Emergency and Critical Care of Pet Birds

Vet Clin Exot Anim 10 (2007) 345–394
Emergency and Critical Care of Pet Birds

Heather Bowles, DVM, DABVP-Aviana,*,
Marla Lichtenberger, DVM, DACVECCb,
Angela Lennox, DVM, DABVP-Avianc
a
Hunt Valley Animal Hospital, 11206 York Road, Cockeysville, MD 21030, USA
b
Thousand Oaks Pet Emergency Clinic, Thousand Oaks, CA, USA
c
Avian and Exotic Animal Clinic of Indianapolis, Indianapolis, IN, USA
Most birds do not show signs of illness in the early stages of disease.
Often birds with chronic disease present as emergencies because of their abil-
ity to mask clinical signs of disease until their condition is severe. In virtually
all cases, the authors advise the receptionist to recommend the bird be
brought in for an examination. If the owner is concerned enough to call,
then the bird is likely sick and needs to be seen. Although all signs reported
by the client can be of concern, sitting at the bottom of the cage, bleeding,
respiratory distress, regurgitation, and anorexia are considered true emer-
gencies. The client should be instructed to bring the bird in a cage or suitable
alternative, (eg, box, cat carrier). The water dish should be emptied, but the
cage should not be cleaned before travel to the hospital.
This article discusses triage techniques, history, physical examination, and
diagnostic procedures. Common treatment procedures are presented, such
as catheterization, nebulization, air sac cannulation, and radiographic tech-
niques. The importance of nutrition precedes discussion on common emer-
gency presentations. The reader should be aware that shock, fluid therapy,
cardiopulmonary–cerebral resuscitation, analgesia, and anesthetic monitor-
ing techniques in birds are presented elsewhere in this issue. The clinician
must stabilize all critically ill birds (see the article by Lichtenberger in this issue).
Triage
Once the bird has arrived, it is ideal to have a trained receptionist call for
an immediate triage by an experienced technician, as prompt, accurate
treatment is vital for a favorable outcome. In cases of bleeding, seizures,
* Corresponding author.
E-mail address: [email protected] (H. Bowles).
1094-9194/07/$ - see front matter Ó 2007 Published by Elsevier Inc.

doi:10.1016/j.cvex.2007.04.001 vetexotic.theclinics.com
346 BOWLES et al
head trauma, and respiratory distress, the bird should be evaluated immedi-
ately by the veterinarian. The veterinarian should proceed immediately to
the section for treatment protocols. If the bird is depressed, weak, or sitting
at the bottom of the cage, it should be placed immediately in a warmed
incubator with oxygen. The optimum temperatures for ill birds are 85 to
90 F (29 to 30 C). Many birds will benefit from symptomatic treatment
such as oxygen supplementation, fluid therapy, broad-spectrum antibiotics
and antifungals, and nutritional support and observation for the first 2 to
8 hours in a warmed incubator before diagnostic testing is preformed.
History
Take a complete history while the bird is being stabilized in the incubator
with oxygen. History should include information such as age, sex (if known)
source of the bird, and presence of other birds in the household. Dietary
history includes types and proportions of foods offered and consumed,
and any changes in food or water consumption. Determine the length of
illness and progression of signs and symptoms. Other important informa-
tion includes exposure to trauma, toxins (plant, airborne, overheated non-
stick cookware, metal, cleansers), and other pets in the household. Inquire
about recent illness in other birds in the household. Other important
information includes changes in droppings, reproductive activity including
courtship behavior and oviposition, and other changes in behavior. Envi-
ronmental history includes information on type of caging, and whether
the bird is able to leave the cage unsupervised.
Preprinted history questionnaires are often extremely useful.
Examination
Initially the bird should be evaluated in its cage. Posture, ability to ambu-
late and perch, respiratory status, interest in the environment, and fluffing of
the feathers are assessed. The cage can be examined for regurgitated material,
blood, or other discharge. If the bird is presented in its regular cage, inspect it
for potential sources of toxins. Examine the feces for color, volume, and con-
sistency. Feces that are scant and green to black suggest anorexia. Urates are
normally white to off white, but may take up color from food dye in the feces.
Urine is normally scant and clear, but many birds display stress-related
polyurea at presentation. Frank blood may be noted either from the gastroin-
testinal (GI) or urinary tract or from hemorrhaging masses in the cloaca.
Perform a complete physical examination as the condition of the bird
allows. Work in a small room with low ceilings, closed window, and no
fans, especially if the bird is flighted. Some birds, particularly finches and
canaries, should be captured in a darkened room. Prior to restraint, have all
equipment ready in advance to minimize handling time, and attempt to deter-
mine if the bird is stable enough for examination. Death during handling
EMERGENCY AND CRITICAL CARE OF PET BIRDS 347
occurs most frequently in birds that are weak and in respiratory distress. In an
authors’ experience, other birds at risk include obese budgerigars on inappro-
priate (seed) diets. It is wise to advise owners of very ill birds that handling and
treatment may result in worsening of condition and even death.
Physical examination must be complete and thorough as in any other
species. Structures unique to birds include the crop, which is palpated for
the presence of food and/or foreign material, and the choanal slit of the oro-
pharynx, which is examined for the presence of inflammatory debris, foreign
material, and blunted papillae suggesting hypovitaminosis A. Feathers of the
rest of the body are parted carefully to examine the skin. The beak is inspected
for bleeding, symmetry, and fractures. Examination of the basilic vein and
determination of refill time is useful to evaluate perfusion status. Hydration
is assessed by skin turgor. Auscultation is challenging in birds because of rel-
atively small size, rigid lungs, and unique respiratory system. Auscultation
may reveal abnormalities in heart rate, rhythm, murmur, and abnormal
lung and/or air sac sounds. As respiratory sounds in birds are normally
minimal, the detection of crackles, wheezes, and clicks are likely abnormal.
The palpable ceolomic space is the area between the ventral keel and
pelvis. The space is normally small, and often the only normal palpable
structure may be the ventral aspect of the ventriculus. Abnormalities that
may be detected include: abdominal distension, intraceolomic fluid, palpable
mass, caudoventrally displaced ventriculus, and/or an egg [1–3]. Overall
body condition is evaluated through palpation of the pectoral muscle
mass. Muscle is reduced and the keel readily palpable in underconditioned
birds. In contrast, in overconditioned birds, the central keel bone often is
obscured. and the pectoral muscle mass takes on a plump, rounded appear-
ance. The vent and cloaca are inspected for the presence of lesions including
masses, swelling, and prolapsed tissue. The feathers surrounding the vent
normally are clean and not matted with feces or debris.
Complete neurologic examination is covered in detail in a later section in
this article. Weigh the bird in grams and observe it in the incubator at the
conclusion of the examination to determine the impact of handling on overall
condition.
In cases where complete physical examination is not recommended
because of poor patient condition, perform a rapid examination while trans-
ferring the bird from cage or carrier to the incubator. Quickly palpate the
pectoral muscle mass and ceolomic space during transfer, and observe the
bird carefully after releasing into the incubator.
Diagnostic testing
Blood work
Blood collection is preformed most commonly by venipuncture of the
right jugular vein, although the medial metatarsal and basilic vein may be
348 BOWLES et al
used in larger species. The amount of blood collected is never more than 1%
of the bird’s total blood volume. One of the authors (Lichtenberger) recom-
mends that a good rule of thumb for the critically ill bird is to collect 0.4 to
0.5 mL/100 g body weight.
Routine hematology and chemistry analysis include a complete blood cell
(CBC) count, and at a minimum aspartate aminotransferase (AST), creatine
kinase (CK), glucose, uric acid, calcium, phosphorus, albumin, and electro-
lytes. Hematology and biochemistry tests are important in the diagnosis of
infectious, metabolic, inflammatory, and some toxic diseases. A packed cell
volume evaluates the patient for the presence of anemia. A blood smear
should be evaluated for blood cell quantity and morphology, the presence
of parasites, evidence of polychromasia, and presence of anisocytosis. It
should be noted that birds have efficient mechanisms for compensation after
blood loss, and begin regeneration within 12 to 36 hours [4].
A white blood cell (WBC) count may be performed with a Neubauer-ruled
hematocytometer using the Eosinophil Unopette 5877 (Becton-Dickinson,
Cockeysville, Maryland) or by using the Natt and Herrick method. Both
methods require that samples be read in a timely fashion to prevent overstain-
ing of cells. An estimated WBC count may be performed, particularly to
corroborate results from the previous techniques or if cell quality is declining
in a sample. A differential cell count in a monolayer blood smear under 40
power is performed, and the total leukocyte count is estimated by dividing the
raw leukocyte count by the number of fields counted and multiplying this
number by 2000. Adjustments must be made in anemic patients, and counts
may not be accurate if the sample quality is poor, for example, slides with
excessive numbers of smudge cells or lacking an adequate monolayer region.
A red blood cell count per microliter of whole, anticoagulated blood, may be
performed using the Natt and Herrick method as well [5].
Heterophil morphology can give important information regarding under-
lying disease status. Although standards for evaluation of cell morphology
have not been established, many authors recommend grading heterophil
abnormalities from 1 to 4þ. Cell abnormalities include basophilic cytoplasm
and cytoplasmic granules, rounding of cytoplasmic granules, nuclear hyper-
segmentation, and cytoplasmic vacuolation. Monocytosis is commonly
present with chronic inflammatory or infectious disease. Severe leukocytosis
has been associated with chlamydiophila infection, mycobacteriosis, and as-
pergillosis, but is not always consistent. Stress alone may significantly raise
heterophil counts in an otherwise healthy bird, especially in young macaws.
Lymphocytosis typically is associated with significant immune stimulation.
Lymphocytes may exhibit reactive change (darker cytoplasm, nuclear
changes, prominent nucleoli, and cytoplasmic scalloping). These changes
have been noted both in the presence of infection and in apparently normal
birds [5].
Thrombocyte counts usually are reported as adequate or decreased.
Normal numbers range from approximately 20,000 to 50,000/uL. Clumping
of thrombocytes should be documented also. Reduced numbers may be

