Vol. 21, No.
3 March 1999
CE Refereed Peer Review
FOCAL POINT
★Veterinarians working with free-
ranging raptors must handle
these animals as wild species
requiring special veterinary care
to achieve the ultimate treatment
goal of a successful release back
into the wild.
KEY FACTS
■ In order to provide long-term
care of raptors, veterinarians
must work in conjunction with a
knowledgeable licensed wildlife
rehabilitator.
■ The most common causes of
morbidity and mortality in free-
ranging raptors in the United
States are traumatic injuries and
intoxications related to human
activity.
■ The diagnostic approach to
raptors with suspected trauma
should include a thorough
evaluation of the ocular and
musculoskeletal systems because
most traumatic injuries result in
ocular and/or orthopedic lesions.
■ The treatment of lead toxicosis
consists of chelation, most
commonly with edetate calcium
disodium (10 to 40 mg/kg
intramuscularly, twice daily, on
a 5-day-on/5-day-off schedule),
and supportive care.
20TH ANNIVERSARY
Raptor Medicine:
Basic Principles and
Noninfectious
Conditions
Wildlife Conservation Society/Bronx Zoo, Bronx, New York
Sharon Lynn Deem, DVM, PhD
ABSTRACT: An understanding of the biology, physiology, and anatomy of raptors as well as
how to medically approach birds of prey is imperative for providing quality care. The two most
common clinical diagnoses of free-ranging raptors are trauma—usually with ocular and/or or-
thopedic involvement—and toxicoses. Acetylcholinesterase inhibitors and lead poisoning ac-
count for the majority of acute toxicities. Treatment of these intoxicated patients can be re-
warding if practitioners apply fast, aggressive therapy while pursuing diagnostics.
T
he word raptor, derived from the Latin rapere, meaning to grip or grasp,
is a general term used for any predatory bird. Two taxonomic orders, Fal-
coniformes and Strigiformes, comprise all raptorial species. The order
Falconiformes (diurnal raptors) consists of five families—Accipitridae (kites,
hawks, harriers, Old World vultures, and eagles), Cathartidae (New World vul-
tures and condors), Falconidae (falcons), Pandionidae (osprey), and Sagittariidae
(secretary birds). The order Strigiformes (nocturnal raptors) consists of two fam-
ilies—Tytonidae (barn and grass owls) and Strigidae (all other owls). There is
debate among taxonomists regarding this classification scheme, particularly in
reference to the New World vultures (which may be reclassified with stork-like
birds) and secretary birds (which may be reclassified with crane-like birds).1
Raptors are highly visible wildlife species that are often used as biomarkers for
environmental conditions. For example, the mid-1900s reduction of raptorial
species was related to environmental contaminants (e.g., dichlorodiphenyl-
trichloroethane, dieldrin, polychlorinated biphenyls) and alerted people to the
carcinogenic potential of pesticides.2,3 Today, the most common causes of mor-
bidity and mortality of raptors in the United States are related to human activity
(e.g., motor vehicles, buildings, guns, power lines) and emphasize the current
environmental problems associated with human population growth.4–6
Private practitioners are often asked to provide veterinary care for injured rap-
tors. Veterinarians who treat birds of prey used for falconry must have an appre-
Small Animal/Exotics 20TH ANNIVERSARY
ciation for the sport (i.e., laws, terminology, principles)
as well as the common diseases in these birds.7,8
BIOLOGY, PHYSIOLOGY, AND ANATOMY
An understanding of the biology, physiology, and
anatomy of raptors is imperative to providing high-
quality veterinary care. When a free-ranging raptor is
admitted to a veterinary hospital, the species must first
be identified to determine its natural diet, geographic
distribution, and ecologic habits. The importance of
this background information can be exemplified by
sharp-shinned hawks (Accipiter striatus), which are
highly specialized bird-catching hawks that capture
their prey in flight. These birds are small; high-strung;
and notoriously difficult to feed in captivity, often re-
quiring force-feeding during hospitalization.
The gastrointestinal (GI) tract of raptors has unique
characteristics, the most important being the act of eges-
tion.9 Egestion is the retrograde discharge of undigested
or indigestible material through the GI tract of carnivo-
rous birds. This phenomenon is believed to involve both
gastric activity and esophageal antiperistalsis.10 Pellets
(i.e., casts) are formed in the ventriculus from the bones
and hair/feathers of prey items and periodically egested.
In owls, a pellet (often containing bones) is egested after
each meal, whereas in diurnal raptors more than one
meal is often consumed before egestion occurs and
bones are usually not present. The quantity and quality
of pellets are important diagnostic indicators for assess-
ing the health of hospitalized patients. Another GI
tract–related physiologic act is the normal regurgitation
seen in stressed vultures; this should not be diagnosed as
a pathologic finding. Anatomic features of note in the
raptor GI tract include a poorly developed crop and ves-
tigial ceca in diurnal raptors; owls have no crop and
well-developed ceca.9
The skeletal structure of raptors is similar to that of
other avian species, although species variations do exist.
The hallux (first digit) is the opposable toe used for
grasping and killing prey. The humeroscapular bone,
which is present in some species of owls and hawks, is a
unique anatomic characteristic not found in other
avian species.11 Smith and Smith state that this bone is
dorsal to the shoulder joint, near the head of the humerus,
and approximately 4 mm from base to apex in the great
horned owl (Bubo virginianus).11 This bone is radio-
graphically visible and should not be misinterpreted as
a pathologic fracture.11 In their paper, the radiographs
and xeroradiographs depicting this bone are taken in a
craniocaudal view, which is a view infrequently used by
practitioners. When evaluating thoracic radiographs,
however, practitioners should be aware of the presence
of this bone in certain species of raptors.
EGESTION ■ SKELETAL STRUCTURE ■ GOOD SAMARITAN LAW
Compendium March 1999
REHABILITATION AND TREATMENT
CONSIDERATIONS
Federal and State Laws
The decision to treat free-ranging raptors should be
based on legal, medical, and practical factors. All raptor
species in the United States are now legally protected
by a number of federal statutes, specifically the Migra-
tory Bird Treaty Act of 1918, the Bald Eagle Protection
Act of 1940, and the Endangered Species Act of 1973.12
Individual states may also have laws protecting raptors.
Persons providing veterinary care for raptors should be
familiar with federal and state laws.
The Good Samaritan law allows licensed veterinari-
ans to provide initial treatment of any raptor, and many
agencies tolerate veterinarians who provide long-term
care of raptors if they work in conjunction with a li-
censed rehabilitator. (The importance of working with
a qualified, knowledgeable licensed wildlife rehabilita-
tor cannot be overemphasized.) However, veterinarians
who are treating an endangered species (e.g., bald eagle
[Haliaeetus leucocephalus], snail kite [Rostrhamus socia-
bilis]) must report the animal to the appropriate state
wildlife agency and the U.S. Fish and Wildlife Service
(USFWS) within 24 hours. The long-term housing of
raptors for educational or exhibit purposes requires a
rehabilitator’s license, which can be obtained through
the USFWS but may take up to 90 days to acquire.
Criteria for Release into the Wild
The ultimate goal of raptor rehabilitation is to return
the bird to the wild. Guidelines for physiologic and
psychologic assessment of raptors prior to release have
been established.13 Important prerelease survival criteria
include 100% function of wings and legs, normal bilat-
eral vision, normal psychology (e.g., not imprinted),
good feather condition, adequate hunting and survival
skills, and suitable location and time of year for release.
All raptors should ideally be test flown in mews (out-
door flight cages) before release to assess their stamina
and ability to properly fly and land. Another factor that
dictates the approach to an individual raptor is the en-
dangered/threatened status of the patient and whether
use in captive breeding and/or education programs is
an option if release into the wild is unlikely.
Nutrition and Husbandry
All raptors are carnivores. The diets of individual
species vary considerably, however, and include inverte-
brates, reptiles, fish, birds, eggs, and mammals. A
whole-prey diet (e.g., invertebrates, mice, rats, fish,
chicks, quail) should be fed based on the preferred prey
of the hospitalized patient to encourage eating and pro-
vide appropriate vitamins and minerals. Most captive
Compendium March 1999 20TH ANNIVERSARY Small Animal/Exotics

