Patología en Fauna Silvestre


Capture Myopathy Protocol
Capture Miopathy
Audubon Institute
Small Animal Emergency Kit
Primate Emergency Drug Doses
Inmobilization Checklist
Emergency Drug Doses

Capture Myopathy Protocol

Capture myopathy is a muscle disease associated with the stress of capture, restraint, and transportation. The disease is characterized by degeneration and necrosis of skeletal and cardiac muscle. Other names for this disease include: exertional Rhabdomyolysis, muscle dystrophy, overstraining disease, capture stress disease, white muscle disease, and idiopathic muscle necrosis.

Numerous species of birds and mammals are susceptible to capture myopathy. It has never been documented in reptiles or lower vertebrates. It seems to be more prevalent in prey species or submissive members of non-prey species which can become easily excited, especially when exposed to unusual stress such as restraint or chasing.

The disease develops within hours and up to 14 days after capture or transport. It may be seen in both animal that exert themselves maximally and those that are relatively quiet although it generally occurs after severe exertion and is often seen following a difficult, prolonged capture. It can occur with either physical or chemical restraint.

Predisposing factors include fear, anxiety, overexertion, repeated handling, failure to allow an exhausted animal to rest before transportation, and constant muscle tensions such as may occur in protracted alarm reactions. A variety of stressors may function in concert or individually to precipitate development of the classical syndrome.

Four different syndromes related to capture myopathy have been described. These four syndromes are the peracture death syndrome, the acute death syndrome, the ataxic myoglobinuric syndrome, and the ruptured muscle syndrome.

The peracute death syndrome is seen in animals shortly after capture. While the animal is undisturbed, it appears ok, but if excited or stressed again, it may suddenly fall and die. A peracute muscle tissue breakdown, which causes a release of cellular contents, (particularly, lactic acid and potassium) is thought to be the underlying mechanism. The potassium causes the heart to be hypersensitive to substances released by the adrenal glands during stress. The heart develops a severe abnormal rhythm and death rapidly follows.

Acute death syndrome occurs 3-4 hours following capture and involves over-heating, shock, adrenal gland exhaustion, and mild, acute muscle breakdown. Alterations in blood ph to create an acidotic state appear to be a critical factor in the development of acute capture myopathy. Clinical signs that may be observed prior to death include depression, shallow, rapid breathing, increased heart rate, cessation of urination, and rapid debilitation.

Ataxic myoglobinuric syndrome occurs hours to days post-capture. The animal becomes progressively more wobbly until it is unable to stand. The urine may appear reddish-brown in color due to the muscle break-down products. Renal failure follows.

In the ruptured muscle syndrome, animal are usually normal and appear healthy when captured, but clinical signs may become noticeable twenty-four to forty-eight hours later and may persist for three to four weeks. Clinical signs include a marked drop in the hindquarters and hyperflexion of the hocks due to bilateral rupture of the gastrocnemius muscles.

The cause of all these syndromes is very similar but complex, involving fear, the sympathetic nervous system and damage to skeletal and cardiac musculature. The biochemistry of stress and fear create an atmosphere of increased metabolic activity and requirements. The muscles use up all available oxygen and resort to anaerobic glycolysis, a normal physiological process in muscle tissue. A by-product of glycolysis is lactic acid. Lactic acid is usually further metabolized in the liver to glycogen, but with sudden strenuous exercise, the massive increase of lactic acid creates a localized acidosis which progresses to a systemic acidosis.

The blood supply is pooled in the muscles and rapidly becomes deoxygenated. Normally, with exercise, there is a "muscle pump," whereby contractions squeeze blood out of the muscle and relaxation again allows pooling. When an animal is captured, there is now an isotonic state of contraction creating poor tissue perfusion and decreased heat dissipation and hypoxia. All of these problems are magnified when the animal is tranquilized and the muscle masses start to relax. A pooling of blood results in the venous system and a sudden drop in blood pressure occurs. Shock can become a complication as in the acute death syndrome. In most cases of capture myopathy, this hypoxia and local acidosis remains localized, especially in well-perfused muscle, and focal muscle necrosis results.