associated with a coagulopathy. Morphologic changes, such as blebbing
or enlargement of the cytoplasm, should be noted, and these may be associ-
ated with recruitment of cells for phagocytic defense [5].
Ancillary diagnostic tests are performed based on history, physical exam-
ination, and results of other diagnostic testing. These may include but are
not limited to: blood lead level, plasma zinc level, protein electrophoresis,
chlamydiophilia testing, and Aspergillus testing. Plasma protein electropho-
resis (EPH) is useful in detecting inflammation associated with many
diseases (eg, chlamydiophilia, aspergillosis, mycobacteriosis, ceolomitis,
liver disease, and renal disease). There is significant controversy regarding
various diagnostic tests for chlamydiophila and aspergillosis, and the reader
is referred to the literature for a more thorough discussion.
Liver function
Enzyme profiles are routinely assessed to detect liver damage. Commonly
measured enzymes include AST, ALP, CK, lactate dehydrogenase (LDH)
and GGT, but it should be kept in mind that correlation of enzyme elevation
with the true presence and severity of liver disease is often poor [6]. A recent
study reported poor correlation between liver enzyme elevation and liver
disease confirmed by means of biopsy in 30 psittacines [7].
The half-lives are 0.71 hours for LDH, 16 hours for alanine aminotrans-
ferase (ALT), and 8 hours for AST [8]. These enzymes are sensitive for liver
disease but not specific. AST sources include liver, skeletal muscle, heart,
kidney, and brain. Elevated levels are usually the result of liver or muscle
damage. Marked increases in AST (greater than four times normal) usually
indicate liver necrosis. Mild-to-moderate increases (two to four times nor-
mal) are usually the result of skeletal muscle injury. Elevation from skeletal
muscle leakage can be differentiated from liver sources by measuring CK
levels. Levels of CK will increase with skeletal muscle damage. Therefore,
a mild-to-moderate increase in AST with an increase in CK is more likely
caused by skeletal muscle injury. Marked increases in AST without
increased CK suggest severe diffuse hepatic damage; however, hepatic dam-
age and inadequate function may be present with normal levels of AST. The
plasma half-life of AST in pigeons is 7 to 9 hours [8]. Bile acid evaluation
may support the diagnosis of liver disease, but absolute confirmation, in-
cluding evaluation of type and extent of disease is only possible with liver
biopsy. LDH is not specific for liver disease, but the advantage is its very
short half-life. Prolonged LDH elevation without CK elevation suggests
that liver damage is more likely than skeletal muscle damage [6].
Serum calcium
Most laboratories report total serum calcium, which is a combination of
ionized calcium, protein-bound calcium, and complexed calcium. It is
a less precise estimate of true calcium status than ionized calcium alone.
350 BOWLES et al
Ionized calcium in normal individuals is maintained within a narrow

range, and deviations are more likely to represent true disease than do de-
viations in total serum calcium [9]. Calcium concentration may decrease
with inadequate calcium in the diet and excessive egg-laying; however cal-
cium usually is mobilized from the bone to maintain calcium blood con-
centration within normal limits. Ovulating hens often have elevated
calcium levels caused by calcium mobilization for egg production. Hens
that suffer from chronic egg laying may develop osteoporosis despite a
normal serum total calcium concentration. Other causes of hypocalcemia
include hypovitaminosis D3, hypoalbuminemia (only total calcium is af-
fected), and hypoparathyroidism [9]. Calcium concentration elevations
may occur with vitamin D toxicosis (dietary or other source) and hyper-
parathyroidism. Artifactual elevations in total serum calcium can occur
with lipemia and hyperproteinemia [9].
Phosphorus and glucose

Phosphorus levels rise along with calcium during egg formation in female
birds. In healthy individuals the calcium:phosphorus range is maintained
above one. Marked deviations in phosphorus (hyperphosphatemia and
hypophosphatemia) have been associated with renal disease in birds. In-
creased phosphorus elevations also may be associated with hyperparathy-
roidism [10]. Glucose may be the mammalian level (about 300 mg/dL).
Hypoglycemia can be seen with starvation in small or very young birds, liver
failure, neoplasia, and septicemia. Hyperglycemia is a common response to
stress and should not be mistaken for diabetes mellitus. Persistent hypergly-
cemia can indicate diabetes mellitus and pancreatitis, and indicates the need
for pancreatic biopsy [10].
Uric acid
Uric acid concentration may increase with renal disease, dehydration, or
gout. Uric acids are the main avian nitrogenous waste product and are
excreted through tubular secretion. Birds eliminate nitrogenous waste by
tubular secretion; they respond to water deprivation by decreasing overall
glomerular filtration rate (GFR), altering blood flow from reptilian-type
nephrons to mammalian-type nephrons. This gradually increases their plasma
osmolality to recover more water from the glomerular filtrate. Uric acid is
mostly unaffected by GFR until GFR is severely reduced, and urine flow is
insufficient to move the uric acid condensates through the tubules. Therefore
uric acid levels only will be elevated in severely dehydrated birds [5].
Loss of two thirds of the functional mass of the kidney is required for uric
acid increase greater than 15 mg/dL. Normal uric acid concentrations do
not guarantee that the kidneys are healthy. When uric acid is greater
than12 mg/dL, the authors recommend treatment for dehydration and
re-evaluation. Persistent uric acid elevations despite rehydration and fluid
therapy are indications for endoscopic biopsy of the kidney [11].
Hypoproteinemia
Hypoproteinemia may occur with malnutrition, chronic renal and hepatic
disease, malabsorption, or blood loss. Plasma albumin and globulin (alpha,
beta, and gamma levels) should be evaluated by serum protein EPH. An
increase in beta globulins may occur with acute inflammation or infection
(ie, nephritis, hepatitis, aspergillosis, chlamydiophila infection, mycobacter-
iosis, egg-related ceolomitis). Increase in gamma globulins is seen commonly
with chronic inflammation and infection. More work needs to be done on im-
proving the test methodology itself, and on correlation of EPH with clinical
disease. Two independent laboratories in the United States found poor cor-
relation on identical samples submitted to both laboratories [12]. Hypoalbu-
minemia is not a consistent finding in birds with renal failure [12]. This
indicates that the disease process is typically not glomerular disease (ie, tubu-
lar nephritis or interstitial nephritis), is early stages of glomerular disease, or
that birds do not lose protein with glomerular disease [11].
Bile acids
Bile acids assays are very sensitive and specific for liver disease. Normally
over 90% of bile salts are reabsorbed by enterohepatic reuptake by the liver.
Controlled studies show postprandial increases in plasma bile acids when
normal birds are tested. Increases in postprandial samples in birds with liver
disease, however, do not overlap with postprandial bile acid values in
normal birds. Therefore a single postprandial can be used to evaluate birds
with suspected liver disease. Presence or absence of a gall bladder in various
bird species does not affect measurement of bile acids. Severe elevations tend
to occur with gall bladder hyperplasia, hepatic fibrosis, and severe hepatic
lipidosis. Mild-to-moderate elevations tend to occur with mild hepatic lipi-
dosis, cholangiohepatitis, and infectious disease (ie, chlamydiosis). It should
be noted that bile acid levels may be normal in the presence of significant
liver disease [8].
Urinalysis
Urinalysis is problematic in birds because of normal mixing of urine and
feces in the cloaca and voided sample, and because of natural intestinal reab-
sorption of water from urine [12]. Therefore urinalysis must be interpreted
with care, and protein, inflammatory cells and red cells may originate from
the GI tract. Urine protein electrophoresis may be a useful test for bird with
glomerulonephritis, but no studies are available. Ureteral cannulation is pos-
sible, but this requires anesthesia and is technically difficult [11].
Evaluation of feces and crop specimens