raptors are fed a limited va- Visual barriers placed at the

riety of domesticated prey front of the cage will pro-
species, which may not pro- vide a sense of security for
vide adequate sources of the bird. Good hygiene;
necessary macronutrients, protective walls; and perch-
vitamins, and/or minerals.14 es of the right size, shape,
Alternatively, a commercial- and texture20 are necessary
ly available bird-of-prey diet to minimize self-inflicted
(e.g., Nebraska Bird of Prey trauma and infectious prob-
Diet; Central Nebraska Pack- lems (e.g., bumblefoot,
ing, Inc., North Platte, NE, aspergillosis). If a raptor re-
or Zu/Preem Bird of Prey quires long-term treatment,
Diet; Hill’s Division Riviana it is best to either house it
Foods, Inc., Topeka, KS) can in a modified outdoor run
be fed. A nutrient analysis or transport it to a rehabili-
comparing these commercial- Figure 1—Tube feeding a male American kestrel. tation center.
ly prepared diets with indi-
vidual prey items is avail- Handling, Restraint,
able.15 and Diagnostic Workups
As a general guideline, the The safety of both the
amount of feed a raptor re- handler and bird must be
quires per day is inversely considered when handling
correlated with its size.16,17 and restraining raptors. Ta-
Small raptors, such as Amer- lons can inflict serious harm
ican kestrels (Falco sparverius), and should be immediately
may require 30% of their controlled (Figure 2); the
body weight (BW) daily, beak and wings can then be
whereas eagles require 8% immobilized. In addition,
to 10% of BW daily.17 The some raptors (e.g., eagles,
metabolic demands (e.g., great horned owls, vultures)
postoperative recovery, ca- do bite and can inflict seri-
chectic state, activity level) ous wounds with their beaks,
of patients also affect meta- although they are less of a
bolic rate and influence the concern than are talons. The
amount of feed required.18,19 use of leather gloves and
Some species are poor drapes helps with capture
feeders while hospitalized and restraint. Hoods (tightly
(e.g., osprey [Pandion hali- fitted leather caps used to
aetus], sharp-shinned hawk, cover the head and eyes) are
Cooper’s hawk [Accipiter also highly effective in calm-
cooperii ]), and food intake Figure 2— Proper method of restraining a golden eagle ing restrained raptors.
and BW must be carefully (Aquila chrysaetos). Note that the handler is wearing gloves A thorough diagnostic
monitored. Some patients and has control of both feet (i.e., talons) and that the wings workup of raptors is best
will require force-feeding by are positioned against the bird’s body. performed with the bird un-
either manually placing der general anesthesia, using
pieces of prey into the esoph- isoflurane at a vaporizer set-
agus or tube feeding (Figure 1). There is debate as to ting of 3% for induction and 1.5% to 2% for mainte-
whether raptors require fresh, clean water in addition to nance. Any raptor in respiratory distress should first be
water obtained from food. I provide all hospitalized placed in a dark, warm oxygen chamber for 15 to 20
raptors with access to fresh water for drinking and minutes before handling. Mask induction and endotra-
bathing. cheal intubation for maintenance is a safe protocol.
Raptors housed at a veterinary hospital for the short This will minimize the stress associated with restraint
term should be in an area with low traffic and noise. in a wild animal that may already be in a severe state of