Capture myopathy is an unfortunate complication of immobilization, restraint, or transport. Prevention is very important by minimizing excitement that can result in overexertion. All immobilizations must be planned in advance to offset possible difficulty in post-anesthetic recovery.

No reliable therapeutic have been documented to treat capture myopathy. Treatment for capture myopathy is supportiive and includes intravenous fluids, sodium bicarbonate to combat acidosis, corticosteroids, vitamin E and selenium supplements, calcium channel blockers, and antibiotics. Many of the pathologic changes are irreversible and, despite drastic supportive measures, animals suffering from capture myopathy often die, so prevention is essential.

GUIDELINES FOR THE PREVENTION OF CAPTURE MYOPATHY

AT AUDUBON PARK ZOO

The following procedures are observed during all planned capture events:

1. Immobilizations are scheduled during early morning hours when temperature and humidity are lowest.

2. Each event is discussed by the veterinary and curatorial staff and a plan of action determined.

3. All necessary equipment is assembled and ready. Hospital staff are required to refer to a capture equipment check list.

4. All persons participating in the capture event will be trained in the use of equipment such as nets, snares, gloves, etc. Use of projective capture equipment is restricted to the hospital and curatorial staff.

5. When using chemical restraint, an adequate dose of the immobilizing agent is administered by the most efficient and least stressful method.

6. Blindfolds are used to decrease visual stimulation.

7. All personnel involved are to proceed quietly. Unnecessary conversation and noise are avoided.

8. All hospital, curatorial and keeper staff are familiar with the human emergency protocol in the event of a narcotic accident. It is required that hospital staff, mammal curator and assistant curator and hoofstock keepers be trained in CPR and that they keep their certification current by attending an annual review course.

9. Due to the possible association between Vitamin E and capture myopathy, diets fed to all hoofstock and marsupials should contain a minimum of .85 IU/kg of Vitamin E and .25 ppm of Selenium. Our current hoofstock ADF 16 diet meets these levels.

10. Temperature, pulse and respiration rates will be checked during all restraint procedures.

11. Animals with temperatures greater than or equal to 106 will be cooled down with water and receive IV fluid therapy if the condition is severe.

12. Animals showing increased heart rates (>250) or species seeming prone to capture myopathy (waterbuck) may prophylactically be given one liter LRS containing 1,000 meq. sodium bicarbonate.

Revised 6/95

CAPTURE MYOPATHY

DRUG DOSES FOR INITIAL THERAPY

Audubon Park Zoo

WEIGHT (#)

DRUG DOSE Route 100 250 400

1. LRS 20cc/# IV 2L 5L 8L

Max. rate = 40cc/#/hr.

---------------------------------------------------------------------------

2. Sodium bicarbonate 1.0 meq/# IV 100.0cc 250.0cc 400.0cc

8.4% (100meq/100ml)

1.0 meq/ml

---------------------------------------------------------------------------

3. Solu-Delta-Cortef 0.5 mg/# IV

Prednisolone

sodium succinate

100mg 5.0cc 12.5cc 20cc

10.0 mg/ml 1/2 1 1/4 2

vial vials vials

500mg 1.0cc 2.5cc 4cc

50.0 mg/ml 1/10 1/4 4/10

vial vial vial

---------------------------------------------------------------------------

4. Banamine 0.5 mg/# IV 1.0cc 2.5cc 4.0cc

50.0 mg/ml

---------------------------------------------------------------------------

5. Trimethoprim/Sulfa 48% 15 mg/# IV 3.1cc 7.8cc 12.5cc

480.0 mg/ml

---------------------------------------------------------------------------

6. Dipyrone 50% 25 mg/# IV,IM or 5.0cc 12.5cc 20.0cc

500.0 mg/ml Subq

--------------------------------------------------------------------------

7. Bo-Se

Vit.E/Selenium (Bo-Se) 0.03cc/# IM 3.0cc 7.5cc 12.0cc

2.19mg Se/ml;

50mg Vit. E/ml

(68 USP Units/ml)