Fecal wet mounts can reveal Giardia spp., Trichomonas spp. (crop wash),
and Macrorbabdus ornithogaster (megabacterium or avian gastric yeast).
352 BOWLES et al
Fecal cytology and Gram’s stain are commonly used screening tools, but
they have a potential for overinterpretation. In most cases, the presence
of large numbers of gram-negative bacteria, budding yeast or clostridium
spores are considered abnormal. Some authors, however, believe that these
findings in a normal bird are may be reflection of poor nutrition and/or
husbandry. An abnormal Gram’s stain in a bird with evidence of illness,
especially GI disease, may be more significant, and culture and sensitivity
are indicated. Treatment with appropriate antibiotics and/or antifungals
can be initiated pending culture results [13].
Nasal flush
Sinusitis and disease of the nares commonly causes upper respiratory dis-
ease. Birds may sneeze, pick their nares with their toenails, or appear gener-
ally ill. There may or may not be a nasal discharge. A nasal flush with sterile
saline is performed easily with physical restraint. Hold the patient with the
head lowered and beak pointed toward a sterile collection container. Infuse
sterile saline into one nare with a syringe while occluding the other nare with
a finger, then repeat on the other side. The fluid is collected in the sterile con-
tainer and used for cytology and culture. Holding the patient in this position
allows the fluid to exit through the choanal slit and leave the mouth, thereby
preventing the fluid from gaining access to the oropharynx. It may be diffi-
cult to flush the nares if there is a significant amount of material in the nasal
and sinus passages. Diagnostic testing results should be interpreted with
caution because of contamination of the sample from the oral cavity. After
collection of diagnostic samples, flushing can be repeated with medication
(antibiotics, antifungals) added to flush solution. The infraorbital sinus
may be sampled as well. Sterile saline is infused into the sinus rostral to
the orbit, aspirated and submitted for diagnostic testing. This technique pre-
vents oral contamination; however, careful restraint or anesthesia is neces-
sary, and sample sizes retrieved are limited.
Radiographs
Radiography is an integral part of avian medicine. The clinician must
have knowledge of normal avian radiographic anatomy before attempting
to interpret abnormal radiographs. Normal avian radiographs require
proper positioning and may be stressful to the conscious avian patient. It
is impossible to obtain proper positioning without anesthesia in most cases.
In the ventral–dorsal position, stretch the neck out and extend all four
limbs. Superimpose the keel over the spine. In the lateral view, stretch the
neck out. Extend the wings above the body. Stretch and separate each leg.
A common dilemma for veterinarians is that the emergency avian patient
may not appear stable enough for anesthesia and radiographs, which re-
quires careful consideration. It should be kept in mind that if the bird is
to be anesthetized, other diagnostic procedures and treatments may be

attempted including venipuncture, blood pressure, ECG, and intravenous
(IV)/intraosseous catheterization (IO) catheterization. Radiographs are
useful to identify ingested metal, GI obstruction, foreign body, presence
of an egg, organ enlargement or displacement, and fractures. The lungs
and air sacs may be evaluated for pathology also, such as changes in radio-
graphic density and masses. Oral contrast media can help evaluate the size
of the GI tract, and to identify GI tract displacement caused by the presence
of a mass or organomegaly. Care must be taken to prevent aspiration of
barium, which can occur both in the anesthetized or conscious patient.
Anesthetized birds therefore should be intubated. Other options include
horizontal beam radiography in the awake bird [14]. Barium sulfate is
administered at 2 mL/100 g BW and radiographs taken at 20 minutes, 1
hour, and 3 hours, depending on patient size and the goal of the study [14].
Ultrasound
Ultrasonography uses the transmission and reflection of sound waves to
produce an image. Sound waves cannot penetrate the gas-filled air sac
system, and this limits organ visualization in the avian patient. Because of
the small size of most birds and the limited window of accessibility, the
ultrasound transducer must have a small contact area. The cranioventral
approach to the heart and coelomic viscera is the most reliable approach
to most psittacine birds. This acoustic window is located on midline just
caudal to the sternum. A transducer frequency of 7.5 MHz or higher is rec-
ommended [15]. The bird is restrained in dorsal recumbency, with the head
and cranial coelom elevated to assist in visualization. Feathers are wetted
with a small amount of isopropyl alcohol. Acoustic coupling gel is applied
to the skin. In the normal bird, liver, heart, and active gonads (usually
the ovaries) are distinguishable. Spleen, normal kidneys, and inactive
gonads are difficult to identify. The indications for ultrasound include inves-
tigation of soft tissue masses, hepatomegaly, cardiac disease (see the article
by Lichtenberger in this issue), renomegaly, disorders of the reproductive
tract, and identification of ascites. Ultrasound guided aspirates also can
be performed [14].
Computed tomography (CT)

CT is a cross-sectional imaging modality that uses radiographs to create
a digital image or slice that is reformatted into planes of view [16]. CT is
used best for evaluating bone and air-filled structures (skull, sinuses, and
lower respiratory tract). Soft tissue resolution is inferior to MRI. The major
advantage of the CT scan is the short time required for the study; with
a typical study can be performed in 10 minutes. General anesthesia is
required.
354 BOWLES et al
MRI
MRI is performed using a strong external magnetic force to align certain
atoms within the body about a desired axis. The magnetic field then is
turned off, and the unit senses energy released as atoms returning to their
resting state [16]. A cross-sectional image is produced. MRI is used for
imaging soft tissue structures. MRI has been used to evaluate the diagnosis
and management of chronic sinusitis in psittacines [16]. General anesthesia
is required. The disadvantage of the MRI study compared with the CT scan
is the longer time required. A typical study may require 30 minutes to 1 hour.
Procedures
Intraosseous catheterization
In many cases IO catheterization is a superior choice over IV catheteriza-
tion, as the latter is often more technically difficult in terms of placement
and maintenance, especially in small birds. If the bird removes an IV cath-
eter unnoticed, significant blood loss could occur.
IO catheters can be placed in most birds in the distal ulna and in the
proximal tibiotarsus (Fig. 1). Short spinal needles (20 to 22 G 3.1 cm)
can be used in larger birds, while 22 to 25 G injection needles can be used
in smaller birds. Should the needle become occluded, appropriate-sized ster-
ilized cerclage wire can be inserted into the needle to remove the obstruction.
To place an ulnar catheter, palpate the dorsal tubercle of the distal ulna.
Pluck the feathers over this area and aseptically prepare the area for better
visualization of the landmark. Lidocaine 2% (0.2 mg/100 g diluted with
saline) is used to block the skin and periosteum over the site. Grasp the
ulna between the fingers of one hand. With the other hand, the spinal needle
is positioned over the distal ulna and aimed between the fingers holding the
Fig. 1. Intraosseous catheterization. Placement of an intraosseous catheter in proximal tibiotar-