FEEDING ■ HOUSING ■ TALONS ■ ANESTHESIA

Small Animal/Exotics 20TH ANNIVERSARY Compendium March 1999

decompensation. I believe and/or orthopedic prob-

that the physiologic stress Noninfectious Conditions of lems. 5,27–29 Early and ag-
caused by short-term isoflu- Free-Ranging Raptors gressive treatment of these
rane is less than that injuries can make the dif-
caused by manually re- Trauma Nutrition ference between release in-
straining debilitated rap- ■ Hit by vehicle ■ Starvation to the wild and death.
tors. If isoflurane is not an ■ Collision with ■ Hypoglycemia The most common causes
option, protocols using building/power line ■ Nutritional secondary of traumatic injuries in
halothane and parenteral ■ Trapped (barbed-wire hyperparathyroidism
free-ranging raptors are
anesthetics are available21,22 gunshot and vehicular or
or the patient can be re- fence) ■ Thiamine deficiency structural collisions. 4–6
ferred to a veterinarian ■ Predation ■ Iron deficiency anemia The damage caused by
with the proper equipment ■ Vitamin A deficiency gunshot is created by lac-
Toxicosis
for isoflurane anesthesia. ■ Vitamin E/selenium eration and crushing of
■ Organophosphates
The minimal diagnostic deficiency bone and soft tissue in
workup should include a ■ Carbamates the immediate path of the
■ Gout
physical examination that ■ Lead bullet. 30 Treatment of
a
emphasizes thorough oph- ■ Organochlorines Orphaned Young gunshot victims depends
thalmologic examination ■ Polychlorinated on the organ(s) damaged
and assessment of the mus- a
Electrocution (e.g., a lacerated liver ver-
biphenyls a
culoskeletal system, BW, a Refer to the literature40–42 if sus fractured long bone)
■ Mercury toxicity is suspected.
complete blood count, and the patient’s clinical
packed cell volume (PCV), ■ Strychninea state. In most cases, prac-
and total solids. Other tests ■ Anticoagulantsa titioners should not at-
that may be beneficial in- ■ Nicotine sulfatea tempt to remove bullets
clude fecal parasite exami- because lead poisoning is
nation; chemistry profile; seldom associated with
culture and sensitivity of lesions; whole-body radiographs; the uptake of lead in tissue and significant harm may
lead and cholinesterase levels; and, in select cases, endo- result from such an attempt.30
scopic evaluation of the respiratory and GI systems. Orthopedic techniques for raptors are based on those
Free-ranging raptors presented to veterinarians may described in the avian literature.31–34 Both external and
be in a state of decompensation from traumatic, met- internal fixation can be used to treat dislocations and
abolic, nutritional, and/or infectious disease and often fractures. Veterinarians must provide perfect surgical re-
require immediate life-saving emergency medical care. duction and fixation, especially for lesions of the wings,
Information on avian emergency treatment is avail- if the patient is to be released back to the wild. Soft tis-
able.23,24 It is important to remember that raptors are sue damage with or without orthopedic lesions is also a
wild animals that can be fatally stressed by handling. common presenting problem of raptors that have suf-
Having all equipment (e.g., ophthalmoscope, blood col- fered traumatic injuries. Practitioners should refer to
lection equipment, catheter for intraosseous place- the literature on soft tissue surgical procedures.35,36
25
ment ) and drugs (e.g., fluids, steroids, antibiotics) ready Raptors’ eyes are tightly encased, large structures with
before treatment will minimize patient stress and de- anterior scleral ossicles, which consist of a variable
crease the time needed for manipulations. The judicious number of interdigitating bones forming a complete
use of isoflurane may also minimize the stress of handling. bony ring within the sclera.28,37 Unilateral lesions in the
anterior chamber are common in traumatic injuries
NONINFECTIOUS CONDITIONS (Figure 3).27 In one study, however, severe lesions of the
Epidemiologic studies conducted in the United States posterior segment (e.g., vitreous hemorrhage, tear or
show that trauma and toxicities, the majority of which rupture of the pecten, retinal detachment, chorioretinal
are directly related to human activity, are the most com- rupture, posterior scleral rupture) were found with little
mon clinical diagnoses in free-ranging raptors4–6,26 (see or no pathology noted in the anterior segment.38 It was
Noninfectious Conditions of Free-Ranging Raptors). suggested that the posterior segment is prone to injury
related to contrecoup forces because of the anatomy of
Trauma the raptor eye.24 For this reason, it is imperative that a
Most traumatic injuries to raptors result in ocular fundic examination be performed to determine wheth-