---------------------------------------------------------------------------

8. Robaxin 25.0 mg/# IV 25.0cc 60.0cc 100.0cc

Methocarbamol

100mg/ml

WEIGHT (#)

DRUG DOSE Route 100 250 400 9. Dextrose 50 % 100- IV 100.0cc 300.0cc 500.0cc

500cc

---------------------------------------------------------------------------

10. Atropine 0.05 mg/# IV

SA 0.54 mg/ml 9.25cc 23.0cc 37.0cc

LA 15.0 mg/ml 0.3cc 0.8cc 1.3cc

SLOW IV TO EFFECT: NOT COMPATIBLE WITH SODIUM BICARBONATE

Revised 4/93


Capture Miopathy

Capture myopathy is a muscle disease associated with the stress of capture, restraint, and transportation. The disease is characterized by degeneration and necrosis of skeletal and cardiac muscle. Other names for this disease include: exertional Rhabdomyolysis, muscle dystrophy, overstraining disease, capture stress disease, white muscle disease, and idiopathic muscle necrosis.

Numerous species of birds and mammals are susceptible to capture myopathy. It has never been documented in reptiles or lower vertebrates. It seems to be more prevalent in prey species or submissive members of non-prey species which can become easily excited, especially when exposed to unusual stress such as restraint or chasing.

The disease develops within hours and up to 14 days after capture or transport. It may be seen in both animal that exert themselves maximally and those that are relatively quiet although it generally occurs after severe exertion and is often seen following a difficult, prolonged capture. It can occur with either physical or chemical restraint.

Predisposing factors include fear, anxiety, overexertion, repeated handling, failure to allow an exhausted animal to rest before transportation, and constant muscle tensions such as may occur in protracted alarm reactions. A variety of stressors may function in concert or individually to precipitate development of the classical syndrome.

Four different syndromes related to capture myopathy have been described. These four syndromes are the peracture death syndrome, the acute death syndrome, the ataxic myoglobinuric syndrome, and the ruptured muscle syndrome.

The peracute death syndrome is seen in animals shortly after capture. While the animal is undisturbed, it appears ok, but if excited or stressed again, it may suddenly fall and die. A peracute muscle tissue breakdown, which causes a release of cellular contents, (particularly, lactic acid and potassium) is thought to be the underlying mechanism. The potassium causes the heart to be hypersensitive to substances released by the adrenal glands during stress. The heart develops a severe abnormal rhythm and death rapidly follows.

Acute death syndrome occurs 3-4 hours following capture and involves over-heating, shock, adrenal gland exhaustion, and mild, acute muscle breakdown. Alterations in blood ph to create an acidotic state appear to be a critical factor in the development of acute capture myopathy. Clinical signs that may be observed prior to death include depression, shallow, rapid breathing, increased heart rate, cessation of urination, and rapid debilitation.

Ataxic myoglobinuric syndrome occurs hours to days post-capture. The animal becomes progressively more wobbly until it is unable to stand. The urine may appear reddish-brown in color due to the muscle break-down products. Renal failure follows.

In the ruptured muscle syndrome, animal are usually normal and appear healthy when captured, but clinical signs may become noticeable twenty-four to forty-eight hours later and may persist for three to four weeks. Clinical signs include a marked drop in the hindquarters and hyperflexion of the hocks due to bilateral rupture of the gastrocnemius muscles.

The cause of all these syndromes is very similar but complex, involving fear, the sympathetic nervous system and damage to skeletal and cardiac musculature. The biochemistry of stress and fear create an atmosphere of increased metabolic activity and requirements. The muscles use up all available oxygen and resort to anaerobic glycolysis, a normal physiological process in muscle tissue. A by-product of glycolysis is lactic acid. Lactic acid is usually further metabolized in the liver to glycogen, but with sudden strenuous exercise, the massive increase of lactic acid creates a localized acidosis which progresses to a systemic acidosis.