sus of a bird.
ulna. Apply a small amount of pressure as the needle is rotated through the
cortex of the bone. Once the cortex is breached, slowly work the needle
along the medullary canal of the bone until the needle is seated in the
ulna. Use a tuberculin syringe and a small amount of heparinized saline
to test the patency of the catheter. The ulnar vein should blanch as the fluid
is injected. The IO space is not elastic (as is a vein), and so some resistance is
expected. This resistance can be minimized by using small-volume syringes
or by giving fluids by constant rate infusion. When the catheter is securely
in place, attach a male adapter plug that has been flushed with heparinized
saline. Some clinicians use injection caps or T ports. The catheter can be
secured into the ulna by placing a small piece of tape at the hub in a butterfly
fashion and suturing it to the skin. The catheter then is incorporated into
a figure- eight wing bandage to minimize movement of the wing. Wing
movement can cause the catheter to move and widen the perforation in
the bone and cause fluid leakage from this site. For IO catheter in the
proximal tibiotarsus, the cnemial crest is palpated easily at the cranial and
proximal portion of the tibiotarsus. The leg is extended and flexed at the
knee, and the area is plucked and aseptically prepared. The needle is inserted
at the cnemial crest at the insertion of the patellar ligament. There is no
vein in which to visualize blanching, so check for patency by injecting fluids,
or if necessary, confirm by obtaining radiographs of the limb in two views [2,3].
Intravenous catheterization
IV catheters can be placed using short, small-gauge catheters in the right jug-
ular, ulnar, and dorsal metatarsal veins. The jugular vein is a large vein that is
easily to catheterize, but this can be difficult to maintain in an active bird.
Many birds do not tolerate the wrapping necessary to maintain the
catheter. An IV jugular catheter can be placed in birds as small as 75 g. Usu-
ally, no feathers need to be plucked, because there is an area of apterylae over
the jugular veins. Prepare the catheterization site aseptically. The vein is
entered at the distal one-half to one-third with a 20 or 22 gauge catheter of
sufficient length to reach the thoracic inlet [2,3].
The basilic vein is visualized easily for catheterization as is passes over the
proximal ulna. Smaller catheters, such as 24 gauge, should be used for this
vein. Once the catheter is stabilized, the wing is wrapped in a figure eight
bandage to limit mobility. The dorsal metatarsal vein has the advantage
of easy visualization of the catheter after placement. The tough lizard-like
skin of the feet helps to hold the catheter firmly in place. This vein can be
used in most birds over 300 g and can be seen as it courses along the dorso-
medial aspect of the tarsometatarsus [2,3].
Nasal flush
Techniques for nasal flush are discussed under diagnostic testing.
356 BOWLES et al
Nebulization
Nebulizers are designed to convert liquids to appropriately sized aerosol
particles for inhalation. The nebulizer consists of a disposable or reusable
nebulizer and a pressurized gas (air or oxygen) source. A small volume of
medication and a larger volume of diluent are placed into the nebulizer
chamber. The aerosol particle size produced by a nebulizer is affected by the
gas flow used to power it, the volume of solution, and the construction of
the nebulizer.
Nebulization can be useful to deliver moisture or topical medications to the
mucous membranes of the respiratory system. Inhalant delivery of aerosolized
medication offers numerous theoretical benefits, including a large absorptive
surface area across a permeable membrane, a low enzyme environment poten-
tially resulting in low drug degradation, avoidance of hepatic first-pass metab-
olism, potential for high drug concentrations directly at the site of disease, and
reduced potential for systemic toxicity [17]. In veterinary medicine, the litera-
ture on inhalant therapy is extremely sparse, and what does exist focuses more
on aerosol drug delivery to horses than to small pet animal or exotic species.
There are only single published studies in conscious, unsedated cats and rats
demonstrating the ability to deliver particles to the lower airways by means
of ultrasonic nebulization [18,19]. Regardless, aerosol delivery of medication
has become popular for treatment of dogs, cats, small mammals, and birds
with respiratory disease. The administration of nebulized particles using pos-
itive-pressure ventilation through an endotracheal tube may be the most effi-
cient method for lower airway particle delivery, but this is not always practical
in a clinical setting. Nebulization also has been administered to birds in
a closed cage, induction chamber or aquarium, or by means of a face mask.
Typically, the systemic drug dose has been empirically diluted in 5 to 10 mL
of saline and delivered over a single 15- to 30-minute nebulization session.
One of the authors (Lichtenberger) has anesthetized avian patients with severe
small airway disease (eg, aerosol hypersensitivity, smoke inhalation), intu-
bated, and nebulized a bronchodilator directly into the endotracheal tube.
The most frequently used antibiotic medications for nebulization are the
aminoglycoside antibiotics, but there are no established guidelines for
administration of these drugs by this route. Amphotericin B has been
used effectively by means of nebulization for lower airway fungal disease
in rats [10]. In the experience of one of the authors, other antifungals
(itraconazole, terbinafine at 10 mg/kg twice daily diluted in 5 mL of saline)
also can be nebulized. Parental bronchodilators such as terbutaline also
have been used empirically by means of nebulization in birds with lower
airway disease. In birds, terbutaline (0.01 mg/kg) often is given initially
intramuscularly or subcutaneously while the bird is placed into an oxygen
environment, and then terbutaline (0.01 mg/kg diluted in 5 to 10 mL of
saline three times daily) is nebulized for subsequent treatment. Mucolytic
therapy with N-acetylcysteine by means of nebulization also has been
used by some clinicians to facilitate the clearance of respiratory secretions.
Because of its potential irritation to the airways, a bronchodilator should

precede therapy with N-acetylcysteine, and nebulization with this drug
should be considered with caution in small exotic animals. N-acetylcys-
teine also has been given at 150 mg/kg by mouth for the first dose
followed by 70 mg/kg by mouth three times daily for 2 to 3 days
(Lichtenberger).
Ultrasonic nebulizers generate an aerosol through ultrahigh-frequency
vibration of a piezoelectric crystal at the bottom of a liquid. The advantages
of an ultrasonic nebulizer include faster nebulization time, longer product
life, smaller particle size (3 to 10 micros), and quieter operation compared
with a jet nebulizer. The nebulizer can be connected to a cage or inhaled
directly through a mask (Fig. 2). The apparatus also can be connected to an anes-
thetized bird with an endotracheal tube. The ultrasonic nebulizer can be pur-
chased for a low cost ($150/unit); therefore it is affordable for both
veterinarians, and in special circumstances, by owners for continued home ther-
apy. Some ultrasonic nebulizers have been designed specifically for the veterinary
market (DVM Pharmaceuticals, Inc., IVAX Corp, Miami, Florida) [18,19].
Other procedures
Air sac cannulation and nutrition (gavage tube feeding and esophagos-
tomy tube placement) are discussed by Chavez and Echols in this issue.
Common diseases and syndromes

Respiratory distress
Acute respiratory distress is usually a life-threatening emergency. Every
bird presenting with respiratory distress will require immediate stabilization
Fig. 2. Nebulization technique. Nebulization using an ultrasonic nebulizer and mask.

358 BOWLES et al
in a warmed oxygenated incubator (oxygen flow at 5 L/min delivers a oxygen

concentration of 78% to 85% in most incubators. In the experience of
one of the authors (Lichtenberger), a bronchial dilator, (eg, terbutaline
0.01 mg/kg intramuscularly every 6 to 8 hours; Brethine, Novartis Pharma-
ceuticals Corporation, East Hanover, New Jersey) and an analgesic with
antianxiety properties, butorphanol (1 to 2 mg/kg intramuscularly every
2 to 3 hours; Torbutrol, Intervet Inc., Mibboro, Delaware) can be adminis-
tered to birds in respiratory distress before placement into the oxygen-
enriched incubator.
The dyspneic patient should be evaluated to determine if the disease
condition involves the upper or lower airway. Typically history, ausculta-
tion, and physical evaluation will allow the clinician to determine this
accurately. Birds also can develop significant dyspnea because of compres-
sion of the air sacs by either intraceolomic fluid or a space occupying
mass. Palpation of the abdomen often will allow the clinician to assess if
there is distension by fluid, a palpable mass, or displaced viscera.
After placing the bird in the incubator, observation of breathing pattern,
respiratory sounds, and a quick, efficient physical examination are the most
important tools for diagnosing and treating respiratory distress [20–24].
Auscultation of the lungs may not reveal subtle respiratory disease because
of the rigidity of the avian lungs. Auscultation, however, can detect abnor-
mal respiratory sounds such as wheezing or clicks and help localize them to
upper or lower airways. Auscultation also is recommended to identify heart
murmur, arrhythmia, and determine heart rate, which is frequently challeng-
ing in birds because of relatively rapid heart rates. The history and physical
examination will help the clinician localize the lesion, which will facilitate
immediate steps to stabilize the patient. The following discussion will give
an anatomical and physiological overview of the five different areas of the
respiratory system and describe history, physical examination, diagnosis,
and treatment protocols for diseases occurring in each area. Respiratory dis-
tress may be caused by an upper airway disease (sinus), large airway disease
(glottis to syrinx), small airway (primary bronchi), parenchymal disease
(lungs or air sacs), or intraceolomic disease (fluid, organ enlargement or
mass), resulting in compression of the air sacs.
Five areas of the respiratory system

Upper airway and infraorbital sinus
Anatomy and physiology
The cere is the area around the most dorsal surface of the maxillary
rhampotheca or upper beak. It may be feathered or unfeathered in various
species of psittacine birds. In adult male budgerigars, the cere is usually blue;
in adult females, it is usually brownish-pink. In each species, it has a charac-
teristic size and shape.
The nares or nostrils are located dorsally within the area of the cere in psit-
tacine birds. The openings may be shaped abnormally as a result of chronic
upper respiratory infection or trauma and should be noted on the physical ex-
amination. Air moves through the nares into the nasal cavity. In psittacines
and many other pet birds, a rounded, keratinized structure called the opercu-
lum is found in the rostral-most extent of the nasal cavity. It acts as a baffle to
deflect and prevent inhalation of foreign material [25].
The nasal cavity in most species is divided by a nasal septum. Within the
lateral walls of the cavity are highly vascularized nasal conchae. Most birds
have three conchae: the rostral, middle, and caudal nasal conchae. The mid-
dle nasal concha is the largest of the three. A clinically important anatomic
feature is the relationship of this concha to the openings of the infraorbital
sinus, the only true paranasal sinus of birds. This sinus opens dorsally into
the middle and caudal nasal conchae. The caudal nasal concha drains only
into the nasal cavity by its dorsal opening into the infraorbital sinus. As a re-
sult, the only passageway for drainage of mucopurulent material in the in-
fraorbital sinus is the caudal nasal concha up through the dorsal opening,
or over the middle nasal concha into the nasal cavity [25].
The infraorbital sinus is located ventromedial to the orbit and has numer-
ous diverticuli. A rostral diverticulum extends into the maxillary rostrum or
bill; a preorbital diverticulum lies rostral to the orbit. A postorbital divertic-
ulum may be subdivided to surround the opening of the ear, and a mandib-
ular diverticulum extends into the mandibulary rostrum. In addition to its
communication with the nasal conchae, the infraorbital sinus also commu-
nicates with the cervicocephalic air sac at its caudal-most extent. Knowledge
of the relationship of this sinus and air sac with the bones of the skull is
important during examination of the upper respiratory system and during
irrigation and surgical drainage procedures [25].
Sinusitis history
The owner often will describe sneezing, picking the nares with their toe-
nails, nasal discharge, redness of the sinus area, and/or ocular discharge,
and some birds will rub their beak on the perch. In some cases, nasal dis-
charge is removed rapidly by the bird, and the only evidence is brownish dis-
coloration of the feathers above the nares.
Pattern of breathing, respiratory sounds, and physical examination