REDUCING STRESS ■ TREATING GUNSHOT VICTIMS ■ FUNDIC EXAMINATION

Small Animal/Exotics 20TH ANNIVERSARY Compendium March 1999

er posterior segment lesions cholinesterase levels or by

are present. Fundic exami- detecting the pesticide in the
nation can often be per- crop or GI contents via gas
formed in the awake raptor chromatography. 51 These
or under isoflurane anesthe- tests are readily available at
sia. If necessary, vercuroni- most veterinary diagnostic
um bromide may be used laboratories. If possible, sam-
for mydriasis39—but only by ples from normal birds of the
specialists or those with ex- same species should be sub-
perience. mitted with samples from
the suspected poisoned birds
Toxicosis to generate control values for
Organophosphate (OP), comparison.
carbamate, and lead toxico- Treatment should be in-
sis are the most common Figure 3A stituted immediately in any
toxicities in free-ranging raptor suspected of having
raptors (see Noninfectious OP or carbamate toxicosis.
Conditions of Free-Ranging Atropine (0.5 mg/kg, 0.25
Raptors). dose intravenously and 0.75
dose intramuscularly) should
Organophosphates and be administered and the an-
Carbamates imal observed for response
Organophosphates and to therapy. The dose should
carbamates are used exten- be repeated intramuscularly
sively in agricultural practice at 3- to 4-hour intervals un-
as pesticides. 43–45 Birds of til all signs have dissipated
prey most often come in con- and residual toxin (e.g., toxin-
tact with these agents by eat- laced food present in the GI
ing contaminated prey (e.g., tract) is absent. Diphenhy-
insects, small vertebrates)44,46 dramine (4 mg/kg intra-
and topically treated live- muscularly three times dai-
stock.47 However, several cas- ly) may also be beneficial; it
es of intentional poisoning has been shown to block
have been reported.48–50 If il- the effect of nicotine-recep-
legal poisoning is suspected, tor overstimulation in mam-
the appropriate law enforce- mals.43
Figure 3B
ment agency should be in- Pralidoxime chloride (20
formed. Figure 3—(A) Bald eagle with corneal edema and vasculariza- mg/kg intramuscularly) will
Organophosphates and tion of the left eye. (B) Eastern screech owl (Otus asio) with break the OP–acetylcholin-
exophthalmia and hyphema of the right eye.
carbamates inactivate the en- esterase bond only if it is
zyme acetylcholinesterase, administered within 24
leading to the buildup of hours of intoxication, but it
acetylcholine and continual stimulation at the motor is contraindicated for carbamate poisoning. The use of
end-plates, which often results in death due to respira- pralidoxime chloride is therefore rarely appropriate be-
tory failure. Clinical signs of OP and carbamate poi- cause the inciting toxin (OP versus carbamate) and
soning in raptors include ataxia, inability to stand, time of intoxication are almost always unknown.
opisthotonos, spastic nictitans, rigid paralysis with Any food present in the crop should be manually ex-
tightly clenched talons, rapid respiration, salivation, tracted with forceps, and activated charcoal (0.02 to
muscle twitching, and alternating miosis and mydri- 0.08 mg orally) should be administered when it is be-
asis.44 The classic signs of parasympathetic overstimula- lieved that the pesticide was recently ingested and is
tion seen in mammals (e.g., GI hypermotility, miosis) still present in the GI tract. Supportive care is also im-
are usually not present. portant and may include fluids, warmth, antifungals,
A definitive diagnosis is based on the plasma or serum antibiotics, and nutritional supplementation as needed.