The blood supply is pooled in the muscles and rapidly becomes deoxygenated. Normally, with exercise, there is a "muscle pump," whereby contractions squeeze blood out of the muscle and relaxation again allows pooling. When an animal is captured, there is now an isotonic state of contraction creating poor tissue perfusion and decreased heat dissipation and hypoxia. All of these problems are magnified when the animal is tranquilized and the muscle masses start to relax. A pooling of blood results in the venous system and a sudden drop in blood pressure occurs. Shock can become a complication as in the acute death syndrome. In most cases of capture myopathy, this hypoxia and local acidosis remains localized, especially in well-perfused mmuscle, and focal muscle necrosis results.

Capture myopathy is an unfortunate complication of immobilization, restraint, or transport. Prevention is very important by minimizing excitement that can result in overexertion. All immonbilizations must be planned in advance to offset possible difficulty in post-anesthetic recovery.

No reliable therapeutic have been documented to treat capture myopathy. Treatment for capture myopathy is supportiive and includes intravenous fluids, sodium bicarbonate to combat acidosis, corticosteroids, vitamin E and selenium supplements, calcium channel blockers, and antibiotics. Many of the pathologic changes are irreversible and, despite drastic supportive measures, animals suffering from capture myopathy often die, so prevention is essential.

6/95

GUIDELINES FOR THE PREVENTION OF CAPTURE MYOPATHY

AT AUDUBON PARK ZOO

The following procedures are observed during all planned capture events:

1. Immobilizations are scheduled during early morning hours when temperature and humidity are lowest.

2. Each event is discussed by the veterinary and curatorial staff and a plan of action determined.

3. All necessary equipment is assembled and ready. Hospital staff are required to refer to a capture equipment check list.

4. All persons participating in the capture event will be trained in the use of equipment such as nets, snares, gloves, etc. Use of projective capture equipment is restricted to the hospital and curatorial staff.

5. When using chemical restraint, an adequate dose of the immobilizing agent is administered by the most efficient and least stressful method.

6. Blindfolds are used to decrease visual stimulation.

7. All personnel involved are to proceed quietly. Unnecessary conversation and noise are avoided.

8. All hospital, curatorial and keeper staff are familiar with the human emergency protocol in the event of a narcotic accident. It is required that hospital staff, mammal curator and assistant curator and hoofstock keepers be trained in CPR and that they keep their certification current by attending an annual review course.

9. Due to the possible association between Vitamin E and capture myopathy, diets fed to all hoofstock and marsupials should contain a minimum of .85 IU/kg of Vitamin E and .25 ppm of Selenium. Our current hoofstock ADF 16 diet meets these levels.

10. Temperature, pulse and respiration rates will be checked during all restraint procedures.

11. Animals with temperatures greater than or equal to 106 will be cooled down with water and receive IV fluid therapy if the condition is severe.

12. Animals showing increased heart rates (>250) or species seeming prone to capture myopathy (waterbuck) may prophylactically be given one liter LRS containing 1,000 meq. sodium bicarbonate.

4/93

CAPTURE MYOPATHY

DRUG DOSES FOR INITIAL THERAPY

Audubon Park Zoo

WEIGHT (#)

DRUG DOSE Route 100 250 400

1. LRS 20cc/# IV 2L 5L 8L

Max. rate = 40cc/#/hr.

-------------------------------------------------------------------------------

2. Sodium bicarbonate 1.0 meq/# IV 100.0cc 250.0cc 400.0cc

8.4% (100meq/100ml)

1.0 meq/ml

-------------------------------------------------------------------------------

3. Solu-Delta-Cortef 0.5 mg/# IV

Prednisolone

sodium succinate

100mg 5.0cc 12.5cc 20cc

10.0 mg/ml 1/2 1 1/4 2

vial vials vials

500mg 1.0cc 2.5cc 4cc

50.0 mg/ml 1/10 1/4 4/10

vial vial vial

-------------------------------------------------------------------------------

4. Banamine 0.5 mg/# IV 1.0cc 2.5cc 4.0cc

50.0 mg/ml

-------------------------------------------------------------------------------

5. Trimethoprim/Sulfa 48% 15 mg/# IV 3.1cc 7.8cc 12.5cc

480.0 mg/ml

-------------------------------------------------------------------------------

6. Dipyrone 50% 25 mg/# IV,IM or 5.0cc 12.5cc 20.0cc

500.0 mg/ml Subq

-------------------------------------------------------------------------------

7. Bo-Se

Vit.E/Selenium (Bo-Se) 0.03cc/# IM 3.0cc 7.5cc 12.0cc

2.19mg Se/ml;