There will be a soft audible breathing sound localized to the nasal cavity,
with open-mouth breathing only with complete, bilateral nasal and/or sinus
obstruction. There will be an increased respiratory rate but usually without
an increased effort.
Etiology
Causes include infraorbital infection (bacterial, fungal, chlamydiophila),
foreign body, neoplasia, abscess, granuloma, fibrinous plug [26], and avian
360 BOWLES et al
pox [27,28]. Squamous metaplasia from nutritional hypovitaminosis A may

affect the epithelium lining the nasal and sinus passages, facilitating opportu-
nistic infection as well. Extension of an infection or inflammation of the nares
into the sinus may cause redness and swelling of the peri-orbital area. The signs
may be limited to the upper respiratory tract or may involve the lower respi-
ratory tract.
Diagnostic tests
A nasal flush or infraorbital sinus aspiration and culture and sensitivity
of the fluid are recommended. Endoscopy of the choanal area and biopsy
of any lesions are the next diagnostic procedures that would be used to
diagnose cases that are nonresponsive to initial treatment. Radiographs
and CT or MRI scans of sinuses may be useful [15].
Treatment
Many times a nasal flush will help remove mucous and discharge so that
the bird can breathe easier. Initial cytology of the fluid can help the clinician
decide on treatment (antibiotics, antifungals) pending cultures and sensitiv-
ities. Nasal antibiotic drops (or ophthalmic drops) and therapeutic nasal
flushes with antibiotic solutions may be used for minor infections and sys-
temic antibiotics for more severe disease.
Large airway (glottis, trachea to the syrinx)

The larynx is composed of four almost ossified cartilages with an overly-
ing mucosa or laryngeal mound. The larynx is not involved in sound
production in birds. The rima glottis represents the laryngeal opening into
the trachea and is not covered by an epiglottis as it is in mammals. The
rima glottis and trachea are larger in diameter on a per weight basis than
they are in mammals. This principle provides one reason why it is easier
to intubate birds than mammals. This increased diameter directly reflects
one physiologic adaptation of birdsdthe use of their beaks for the manip-
ulation of objects. The increased length of the trachea is part of an adapta-
tion in birds whereby the increased length of their necks allows use of their
beak to manipulate objects. The increase in length causes an increased air
resistance, however. A wider rima glottis, and a wider trachea, are necessary
to reduce this resistance. To compensate for the wider and longer trachea
and its corresponding increase in dead space, the respiratory rate of birds
is less than that of mammals, with a larger tidal volume. These anatomic
and physiologic differences are important when selecting endotracheal tubes
for anesthetic procedures. In addition, the tracheal rings of birds are
complete. They are shaped like a signet ring and overlap to form a more
rigid trachea than that of a comparably sized mammal. These two facts
are important to reduce the possibility of tracheal kinking when moving
the neck. Overinflation of cuffed endotracheal tubes is potentially easier in a

bird because of the less expansive nature of the trachea, and this can lead to
mucosal edema and difficulty breathing. Whenever possible, uncuffed endo-
tracheal tubes should be used [29].
The trachea often bifurcates immediately after entering the thoracic inlet.
At this bifurcation is the syrinx, which represents the voice box of birds. The
syrinx is highly variable among species but represents numerous cartilages,
which may be ossified, and syringeal muscles and membranes. Most
syringeal muscles are external to the tracheal birfurcation. Depending on
the species, birds also may have internal syringeal muscles within the space
of the trachea and/or bronchi. This narrowed internal diameter of the syrinx
is a common site for tracheal granulomas and foreign bodies [29].
History
Owners may report a voice change and/or intermittent respiratory stridor
increasing in intensity with time. Birds may present in respiratory distress, in
some cases with no previous clinical signs.
The bird may have demonstrated a change in voice or intermittent respi-
ratory stridor noise that has increased in intensity over weeks and presents
with respiratory distress. Some birds present with sudden onset of respira-
tory distress with no previous clinical signs.

There is loud inspiratory stridor and often an increased rate and effort
with open-mouth breathing. The bird may have no other abnormal physical
examination findings. In cases of near-complete obstruction, the bird may
present in extreme dyspnea, gasping for air. If there is a complete obstruc-
tion, the bird will present gasping for air and eventually will fall over and go
into respiratory arrest.
Etiology. The most common cause of large airway obstruction is foreign

body inhalation, in particular seed hulls in smaller birds. Other causes of
obstruction include Aspergillus granuloma (especially African gray parrots),
and tracheal trauma, including fibrinous stenosis secondary to recent endo-
tracheal intubation [29].
Diagnostic tests
Radiographs, blood work, endotracheal wash, and endoscopy can help
diagnose the cause of airway obstruction. Foreign bodies rostral to the
syrinx often can be visualized by means of transillumination of the trachea.
Treatment
Large airway obstruction requires rapid anesthetic induction with
sevoflurane/isoflurane anesthesia and rapid intubation and ventilation
362 BOWLES et al
with 100% oxygen. It should be noted that birds in extreme respiratory

distress often breathe much easier under general anesthesia, likely because
of reduction of fear and stress associated with dyspnea. Emergency air sac
cannulation is performed (see article by Chavez and Echols in this issue).
The cannula remains in place until the obstruction is relieved or removed
medically or with surgery. Successful relief of airway obstruction can be
tested by manually occluding the air sac cannula for several minutes while
observing respirations. One of the authors (Lichtenberger) has maintained
air sac tubes in place for 2 days to up to 5 weeks.
In larger birds, endoscopy can occasionally be used to successfully remove
an obstruction. In some cases, a flexible feeding tube or catheter can be used to
aspirate foreign material out of the trachea by using a syringe and applying
negative pressure. Foreign material located rostral to the thoracic inlet can
be flushed out of the trachea and into the mouth by inserting a needle through
the trachea just below the foreign material and carefully introducing air or sa-
line while holding the bird in an upside down position.
Surgical approaches to the trachea and syrinx have been described [20].
Small airway
The mainstem or primary bronchi represent the continuation of the
syrinx. Each perforates the septal surface of the lung and continues into
the lung parenchyma as the intrapulmonary primary bronchus. The portion
of the bronchus is long as it continues to the caudal extremity of the lung. Its
diameter is variable among species but is widest at its entrance into the lung
tissue and then tapers progressively. The epithelium of the primary
bronchus is pseudostratified with goblet cells, and there are areas with ridges
carrying cilia. There are four groups of secondary bronchi that arise from
the primary bronchus. Their anatomy are described with the description
of the lung parenchyma [29].
History
History may include recent exposure to airborne toxins, including
aerosols, smoke, or fumes from overheated nonstick cookware. Blue and
gold macaws (Ara ararauna) may present with history of exposure to cock-
atoo dander.