ACETYLCHOLINESTERASE ■ DEFINITIVE DIAGNOSIS ■ ATROPINE

Compendium March 1999 20TH ANNIVERSARY
Lead
Lead poisoning is seen in
raptors that ingest lead (e.g.,
intact lead shot in the bodies
of prey). Acute and chronic
lead poisoning have been di-
agnosed in many raptor
species.52–54 Lead poisoning
is often pansystemic, affect-
ing the GI, nervous, renal,
immunologic, and hemato-
poietic systems. The rate of
exposure (acute versus chron-
ic) will influence clinical Figure 4—Lateral radiograph of a black vulture (Coragyps ly dehydrated (10% to 15%)
signs. Signs of acute toxicity atratus) with lead shot in the ventriculus.
include anorexia, vomiting,
diarrhea, and neurologic ab-
normalities (e.g., wing droop, poor mentation, muscle
twitches, seizures). Similar clinical signs may be seen
with chronic exposure, but neurologic deficits are usual-
ly limited to paresis or paralysis and the bird may be
weak and emaciated because of anemia and progressive
weight loss, respectively. A definitive antemortem diag-
nosis is based on whole-body radiographs (Figure 4),
blood lead levels, and/or decreased aminolevulinic acid
dehydratase activity.55
Initial therapy of lead toxicosis consists of chelation,
fluids, and supportive care. Edetate calcium disodium
(10 to 40 mg/kg intramuscularly twice daily on a 5-day-
on/5-day-off schedule until signs of toxicosis have re-
solved and/or blood lead levels are within normal range)
is the most commonly used chelating agent. Alternative-
ly, the oral chelating agent D-penicillamine (55 mg/kg
twice daily for 3 to 6 weeks) can be administered. Both
of these agents can be nephrotoxic and cause GI side ef-
fects. Meso-dimercaptosuccinic acid has recently been
shown to produce lower blood lead levels than does ede-
tate calcium disodium when administered for 5 days at
30 mg/kg/day.55 Activated charcoal, cathartics, and endo-
scopic or surgical intervention may be necessary to re-
move the lead material. Periodic whole-body radiographs
and/or serial blood lead levels will help practitioners assess
when chelation therapy can be discontinued.
Nutritional Deficiencies
Starvation and emaciation are common presenting
conditions in free-ranging raptors; underlying causes
(e.g., orphaned young, traumatic injury, toxicosis, viral
infection) must be elucidated. Treatment of starvation
should be directed at rehydration and establishing nor-
moglycemia.
It is imperative to correct dehydration before feeding
solid foods to avoid vomiting and/or improper diges-
CHELATION THERAPY ■ DEHYDRATION ■ BLOOD TRANSFUSION
Small Animal/Exotics
tion in the dehydrated pa-
tient. Hydration status can
be assessed by evaluating the
skin turgor around the eyes,
turgescence of the ulnar vein
and artery, and PCV and
total plasma solids. Fluids
can be administered orally
or subcutaneously in birds
with mild dehydration (5%)
but are best administered
either by the intravenous or
intraosseous route in severe-
birds.56,57 Sites for intraven-
ous fluid administration are
the right jugular, brachial,
or medial metatarsal veins. The usual sites of in-
traosseous catheter placement are the distal ulnar and
proximal tibiotarsus.25 The amount of fluid can be cal-
culated using the following equation:
BW (g) × Percent of dehydration (decimal value) =
Estimated deficit (ml)
The raptor should receive one quarter to one half of the
necessary fluids within 2 to 4 hours and the remaining
volume during the next 22 to 24 hours.58 Alternatively,
fluid and electrolyte requirements can be determined
using metabolic scaling. 59 For intravenous and in-
traosseous administration, a 50:50 mix of lactated
Ringer’s solution and 5% dextrose is appropriate for
most patients. Severely hypoglycemic birds can be ad-
ministered a slow (intravenous or intraosseous) bolus of
50% dextrose (0.5 to 1.0 ml/kg) in a crystalloid fluid,
not exceeding 10 to 20 ml/kg.
In raptors with a PCV below 15%, blood transfusion
is a therapeutic option. Short-term benefits of homolo-
gous whole-blood transfusions have been demonstrated
in domestic pigeons. 60 However, erythrocytes were
rapidly destroyed in another study using heterologous
blood transfused from pigeons to selected raptor
species,61 suggesting that heterologous transfusions may
be detrimental. Because of the lack of availability of ho-
mologous blood and the often favorable response of
anemic birds to parenteral crystalloid fluids and iron
dextran therapy,62 I use blood transfusion only in rap-
tors that have experienced acute, life-threatening blood
loss. Donor blood (donor PCV should be in the nor-
mal range for that species and hemoparasites not pres-
ent) is collected in a heparinized syringe and adminis-
tered as a bolus at the rate of 8 to 10 ml/kg.
Solid foods should be slowly introduced to cachectic
Small Animal/Exotics 20TH ANNIVERSARY Compendium March 1999

patients. In mammals, it has been shown that excess
calories given to starved patients often result in life-
threatening hypophosphatemia, a condition referred to
as the refeeding syndrome.63 Although not proven, it is
probable that the refeeding syndrome also occurs in
birds. One protocol is to use a 2:1 recipe of lean meat
(e.g., baby food or low-calorie dog food) mixed in a
30% solution of Nutri-Cal® (Evsco Pharmaceuticals
Affiliate of IGI, Inc., Buena, NJ) in electrolytes. 16
Three feedings daily using 20 to 30 ml/kg/BW per
feeding (based on the Kcal/L content of this formula)
may be necessary for the first few days.16 Alternatively,
the Kcal/kg daily requirement can be calculated for an
individual patient based on its metabolic rate.16,19
Nutritional secondary hyperparathyroidism15 and thi-
amine deficiency64 may occur in free-ranging raptors fed
inappropriate diets during rehabilitation efforts. Less
common nutrition-related diseases include iron defi-
ciency anemia, vitamin A deficiency, vitamin E/seleni-
um deficiency, and gout.65
ENDIU
MP
Orphaned Young
M’
of raptors.68,69 Electrocuted birds are often found dead
near or under power lines. In raptors that survive elec-
trocution, burns with electrolyte and physiologic de-
rangements are the initial concerns. Standard emergen-
cy care70 and topical treatment (1% silver sulfadiazine
cream) of burn wounds should be provided immediate-
ly. Immunosuppression and secondary bacterial infec-
tion of burn sites often result in severe infectious dis-
eases (e.g., aspergillosis, septicemia) and must be
addressed during the often protracted recovery period
of these patients.
REFERENCES
1. Johnsgard PA: Evolution, classification, and zoogeography,
in Hawks, Eagles, and Falcons of North America. Washington
DC, Smithsonian Institute, 1990, pp 3–21.
2. Blus LJ, Wiemeyer SN, Henny CJ: Organochlorine pesti-
cides, in Fairbrother AN, Locke LN, Hoff GL (eds): Nonin-
fectious Diseases of Wildlife, ed 2. Ames, IA, Iowa State Uni-
versity Press, 1996, pp 61–70.
3. O’Hara TM, Rice CD: Polychlorinated biphenyls, in Fair-
brother AN, Locke LN, Hoff GL (eds): Noninfectious Dis-
eases of Wildlife, ed 2. Ames, IA, Iowa State University Press,