50mg Vit. E/ml

(68 USP Units/ml)

-------------------------------------------------------------------------------

8. Robaxin 25.0 mg/# IV 25.0cc 60.0cc 100.0cc

Methocarbamol

100mg/ml

-------------------------------------------------------------------------------

9. Dextrose 50 % 100- IV 100.0cc 300.0cc 500.0cc

500cc

-------------------------------------------------------------------------------

10. Atropine 0.05 mg/# IV

SA 0.54 mg/ml 9.25cc 23.0cc 37.0cc

LA 15.0 mg/ml 0.3cc 0.8cc 1.3cc

SLOW IV TO EFFECT: NOT COMPATIBLE WITH SODIUM BICARBONATE


--------------------------------------------------------------------------------

AUDUBON INSTITUTE

AUDUBON PARK ZOO

ANIMAL HEALTH CARE CENTER

SMALL ANIMAL EMERGENCY KIT

Equipment:
1 – Stethoscope

1 – Laryngoscope

2 – Laryngoscope Heads

1 - Thermometer

1 – Tube of K-Y jelly

1 – E.T. tube –

1 – E.T. tube –

1 – E.T. tube –

1 – E.T. tube –

1 – E.T. tube –

1 – E.T. tube –

1 – E.T. tube –

2 – Stylets

1 Cut Down Pack

1 – Scissors

1 – Scalpel Handle

1 – Disposable Scalpel

1 – Forceps

1 – Hemostat

Supplies:

5 – ½ cc Syringes w/ needle 1 –

5 – 1 cc Syringes w/ needle 1 –

5 – 1cc Syringes w/o needle

12 – 3 cc Syringes

5 – 6 cc Syringes w/ needle

4 – 12 cc Syringes w/ needle

1 Slot – 14 ga. Needles 1 "

1 Slot – 18 ga. Needles 1 ½ "

1 Slot – 18 ga. Needles 1 "

1 Slot – 20 ga. Needles 1" & 1 ½ "

1 Slot – 22 ga. Needles 1" & 1 ½ "

1 Slot – 23 ga. Needles 1 "

1 Slot – 25 ga. Needles 5/8 "

1 – Roll 1" tape

1 – Roll – 2" tape

2 – Rolls – 2" Vetwrap

1/3 – 3 X 3 Gauze Squares

1 – Large Animal IV Set

2 – IV Sets

1 – Alcohol prep jar

1 – Betadine prep jar

2 – 2-0 PDS

2 – 2-0 Dexon

2 - # 10 Blades

3 – 16 ga. Catheters

3 – 18 ga. Catheters

3 – 20 ga. Catheters

2 – 18 ga. Catheters (Termo)

2 – 20 ga. Catheters ( Termo)

2 – 19 ga. Catheters (Butterfly)

2 – 21 ga. Catheters (Butterfly)

2 – 23 ga. Catheters (Butterfly)

Drugs

Aminophylline – 1 bottle

Atropine SA – 1 bottle

Dexamethasone – 1 bottle

Dopram – 1 bottle

Epinephrine – 1 bottle

Heparin – 1 bottle

Ketamine – 1 bottle

Lasix – 1 bottle

Lidocaine – 1 bottle

Rompum SA – 1 bottle

Sodium Bicarb 100 ml. – 1 bottle

Solu-Delta-Cortef – 100 mg – 2 bottles

Solu-Delta-Cortef – 500 mg – 3 bottles

Valium – 1 bottle

Versed – 2 bottles

Fluids:

1000 ml LRS – 1 bag

500 ml LRS – 1 bag

Miscellaneous:

Emergency drug dose chart

Capture Myopathy protocol


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