Birds present in variable stages of respiratory distress, often severe. Many
present with a soft expiratory wheeze. Stress and handling often exacerbate
clinical signs.
Etiology. Small airway disease includes exposure to inhalant respiratory

irritants and toxins including overheated polytetrafluoroethylene or similar
compounds in nonstick cookware or newly installed furnaces, smoke, aero-

sols, candles, or other potential airborne toxins [21,22]. A hypersensitivity
syndrome has been identified in blue and gold macaws raised in close
proximity cockatoos [25]. Infectious pneumonia (bacterial, fungal) is not un-
common in pet birds.
Diagnostic tests
Stabilize the bird for 12 to 24 hours with bronchodilators and oxygen
before performing diagnostic tests. There are no specific tests for airborne
toxins or allergic syndrome of blue and gold macaws. Diagnostic tests in-
clude complete blood count, serum chemistries, radiographs, endoscopy, as-
pergillus serology, and PCR. While these diagnostics are often
unremarkable in cases of inhalant toxins, leukocytosis, polycythemia, in-
creased lung and/or air sac density, granuloma, hyperinflation of air sacs
may be evident in cases of infectious disease and hypersensitivity.
Treatment
The most effective bronchodilators are pharmaceutical agents that stim-
ulate b-adrenergic receptors in bronchial smooth muscle and promote
smooth muscle relaxation. For this reason they have become an authors’
first line of treatment for bronchoconstriction causing acute respiratory
distress. These b-receptor agonists are most effective and least toxic when
they are given as an aerosol that is inhaled. b-agonists, such as terbutaline
can be given intramuscularly in birds (0.01 mg/kg every 6 to 8 hours)
initially for immediate effect (improvement seen within 5 minutes) and
then continued by nebulization for 24 to 48 hours (see nebulization in pro-
cedures in this article). A sedative such as butorphanol can be used to reduce
fear and anxiety associated with respiratory distress. Prior to beginning
diagnostic testing or more invasive treatment, test the bird by turning off
the oxygen and observe the breathing pattern. If the bird is able to breath
normally at rest, test the bird’s ability to withstand more aggressive han-
dling. At this point, it is likely the bird can be anesthetized for radiographs
and blood work to rule out other disease components.
Birds that improve with therapy and are stable can be sent home on oral
terbutaline for 3 to 4 days. At-home nebulization may be beneficial in some
cases. Advise the owner to remove the source of the aerosol toxin.
If no improvement is seen within 24 hours of therapy, one of the authors
(Lichtenberger) places the bird under inhalant anesthesia and intubates.
Tracheal and ceolomic endoscopy with biopsy as indicated is performed
to help identify the severity of the disease. In the author’s experience, smoke
or Teflon toxins can cause the most significant damage to not only the
small airways, but also to the lungs. Nonsteroidal anti-inflammatory drugs
(NSAIDS) can be used if inflammation of the trachea is severe. The bird is
nebulized (see nebulization methods) with terbutaline (0.01 mg/kg) and then
followed in 5 minutes with acetylcysteine 100 mg/mL (Mucomyst, Bristol)
364 BOWLES et al
nebulization (10 mL in 4 mL saline) by means of the endotracheal tube. This

may be repeated twice a day until there is improvement. Broad spectrum an-
tibiotics and/or antifungals should be initiated in those patients with evi-
dence of infectious disease.
Coelomic cavity disease (mass, fluid, or organomegaly)

The coelomic cavities of birds are similar between species, and in general
there are 16 distinct and separate cavities in the adult bird. Eight of the
cavities are air sacs, and the remaining eight are cavities of the coelom
proper, with five as peritoneal cavities, and the remaining three represented
in mammals as well. The mammalian cavities include: the right and left
pleural cavities and the pericardial cavity. The five peritoneal cavities of
birds include the left and right ventral hepatic peritoneal cavities, the left
and right dorsal hepatic cavities, and the intestinal peritoneal cavity [25].
History
There is often no prior history, and many birds will present with acute
respiratory distress. In case of a large egg compressing the air sacs or egg
ceolomitis, there may be a history of egg laying. Some birds may present
with vague history of decreased appetite and lethargy before presentation.

The bird will have increased respiratory rate and effort, which increases
with stress and handling. There are usually no abnormal respiratory sounds.
In many cases, the ceolomic space (space between the ventral keel and
pelvis) is wider than normal, and there may be a palpable mass or fluid.
Etiology
Any ceolomic mass or disease producing organ enlargement or fluid
can cause ceolomic distention. Common causes of coelomic distension are
fluid accumulation,heart disease, hypoalbuminemia, liver disease, egg-related
ceolomitis [30], or presence of a mass (neoplasia, abscess, egg).
Diagnostic tests and treatment

Ascites. Ascites resulting in coelomic distension and respiratory distress
requires immediate coelomocentesis. Coelomocentesis may be performed
on the right lateral coelom just cranial to the cloaca or on the ventral mid-
line. Use a 25 to 22 gauge needle and 12 mL syringe (Fig. 3). Often, ultra-
sound can help guide coelomocentesis if the fluid is located within a specific
loculated space and difficult to aspirate.
Save any fluid recovered for culture/sensitivity and cytology. Transudate
is characterized by a clear to pale-yellow color, with a low specific gravity
(!1.020), low protein (1 g/dL) and a low cellularity. The most common
Fig. 3. Coelomocentesis. Removal of fluid within the coelom of a bird using a syringe and
22-gauge needle.
causes of a transudate are liver failure (eg, cirrhosis) or heart failure.

Exudate is characterized by a high specific gravity (O1.020), a high protein
content (O3 g/dL) and presence of inflammatory cells and mesothelial cells.
Cytology of the septic fluid may show a large number of white cells with in-
tracellular bacteria. One of the authors (Lichtenberger) uses comparison of
ceolomic fluid and serum glucose to differentiate septic ceolomitis from non-
septic [31]. In cases of septic ceolomitis, ceolomic fluid glucose is usually
lower than serum glucose. Turbid yellow, green or brown yolk-like fluid,
or inspissated yolk material in the coelomic cavity is indicative of ectopic
ovulation or a ruptured oviduct. Cytology reveals yolk material and fat
particles. Small–to–moderate amounts of free yolk in the abdomen may
be absorbed by the body, and associated inflammation is treated with
NSAIDs. The presence of ceoloc bacteria indicates antibiotic therapy is
necessary. Ectopic eggs and large amount of celomic yolk usually require
exploratory surgery, removal, and often salpingohysterectomy. More
information on treatment of reproductive-related disease is presented here.
Ceolomic neoplasia often produces fluid containing blood and occasion-
ally exfoliated neoplastic cells on cytology. Abdominal ultrasound is
performed to identify presence of an abdominal mass. A 22 gauge needle
can be used for ultrasound-guided aspiration of the mass. Confirmation
of and identification of ceolomic masses are also possible with endoscopy
and/or exploratory surgery. Ideally, a coagulation profile should be per-
formed prior to fine needle aspirate or surgery.
Careful auscultation is indicated for a heart murmur, gallop, or other ar-
rhythmia, or crackles suggestive of cardiogenic edema. If heart failure is sus-
pected, administer furosemide (2 to 4 mg/kg IV) and nitroglycerine ointment
on the tongue and allow the bird to stabilize before further diagnostics. If
there is ceolomic effusion, coelomocentesis is performed. A cardiac workup
366 BOWLES et al
will require blood pressure measurements, radiographs, and an echocardiog-

raphy. If there is significant coelomic fluid present secondary to heart dis-
ease, coelomocentesis should be performed (see section on coelomic
enlargement in respiratory distress). There have been no reports of cardiac
failure and documented hypertension (hypertension is discussed as a separate
topic). The most common heart problems reported in psittacine birds are
right-sided congestive heart failure with ascites and hydropericardium
[15]. Pericardiocentesis is recommended when hydropericardium is present.
Left-sided heart failure is less common in psittacines reported thus far. Re-
ports of thickened mitral valve and left and right side failure have been re-
ported [15]. Heart medications commonly used are enalapril at 2.5 mg/kg
BID, and furosemide, 0.15-2.0 mg/kg PO, IM SID-BID [15]. The author
(Lichtenberger) prefers benazepril at 0.5 mg/kg PO BID. If contractility
is poor and/or dilated cardiomyopathy is identified on echocardiogram,
digoxin has been recommended at 0.02-0.05 mg/kg BID [15]. No clinical
studies on the toxicity of any cardiac drugs have been performed in birds.
Parenchymal disease (lungs and/or air sacs)