20th

CO

1996, pp 71–86.
S

1 9 7
9 - 1
9 9 9 Fledgling raptors may tru- 4. Coon NC, Locke LN, Cromartie LE, et al: Causes of bald
ANNIVERSARY ly be orphaned due to aban- eagle mortality, 1960–1965. J Wildl Dis 6:72–76, 1970.
donment or they may have 5. Fix AS, Barrows SZ: Raptors rehabilitated in Iowa during

A LookBack been incorrectly presented

There have been many advances
in the veterinary care of raptors
during the past 20 years. These
developments have largely been
a result of concurrent advances
in avian medicine as a
subspecialty of veterinary
medicine as well as the
integrated approach of falconers,
rehabilitators, field biologists,
and veterinarians to address the
specific needs of raptors. The
most important of these
advances are improvements in
the captive propagation of
endangered raptor species, the
routine use of isoflurane
anesthesia, and highly refined
orthopedic techniques.
by well-meaning people. It
is important to determine
the health status of the “or-
phaned” raptor because
management will vary
based on initial evaluation.
In addition to the inherent
problems of avian pediatric
medicine, 66,67 irreversible
imprinting of a young rap-
tor to humans can occur
quickly and will result in a
nonreleasable bird. Im-
printing in raptors most
commonly occurs during a
relatively short period, gen-
erally from the second or
third week (as the chick is
opening its eyes and focus-
ing) to the sixth week of
life. It is imperative that the
chick has minimal human
contact during this time.
Electrocution
Power lines are an impor-
tant cause of electrocution
1986 and 1987: A retrospective study. J Wildl Dis 26:18–21,
1990.
6. Deem SL, Terrell SP, Forrester DJ: A retrospective study of
morbidity and mortality of raptors in Florida: 1988–1994. J
Zoo Wildl Med 29:160–164, 1998.
7. Redig PT: Health management of raptors trained for falcon-
ry. Proc Annu Assoc Avian Vet Conf:258–264, 1992.
8. Suedmeyer WK: An introduction to falconry. Proc Annu As-
soc Avian Vet Conf:164–172, 1993.
9. Duke GE: Raptor physiology, in Fowler ME (ed): Zoo and
Wild Animal Medicine, ed 2. Philadelphia, WB Saunders Co,
1986, pp 370–376.
10. Duke GE, Evanson OA, Redig PT, et al: Mechanism of pel-
let egestion in great–horned owls (Bubo virginianus). Am J
Physiol 231:1824–1829, 1976.
11. Smith BJ, Smith SA: The humeroscapular bone of the great
horned owl (Bubo virginianus) and other raptors. Anat Histol
Embryol 21:32–39, 1992.
12. Wells-Mikota SK: Wildlife laws, regulations, and policies, in
Fowler ME (ed): Zoo and Wild Animal Medicine: Current
Therapy 3. Philadelphia, WB Saunders Co, 1993, pp 3–10.
13. Chaplin SB, Mueller LR, Degeneres LA: Physiological as-
sessment of rehabilitated raptors prior to release, in Redig
PT, Cooper JE, Remple JD, Hunter DB (eds): Raptor Bio-
medicine. Minneapolis, University of Minnesota Press, 1993,
pp 167–173.
14. Clum NJ, Fitzpatrick MP, Dierenfeld ES: Nutrient content
of five species of domestic animals commonly fed to captive
raptors. J Raptor Res 31:267–272, 1997.
15. Fowler ME: Metabolic bone disease, in Fowler ME (ed): Zoo
and Wild Animal Medicine, ed 2. Philadelphia, WB Saunders
Co, 1986, pp 70–90.
16. Redig PT: Raptor nutrition and feeding, in Medical Man-
agement of Birds of Prey. St Paul, University of Minnesota

