine = improved ventilatory function
Commercially available at 30, 50 mg/ml: high concentration formulations greatly increase utilization for remote delivery
Naltrexone
most versatile, lowest chance of narcotization
Rapid antagonism of mu-opioid receptor antagonism
Reliable antagonism of longer-acting opioids (carfentanil), IM or IV
* Dose of 100 mg:1 mg of carfentanil
* 10-30 mg of naltrexone: 1 mg thiafentanil
Drug Choices in Human Overdoses
Naloxone, naltrexone
Naloxone
Pure narcotic antagonist, may reverse all opioids listed above
Reverse in 1-3 min IV
Short half life, renarcotization seen with carfentail
Dose given to elk of 2 ucg for every 1 ucg of carfentanil given
Diprenorphine
Antagonist used to reverse etorphine, agonistic properties on own
* Acts as antagonist when given after etorphine
Rapid reversal
Adverse effects = rare
* Overdosing: continued immobilization DT partial agonist activity
Human accidently gets etorphine, no diprenorphine (DT agonist effects)
Cyclohexamines
Adverse effects: hyperthermia, excessive salivation, catecholamine release, convulsions
Act fast, relatively wide margin of safety, cardiorespiratory depression only moderate
Laryngeal function somewhat preserved
Combined with a benzo or alpha-2 agonist= additive or synergistic
Particularly effective in carnivores, primates, birds; no known antagonist
Ketamine in Wildlife
Never used as a sole immobilizing agent, co-administer with tranquilizer-sedative
Optimum dose, first effects = 2-5 min post IM, full effects 5-10 min - duration 45min-2hr
Ketamine based combos = unreliable in bears, do not use in vultures
Telazol
First effect = 1-2 min, full effects 15-30 min
Onset usually smooth with good muscle relaxation, somatic analgesia
Duration of effect, quality of emergence, duration of recovery vary with species: tiletamine, zolazepam metabolized at different rates
Recovery in 3-8 hours, may be prolonged in some species
If reconstitute with a2 agonist – decrease volume injected, enhance analgesia, decrease recovery times following antagonism of a2 agonist
No Telazol in…
Tigers, other big cats (debated)
Rough recoveries in ungulates - ruminants, swine
NZWR
Alpha 2 Agonists
Alone = unreliable immobilization in most species
hypoxia in ungulates, hypertension +/- bradycardia
Contribute to ruminal tympany, regurgitation in ungulates
Also alters thermoregulation
Very excited animals –> not predictable level of immobilization
Xylazine, Detomidine Reverals
1 mg of atipamezole : 10 mg xylazine (IM)
5 mg atipamezole : 1 mg detomidine (IM)
Medetomidine
Produce sedation, analgesia, and muscle relaxation
Unreliable alone: medetomidine + low dose ketamine or Telazol
Antagonism with atipamezole = 3-5x medetomidine dose
a2 Reversals
Atipamezole = most selective, can be used in all species
Species-dependent differences in response to yohimbine, tolazoline but less with atipamezole
Yohimbine not particularly effective in wild bovids
IM unless emergency: CNS excitation, tachycardia, hypotension followed by hypertension with IV
—Animals may arouse rapidly without warning following IV
—Potentially dangerous species = may not give you time to escape
ACP, Droperidol (neuroleptic agents)
-typically paired with opioids (etorphine)
-long-acting tranquilizer to facilitate translocation
-overall stress reduction
-effects = days to weeks
Perphanazine enanthate
Slow-onset, long-acting PTZ derivative formulated in sesame oil vehicle
Onset 12-16 h, effects last up to 10 days
Zuclopenthixol acetate
Thioxanthene derivative, lasts up to 3-4 days – 1mg/kg IM in most studies
Occasionally, extrapyramidal signs
Azaperone
Butyrophenone drug, used as a tranquilizer in pigs
+/- alpha 2, +/- opioids for ax, immobilization of wild/farmed ungulates
Pigs = DOA of 6 h
Anticipated Drug Needs
Budget for at least 50% more drug than is actually needed
Help offset drug wasted from lost darts or poor dart placement
Dart Loading Once Target Located
Metal darts not loaded for >12hr: possible corrosive action of drugs may impair injection mechanism
Preloaded darts with air-activated discharge should not be pressurized; have tendency to lose pressure if armed for extended period
How far does the animal need to be for accurate dart delivery?
within 30-40m
Animals may be stalked, baited, approached in a vehicle or helicopter, or trapped or snared prior to approach
Trapped animals advantage of limiting movement during capture
* May be more stressful than helicopter capture, esp for bears
How long should capture take?
2-5min
What is the most important determinant of induction time?