The lungs are paired and attached firmly to the ribs and dorsal body wall.
They appear spongy on radiographs and are visualized best using a lateral
view. The mainstem bronchi divide into secondary bronchi. These bronchi
subsequently divide into parabronchi. All parabronchi anastomose freely
with other parabronchi and have expansions within their walls, called atria,
which allow gas exchange. Parabronchi maintain a constant mean diameter
within a species [25,32].
The mediodorsal and medioventral secondary bronchi connect to form
a functional unit. These bronchi terminate at the cranial pulmonary air sacs
and form the basis of the paleopulmonic respiratory system. The parabronchi
of the lateroventral secondary bronchi connect with the laterodorsal second-
ary bronchi, and they in turn are connected to the mediodorsal secondary
bronchi. The cranial pulmonary air sacs are expandable sacs that are con-
nected to the lungs by these bronchial arrangements and include the cervical,
clavicular, and cranial thoracic air sacs. The lateroventral bronchi are con-
nected with the caudal pulmonary air sacs of the lungs. These caudal air
sacs are the caudal thoracic and abdominal air sac. This latter arrangement
represents the neopulmonic respiratory system. Air sacs, in general, are similar
histologically to a peritoneum, with squamous to columnar epithelium, a base-
ment membrane, and an underlying connective tissue support. Only in the area
immediately surrounding an opening of a parabronchus does the tissue change
to ciliated columnar epithelium. The paleopulmonic and neopulmonic sys-
tems are defined best physiologically rather than anatomically [32].
Birds do not have a diaphragm and therefore rely on changes in pressure
between their air sacs relative to the atmospheric pressure to move air
through a nonexpandable lung. The pressure changes within the air sacs are
the result of volume changes in the thoracoabdominal cavity. On inspira-
tion, the ribs move cranioventrally, thereby increasing the thoracoabdomi-
nal space. This results in a lowering of the pressure in the air sacs. On
expiration, the ribs move caudodorsally, thereby reducing the space in the
chest and increasing the pressure in the air sacs. Expiration is an active
process requiring skeletal muscle contraction. For this reason, it is extremely
important during restraint that the sternum can move freely, or the bird may
suffocate. It also should be noted that ventilation of the apneic bird can be
accomplished by gently compressing the sternum and allowing it to recoil
into normal resting position [32].
Gas exchange occurs in the walls of the parabronchi, the atria, and more
importantly in the air capillaries, which are the avian equivalent of alveoli.
The blood–gas barrier of birds is similar to that of mammals in that it
consists of an endothelial capillary cell, a common basal lamina, and an
air capillary epithelium of squamous cells. The difference is that the
blood–gas barrier is much thinner in birds than in mammals. The diameter
of the air capillaries of birds is much smaller than that of a mammalian al-
veolus, allowing for a much larger number of air capillaries in a given space
when compared with mammals [32].
Because of the unidirectional continuous flow of air of the paleopulmonic
system, birds are more efficient than mammals in capturing oxygen (O2) and
removing carbon dioxide (CO2). The nonoxygenated blood enters at an
approximately 90 angle from the parabronchus. This cross-current gas
exchange enhances the ability to oxygenate the blood [32].
The epithelial cells of the lung act as fixed macrophages and transfer
engulfed material to interstitial macrophages. Air that enters the caudal air
sacs is filtered to a lesser degree than air in the cranial air sacs, making the
caudal air sacs more susceptible to disease [25,32].
History
There is usually a history of not doing well, lethargy, and anorexia. These
birds are usually sick with weight loss caused by the chronic disease process.
Pattern of breathing, respiratory sounds and physical examination

Birds often exhibit signs of increased respiratory rate and/or effort and
are in general poor body condition. There are generally no respiratory
sounds.
Etiology
Causes of parenchymal disease include: cardiogenic pulmonary edema
(discussed in previous section on coelomic diseases), smoke inhalation,
aspiration pneumonia, aspergillosis, chlamydophilosis, gram-negative bacte-
ria, poxvirus, Pacheco’s disease, reovirus, encephalitozoonosis [30], and
neoplasia [31].
368 BOWLES et al
Diagnostics
Radiographs and an echocardiogram are performed to rule out cardiac
disease and evaluate the lungs and air sacs. An endotracheal wash, culture,
and sensitivity are useful in cases of bacterial infection. A chlamydiophila
test should be performed. Ceolomic endoscopy with biopsy is useful to de-
tect neoplasia and disease processes producing distinct lesions or granulo-
mas. Complete blood count, serum chemistries, and aspergillus serology
and PCR are also useful diagnostic tests.
Treatment
Parenchymal disease may benefit from use of parental or nebulization of
bronchodilators and antibiotics. An air sac tube may improve respiration
partially in birds with small airway and primary lung.
Birds with a history of regurgitation or vomiting and possible aspiration
pneumonia may benefit from broad-spectrum antibiotics (eg, enrofloxacin,
cephalosporins, trimethoprim sulfadiazine) and bronchodilators.
Birds suspected of aspergillosis (leukocytosis and pulmonary nodules)
can be treated with terbinafine hydrochloride (Lamisil) or itraconazole at
10 to 15 mg/kg twice daily for 4 weeks. Itraconazole should be used with
caution in African gray parrots.
Birds suspected of psittacosis (leukocytosis, clinical signs varying from
chronic unthriftiness to acute anorexia, diarrhea and respiratory distress,
and lime green feces) should be treated with drugs inhibiting the growth
of Chlamydiophila, such as doxycycline, macrolides, chloramphenicol,
and/or fluoroquinolones). Diagnosis of psittacosis is problematic in avian
species. There is no gold standard that can be used to unequivocally deter-
mine if a particular test is accurate. One author recommends the use of two
tests run simultaneously (eg, serology antibody test and a PCR test) to
lessen chances of false-positive and false-positive results. Treat with doxycy-
cline for 6 weeks. Many protocols are recommended (see psittacosis treat-
ment later in this article under GI disease). There is no treatment for viral
infections and many birds die within a short time.
Trauma
Traumatic injuries and fractures occur commonly in the avian pet bird
and control of hemorrhage, oxygen and heat support, analgesics, and pa-
rental antibiotics are the initial treatment protocol for all birds with
injuries.
Most common injuries are lacerations, bite wounds, self-mutilation, ther-
mal wounds, or fractures. Lacerations and abrasions in birds are caused
commonly by enclosure wires, inappropriate toys, collision during flight,
other birds, or household pets. Birds sustaining bite wounds from dogs,
cats, or other birds are encountered frequently. Injuries from metal leg
bands are also common. Open-style steel bands may cause problems if
the band gap is large enough to allow the bird to get hung up on the cage
wire. Inappropriately sized bands may cause soft tissue swelling and vascu-
lar compromise to the distal leg and toes. Feather, toenail, and beak injuries
can cause significant hemorrhage. Self-mutilation behavior may cause ex-
tensive soft tissue wound injuries. Thermal injuries most commonly occur
in the crop of neonates fed improperly heated hand-feeding formula, in
most cases heated in the microwave without proper mixing. Accidental
burns may occur when birds come in contact with hot liquids, hot surfaces,
or electrical wires. Fractures should be splinted to prevent further compli-
cation as soon as the bird’s condition is stable. Simple bandaging techniques
may be used to provide adequate stability until definite treatment is possible
[3].
Treatment protocols
General emergency and supportive care
External hemorrhage must be stopped immediately. Birds with broken blood
feathers often present as an emergency. The developing feather contains
a rich blood supply, which retracts when the feather is mature. This shaft
can bleed when fractured, especially if the feather is large. Pressure at the
base of the follicle often will stop the bleeding. In some cases, larger feathers
with fractured shafts must be removed. This is accomplished by grasping the
feather at its base with a hemostat, and extracting the feather from the
follicle. In the case of large primary wing feathers (remiges), it is important
to support the bones of the wing during extraction to prevent fractures.
Occasionally the follicle will continue bleeding, but this usually can be
controlled with digital pressure or fine absorbable suture. Hemostatic agents
such as silver nitrate may damage or destroy the feather follicle, resulting in
feather loss or growth of abnormal feathers.
Excessive hemorrhage also may occur following nail or beak injury.
Hemostatic agents or a hand-held cautery unit may be used to stop bleeding
from the nail tip. It is difficult to stop bleeding of the beak in a conscious,
struggling bird; therefore the authors recommend inhalant anesthesia. The
tip of the beak can be cauterized with a hand-held or electric cautery unit.
Hemostatic agents such as silver nitrate can be used also, but care should
be taken to use these products sparingly to avoid ingestion after recovery
from anesthesia.
Wounds and open fractures

Wounds and open fractures are commonly treated with beta-lactams
(eg, piperacillin 100 to 200 mg/kg intramuscularly, IV every 6 to 8 hours),
trimethoprim-sulpha, or fluoroquinolones [33].
Analgesics
Administration of analgesics is necessary in birds that have experienced
a fracture or soft tissue trauma. Studies in pigeons have demonstrated
370 BOWLES et al
that they have more kappa opioid receptors in the forebrain than mu opioid
receptors. This may explain why birds do not respond to mu agonists, such
as morphine, fentanyl, and buprenorphine, in the same manner as mam-
mals. Butorphanol has been shown as a useful analgesic is birds. Post-
traumatic administration of NSAIDs may decrease soft tissue sensitization
and may reduce the dose of opioid drug required. NSAIDs such as melox-
icam, ketoprofen, and carprofen (Metacam,) at 0.5 mg/kg intramuscularly
can be used for pain relief, when the bird is well perfused, and kidney func-
tion is normal [34,35].
Lidocaine can be used safely in birds at doses below 2 mg/kg. When giv-
ing 1 to 2 mg/kg to small birds, the commercially available concentration of
lidocaine should be diluted at least 1:10. Lidocaine can be mixed with bupi-
vicaine 0.5% (1 mg/kg). This mixed dose can be injected intramuscularly or
infiltrated locally at the surgery or wound site [35].
Punctures and small contaminated wounds can be left open to drain