REFEEDING SYNDROME ■ HYPERPARATHYROIDISM ■ IMPRINTING

Compendium March 1999 20TH ANNIVERSARY
Press, 1993, pp 61–72.
17. Cooper JE: Nutritional diseases, including poisons, in Vet-
erinary Aspects of Captive Birds of Prey. Gloucestershire, Eng-
land, Standfast Press, 1985, pp 124–135.
18. Bennett PM, Harvey PH: Active and resting metabolism in
birds: Allometry, phylogeny and ecology. J Zool Lond 213:
327–363, 1987.
19. Quesenberry K: Avian nutritional support, in Kirk RW (ed):
Current Veterinary Therapy. XI. Small Animal Practice.
Philadelphia, WB Saunders Co, 1992, pp 1160–1163.
20. Redig PT: Guidelines for perch design, in Medical Manage-
ment of Birds of Prey. St Paul, University of Minnesota Press,
1993, pp 181–182.
21. Altman RB: Avian anesthesia, in Hoefer HL (ed): Practical
Avian Medicine: The Compendium Collection. Trenton, NJ,
Veterinary Learning Systems, 1997, pp 132–137.
22. Heard DJ: Anesthesia and analgesia, in Altman RB, Clubb
SL, Dorrestein GM, Quesenberry K (eds): Avian Medicine
and Surgery. Philadelphia, WB Saunders Co, 1997, pp 807–
827.
23. Kaufman GE: Avian emergencies, in Murtaugh RJ, Kaplan
PM (eds): Veterinary Emergency and Critical Care Medicine.
St. Louis, Mosby-Year Book, 1992, pp 453–463.
24. Murray MJ: Management of the avian trauma case. Semin
Avian Exotic Pet Med 3:200–209, 1994.
25. Ritchie BW, Otto CM, Latimer KS, et al: A technique of
intraosseous cannulation for intravenous therapy in birds.
Compend Contin Educ Pract Vet 12(1):55–59, 1990.
26. Morishita TY, Aye PP, Brooks DL: A survey of diseases of
raptorial birds. J Avian Med Surg 11:77–92, 1997.
27. Murphy CJ, Kern TJ, McKeever K, et al: Ocular lesions in
free-living raptors. JAVMA 181:1302–1304, 1982.
28. Murphy CJ: Raptor ophthalmology. Compend Contin Educ
Pract Vet 9(3):241–263, 1987.
29. Davidson M: Ocular consequences of trauma in raptors.
Semin Avian Exotic Pet Med 6:121–130, 1997.
30. Pavletic MM: Gunshot wound management. Compend Con-
tin Educ Pract Vet 18(12):1285–1299, 1996.
31. Bennett RA, Kuzma AB: Fracture management in birds. J
Zoo Wildl Med 23:5–38, 1992.
32. Orosz SE, Ensley PK, Haynes CJ: Avian Surgical Anatomy:
Thoracic and Pelvic Limbs. Philadelphia, WB Saunders Co,
1992.
33. Martin HD, Ritchie BW: Orthopedics, in Ritchie BW, Har-
rison GJ, Harrison LR (eds): Avian Medicine: Principles and
Application. Lake Worth, FL, Wingers Publishing, 1994, pp
1137–1169.
34. Bennett RA: Orthopedic surgery, in Altman RB, Clubb SL,
Dorrestein GM, Quesenberry K (eds): Avian Medicine and
Surgery. Philadelphia, WB Saunders Co, 1997, pp 733–766.
35. Bennett RA, Harrison GJ: Soft tissue surgery, in Ritchie
BW, Harrison GJ, Harrison LR (eds): Avian Medicine: Prin-
ciples and Application. Lake Worth, FL, Wingers Publishing,
1994, pp 1096–1136.
36. Altman RB: Soft tissue procedures, in Altman RB, Clubb
SL, Dorrestein GM, Quesenberry K (eds): Avian Medicine
and Surgery. Philadelphia, WB Saunders Co, 1997, pp 704–
732.
37. Murphy CJ: Ocular lesions in birds of prey, in Fowler ME
(ed): Zoo and Wild Animal Medicine: Current Therapy 3.
Philadelphia, WB Saunders Co, 1993, pp 211–221.
38. Buyukmihci NC: Lesions in the ocular posterior segment of
raptors. JAVMA 187:1121–1124, 1985.
39. Mikaelian I, Paillet I, Williams D: Comparative use of vari-
Small Animal/Exotics
ous mydriatic drugs in kestrels (Falco tinnunculus). Am J Vet
Res 55:270–272, 1994.
40. Heinz GH: Mercury poisoning in wildlife, in Fairbrother
AN, Locke LN, Hoff GL (eds): Noninfectious Diseases of
Wildlife, ed 2. Ames, IA, Iowa State University Press, 1996,
pp 118–127.
41. Bauck L, LaBonde J: Toxic diseases, in Altman RB, Clubb
SL, Dorrestein GM, Quesenberry K (eds): Avian Medicine
and Surgery. Philadelphia, WB Saunders Co, 1997, pp 604–
613.
42. Plumlee KH: Toxicant use in the zoo environment. J Zoo
Wildl Med 28:20–27, 1997.
43. Meerdink GL: Organophosphorous and carbamate insecti-
cide poisoning, in Kirk RW (ed): Current Veterinary Thera-
py. X. Small Animal Practice. Philadelphia, WB Saunders Co,
1989, pp 135–137.
44. Porter SL: Pesticide poisoning in birds of prey, in Redig PT,
Cooper JE, Remple JD, Hunter DB (eds): Raptor Bio-
medicine. Minneapolis, University of Minnesota Press, 1993,
pp 239–245.
45. Fairbrother A: Cholinesterase-inhibiting pesticides, in Fair-
brother AN, Locke LN, Hoff GL (eds): Noninfectious Dis-