Dart placement = most important determinant of induction time
Location of Dart Placement
Facilitate fast drug absorption –> muscle mass of neck, shoulder, or hindquarters must be injected
How Dart Placement Changes During Time of Year
Brown bears: dart in hindquarter when they emerge from spring dens
In fall due to large fat stores, dart in shoulder or neck
Use hindquarters to spring
Hair falls on neck and shoulders
Drug Selection and Movement of Immobilized Wildlife
When a2 used, animals head or limbs should not move prior to approach
Telazol alone or with narcotics, may be some involuntary movement
Carnivore Positioning
lateral or sternal
Management of Ruminal Tympany
in sternal – help prevent tympany
* If problem, rock animal back and forth to stimulate eructation
* Pass tube orally/nasally if needed: may predispose to regurgitation, aspiration
* Tympany severe: finish procedure, antagonize agents
* Alpha2 antagonist will increase ruminal activity to help
Timing of Procedures during Wildlife
Painful procedures first after initial sedation when in deepest plane of anesthesia
Hypoxemia in Wildlife Capture
common during wildlife immobilization
Hypoxemia + hyperthermia is very serious
* Increased metabolism, tissue oxygen demand
* Increases risk of inducing exertional myopathy
Supplemental oxygen with pulse oximetry being measured
Tachycardia followed by severe bradycardia (HR <30 bpm) = warning sign that hypoxemia is very severe
Temperature Monitoring in Wildlife
Ungulates more prone to hyperthermia, especially after long chase
Planning immobilization during cooler periods of day or at cooler times
Temps >40 Degrees C (104 F)= cause for concern
Temp > 41 C = emergency and treated aggressively
Other Stimuli in Wildlife Capture
Loud noises increase risk of sudden arousal, especially the vocalizations of distressed offspring
Changing positions
Painful stimuli
Signs of CNS Depression
Spontaneous blinking will reappear
Carnivores often develop chewing and paw movements
* Progresses to head lifting
Xyla-ket or medet-ket immobilization, head lifting or limb movement = animal minimally obtunded and should NOT be approached
Recovery and Reversal
Reversible drug combination not used: animal should be observed until it can ambulate
Place in a comfortable position
Final set of vitals taken
TWO people to administer reversal, typically IM
Pulse Monitoring Locations in Wildlife
Femoral a
Auricular a
Depends on species
Hyperthermia
Most immediate sign = critical rise in body temp (>40-41 C)
Rapid shallow breathing, panting, and weak, rapid, or irregular heart rate
Moving the animal into shade or spraying it with cold water
Also can pack ice/snow around it, cold water enemas
Hypothermia
low temps, characterized as temp <35 C
Mostly in young animals, animals with low body mass, poor condition
Prolonged recovery, acidosis, coagulopathies, and arrhythmias
Dry and cover animal + external heat source
Capture Myopathy
Most commonly associated with pursuit, capture, restraint, transportation
Prey species, particularly ungulates predisposed
* Also long legged wading birds
* Less common in carnivores but can occur under certain conditions
Pathophysiology of Capture Myopathy
Effects of sympathetic exhaustion + sustained stress + intense muscular exertion
Sustained muscular exertion = production, buildup of lactate in muscle
Leads to metabolic acidosis, death of SkM; release of intracellular K+, Ca2+, myoglobin
High amounts of myoglobin in plasma, ultrafiltrate in renal tubules = ARF
Hyperkalemia, acidosis, acute arrhythmias, circulatory failure
Capture Myopathy Tx, Prevent
Difficult to treat PREVENTION IS KEY
Chase limited to 2 min
Capture efforts not resumed for at least 1 day if failed
If several individuals from same herd require capture, advisable to have enough handlers to capture multiple at same time rather than repeatedly stressing herd
4 Clinical Capture Myopathy Syndromes
- Acute Death Syndrome/Capture Shock Syndrome
- Delayed Peracute Death Syndrome
- Ataxia-Myoglobinuric Syndrome
- Muscle Rupture Syndrome
Acute Death Syndrome/Capture Shock Sydrome
during mobilization or within short time after capture, death usually within 1-6hr post capture
Depression, tachypnea, tachycardia, hyperthermia, weak thready pulses, death
Elevations in AST, CK, LDH
Postmortem lesions: small intestinal, hepatic congestion plus pulmonary congestion and edema
Histopath: small areas of necrosis in SkM, brain, liver, heart, adrenals, lymph nodes, spleen, pancreas, renal tubules
Delayed Peracute Death Syndrome
RARE, animals in captivity >24hr
–Animals appear normal if left undisturbed
–If stressed/captured, try to run or escape but stop abruptly and stand/lie still for a few moments
o Eyes dilate, death ensues within several minutes
* Cause of death: ventricular fibrillation
Elevations in AST, CK, LDH
No gross or histopathologic lesions post mortem
Ataxic Myoglobinuric Syndrome
Most common, several hours to days post capture
Clinical signs: mild to severe ataxia, torticollis, myoglobinuria
Elevations in AST, CK, LDH, BUN
Post mortem: main lesions in kidney, SkM
Muscle Rupture Syndrome
24-48hrs post capture, animals normally appear normal
Clinical signs: marked drop in hindquarters, hyperflexion of hock due to unilateral or bilateral rupture of gastrocnemius muscle
Elevations in AST, CK, LDH
Most animals die within few days
Postmortem: massive subcutaneous hemorrhage of the rear limbs, muscular lesions similar to ataxic myoglobinuric syndrome but more severe, widespread
When do most deaths related to wildlife capture occur?
early phase of large capture project before immobilization protocols have been refined, drug dosages adjusted, team members experienced
> 2% mortality during trapping = unacceptable
Three Categories of Capture Mortality of Free Ranging Mammals
- Direct effect of immobilizing agents themselves
- Indirect effects of drug(s) used
- Secondary Effects caused by capture process itself
Three Categories of Capture Mortality of Free Ranging Mammals
- Direct effect of immobilizing agents themselves
- Indirect effects of drug(s) used
- Secondary Effects
Indirect Effects of Drugs Used
Drowning, pneumothorax
Etorphine often induces hyperthermia –> animal seeks water then drowns
Secondary Effects Caused by Capture Process Itself
- Trauma traps
- Long term effects form chasing
- Have nothing to do with ax risk per se, treated as a separate entity