eases of Wildlife, ed 2. Ames, IA, Iowa State University Press,
1996, pp 52–60.
46. Elliot JE, Langelier KM, Mineau P, et al: Poisoning of bald
eagles and red-tailed hawks by carbofuran and fensulfothion
in the Fraser Delta of British Columbia, Canada. J Wildl Dis
32:486–491, 1996.
47. Henny CJ, Kolbe EJ, Hill EF, et al: Case histories of bald
eagles and other raptors killed by organophosphorus insecti-
cides topically applied to livestock. J Wildl Dis 23:292–295,
1987.
48. White DH, Hayes LE, Bush PB: Case histories of wild birds
killed intentionally with famphur in Georgia and West Vir-
ginia. J Wildl Dis 25:184–188, 1989.
49. Allen GT, Veatch JK, Stroud RK, et al: Winter poisoning of
coyotes and raptors with furadan-laced carcass baits. J Wildl
Dis 32:385–389, 1996.
50. Stroud RK, Adrian W: Forensic investigational techniques
for wildlife law enforcement investigations, in Fairbrother
AN, Locke LN, Hoff GL (eds): Noninfectious Diseases of
Wildlife, ed 2. Ames, IA, Iowa State University Press, 1996,
pp 3–18.
51. Hill EF, Fleming WJ: Anticholinesterase poisoning of birds:
Field monitoring and diagnosis of acute poisoning. Environ
Toxicol Chem 1:27–38, 1982.
52. Jacobson E, Carpenter JW, Novilla M: Suspected lead toxi-
cosis in a bald eagle. JAVMA 171:141–144, 1977.
53. Reiser MH, Temple SA: Effects of chronic lead ingestion on
birds of prey, in Cooper JE, Greenwood AC (eds): Recent
Advances in the Study of Raptor Diseases. West Yorkshire,
England, Chiron Publications, 1981, pp 21–25.
54. Janssen DL, Oosterhuis JE, Allen JL, et al: Lead poisoning
in free-ranging California condors. JAVMA 189:1115–1117,
1986.
55. Mautino MM: Lead and zinc intoxication in zoological
medicine: A review. J Zoo Wildl Med 28:28–35, 1997.
56. Abou-Madi N, Kollias GV: Avian fluid therapy, in Kirk RW
(ed): Current Veterinary Therapy. XI. Small Animal Practice.
Philadelphia, WB Saunders Co, 1992, pp 1154–1159.
57. Morrisey JK: Avian emergency medicine and critical care, in
Hoefer HL (ed): Practical Avian Medicine: The Compendium
Collection. Trenton, NJ, Veterinary Learning Systems, 1997,
pp 53–57.
Compendium January 1999 20TH ANNIVERSARY
58. Schaer M: General principles of fluid therapy in small ani-
mal medicine. Vet Clin North Am 19(2):203–212, 1989.
59. Sedgwick CJ: Allometric scaling and emergency care: The
importance of body size, in Fowler ME (ed): Zoo and Wild
Animal Medicine: Current Therapy 3. Philadelphia, WB
Saunders Co, 1993, pp 34–37.
60. Finnegan MV, Daniel GB, Ramsay EC: Evaluation of whole
blood transfusions in domestic pigeons (Columba livia). J
Avian Med Surg 11:7–14, 1997.
61. Sandmeier P, Stauber EH, Wardrop KJ, Washizuka A: Sur-
vival of pigeon red blood cells after transfusion into selected
raptors. JAVMA 204:427–429, 1994.
62. Redig PT: Fluid therapy and acid-base balance in the criti-
cally ill avian patient. Assoc Avian Vet Proc Inter Conf Avian
Med:59–73, 1984.
63. Hardy RM, Adams LG: Hypophosphatemia, in Kirk RW
(ed): Current Veterinary Therapy. X. Small Animal Practice.
Philadelphia, WB Saunders Co, 1989, pp 43–47.
64. Ward FP: Thiamine deficiency in a peregrine falcon. JAVMA
159:599–601, 1971.
65. Murnane RD, Garner MM: Visceral gout in a rough legged
hawk (Buteo lagopus). J Wildl Dis 23:515–517, 1987.
66. Joseph V: Raptor pediatrics. Semin Avian Exotic Pet Med
2:142–151, 1993.
Small Animal/Exotics
67. Clubb SL: Psitticine pediatric husbandry and medicine, in
Altman RB, Clubb SL, Dorrestein GM, Quesenberry K
(eds): Avian Medicine and Surgery. Philadelphia, WB Saun-
ders Co, 1997, pp 73–95.
68. Cooper JE: Physical injury, in Fairbrother AN, Locke LN,
Hoff GL (eds): Noninfectious Diseases of Wildlife, ed 2. Ames,
IA, Iowa State University Press, 1996, pp 157–172.
69. Hass D: Clinical signs and treatment of large birds injured
by electrocution, in Redig PT, Cooper JE, Remple JD,
Hunter DB (eds): Raptor Biomedicine. Minneapolis, Univer-
sity of Minnesota Press, 1993, pp 180–183.
70. Redig PT: Management of medical emergencies in raptors,
in Kirk RW (ed): Current Veterinary Therapy. XI. Small Ani-
mal Practice. Philadelphia, WB Saunders Co, 1992, pp
1134–1138.
About the Author
Dr. Deem is affiliated with the Field Veterinary Program,
Wildlife Health Sciences, Wildlife Conservation Society/
Bronx Zoo, Bronx, New York. She is a Diplomate of the
American College of Zoological Medicine.