Large lacerations treated within a few hours are flushed with sterile saline
solution and sutured partially closed. Older wounds should be cleaned, de-
brided, and bandaged twice daily, then closed as needed after the infection is
minimized. Alternatively, 50% dextrose, sugar, and honey have been advo-
cated as a wound dressing to treat large contaminated wounds. Sugar,
honey, and 50% dextrose are readily available inexpensive materials that
when applied to a wound are considered bactericidal because of their high
osmolality. Additionally, they provide the wound with a local nutrient
source to promote granulation tissue. This high osmolality is also responsi-
ble for moving edematous fluid out and drawing macrophages into the
wound. The wound is debrided and flushed with saline. The sugar or honey
is applied to the wound, and it is covered by a wet-to-dry bandage.
Topical wound treatments are products that are applied to wounds to
stimulate wound healing. They promote wound healing by stimulating
production of cytokines or growth factors within the wound. Topical prep-
arations that have shown some effect on wound healing include acemannan,
D-glucose polysaccharide, hydrolyzed bovine collagen, porcine collagen
products, and tripeptide-copper complex [36,37]. Topically applied platelet
derived growth factor (Regranex) has been shown to improve healing in
chronic diabetic foot ulcers in people. It has also proven effective in healing
a large defect in a fish suffering from lateral line disease (B. Whitaker, per-
sonal communication, 2004). Sugar and honey have been advocated as
a wound dressing to treat large contaminated wounds. Sugar and honey
are readily available inexpensive materials that when applied to a wound
is considered bactericidal due to the high osmolality and provides the wound
with a local nutrient source to promote granulation tissue. This high osmo-
lality is also responsible for moving edematous fluid out and drawing mac-
rophages into the wound.
Treatment for self-mutilation

Treatment for self-mutilation may include temporary collaring while
treating the underlying cause, which may be pathological or behavioral.
The area should be cultured and cleaned, treated with silver sulfadiazine
cream, and bandaged with a moisture-permeable dressing if possible.
Scaly mites
Scaly mites (knemidoptes pilae) cause hyperkeratotic lesions on the feet
and base of the beak in parakeets. The birds are brought in for treatment
for rubbing their beak on the perch and/or for growths/wounds on the
beak and feet. The mites are rarely seen on microscopic examination. Treat-
ment involves placing 0.2 mg/kg ivermectin in a tuberculin syringe and
dropping it over the right jugular vein. This is repeated in 2 to 3 weeks [33].
External burn injuries

External burn injuries are treated with cold compresses for a period of 20
to 30 minutes. Superficial burns should be cleansed gently using sterile
saline. Partial or full-thickness burns should be cleansed gently and debrided
daily and treated topically with a water-soluble antibiotic dressing as silver
sulfadiazine (Silvadine cream 1%). This procedure is very painful, and it
should be done under general anesthesia with appropriate analgesia.
Surgical repair of crop fistulas is performed only after complete granula-
tion of the wound edges has occurred with clear demarcation between
healthy and diseased tissue. Attempting to suture the necrotic infected tissue
may result in dehiscence. The bird can continue eating or be tube-fed
throughout this time. The bird should be started on antibiotics. Monitor
until the wound contracts, and a fistula appears (7 to 14 days). When the
wound heals and fistula forms, the scab is removed and necrotic skin and
crop are excised surgically. Surgery before wound contraction is often un-
successful because of the difficulty in distinguishing apparently healthy tis-
sue from tissue that will ultimately necrose. Surgical glue can help seal the
wound to prevent leakage of food until surgery is preformed. Surgical repair
to cover affected areas may include techniques such as advancement flaps
and skin grafts depending upon the location and extent of skin loss [38].
Fractures
Fractures are usually not life-threatening, and they may be supported
with external coaptation depending upon the location. The patient should
be evaluated thoroughly for any open or closed fracture and soft tissue
trauma. If an open fracture is present, exposed tissues are treated with irri-
gation, debridement, and bandaging. The bone segment(s) should be pro-
tected by replacing it(them) under the skin or with appropriate
372 BOWLES et al
bandaging. A figure-eight bandage is applied to stabilize fractures of the ra-

dius, ulna, or carpometacarpus (see surgery and endoscopy article in this is-
sue, by Chavez and Echols). The wing is bandaged in a figure eight fashion
and to the body for fractures of the humerus. Fractures distal to the knee
are stabilized with a lateral splint, or in smaller species (less than 100 g
body weight), a tape splint may be applied (see surgery and endoscopy ar-
ticle by Chavez and Echols in this issue). Femoral fractures may be stabi-
lized using a spica splint or an off weight-bearing sling until surgery is
possible (see surgery and endoscopy article by Chavez and Echols in this is-
sue). If the patient is stable enough to perform immediate surgery, appropri-
ate surgical repair may be performed after radiographs are performed.
Immediate fracture repair offers the advantage of early stabilization and
less postfracture muscle contracture, which facilitates surgical repair.
Closed reduction and repair have been associated with significantly less
soft tissue, nerve, and vascular damage [30,31,39–41].
Reproductive-related emergencies
Chronic egg laying
Chronic egg laying occurs when a hen lays repeated clutches or larger
than normal clutch size without regard to the presence of a mate or accurate
breeding season. This process often physically exhausts the reproductive
tract and is a serious metabolic drain, particularly on calcium stores, all
of which may predispose the hen to egg binding, yolk peritonitis, and
osteoporosis. Commonly affected species include cockatiels, finches, and
lovebirds; however, any species may be affected. Diagnosis of chronic egg
laying is based on history and physical examination. There typically is a his-
tory of the hen laying large numbers of eggs with or without a pause period
in between clutches. A thorough history of the home environment will often
reveal several reproductive stimuli and a mate relationship with one or more
members of the household or an inanimate object. Physical examination
may reveal normal findings, a palpable egg in the coelom, or other second-
ary disease conditions such as a pathologic fracture secondary to osteoporo-
sis. Serum chemistries may reveal hypercalcemia, hypercholesterolemia, and
hyperglobulinemia supportive of an ovulating hen. There may be a hypocal-
cemia present if the hen’s calcium stores are depleted, and particularly if she
is consuming a low-calcium diet such as seed [42–44]. The owner should
be instructed on methods to stop the chronic egg laying as decreasing the
light cycle, removing the male bird, and/or changing location of the cage.
Elimination of an inappropriate sexual bond and restoration of proper
social bond often requires behavioral modification technique and coopera-
tion from all members of the household. Other options include the use of
drugs such as leuprolide acetate (Lupron, TAP Pharmaceuticals) or salpin-
gohysterectomy with or without partial ovariectomy.
Egg binding
Cockatiels, canaries, and finches most commonly are reported to be
affected and seem to present with more severe clinical signs, possibly because
of their small size. Clinical signs associated with egg binding and dystocia vary
according to severity, size of the bird affected, and degree of secondary
complications. Common signs include acute depression, abdominal straining,
persistent tail wagging, a wide stance, failure to perch, abdominal distension,
dyspnea, and/or sudden death. An egg lodged in the pelvic canal may
compress the pelvic blood vessels, kidneys, and ischiatic nerves, causing circu-
latory disorders, lameness, paresis, or paralysis. Pressure necrosis of the
oviductal wall may occur. Dystocia may cause metabolic disturbances by in-
terfering with normal defecation and micturition, and cause ileus and renal
disease, respectively. The severity of the patient’s condition can be estimated
by the degree of depression and the length of time clinical signs have been
present [42–44].
Diagnosis of egg binding or dystocia in a severely compromised patient
may be made based on history and physical examination alone, and the
patient may not be stable enough to survive other diagnostic procedures.
Rapid diagnosis and therapy are crucial for a successful outcome. Physical
examination may reveal depression, lethargy, a thin or normal body condi-
tion, and dehydration. There may be dyspnea or an increased respiratory
rate caused by compression of the caudal thoracic and abdominal air
sacs. The hen may not be able to perch, and may demonstrate pelvic limb
paresis, paralysis, or cyanosis. Owners may report lack of recent stool
production. An egg typically, but not always, is palpable in the caudal
abdomen. Cranially located, soft-shelled, and nonshelled eggs may not be
detected on abdominal palpation. Palpable, calcified eggs may be located
within the oviduct or be free in the ceolom subsequent to uterine rupture.
Careful celomic palpation, cloacal examination, radiographs, coelomic
ultrasound, laparoscopy, and/or laparotomy may be required to determine
the egg’s position [42–44].
It should be kept in mind that the presence of palpable egg does not
always represent an abnormal medical condition. A normal egg is palpable
within the ceolomic cavity within up to 24 hours of normal oviposition.
Radiography and ultrasonography aid in evaluation of the position and
characterization of the egg(s). General confirmation of the presence of an
egg can be done with the bird simply standing awake on the radiographic
cassette. There may be multiple eggs identified in the coelom because of an
obstruction distally or secondary to motility disorders. Osteomyelosclerosis
or hyperostosis of the femurs, tibiotarsi, radii, ulnas and/or spine is a common
finding in birds with estrogenic stimulation, and appears as a general filling or
calcification of the normally hollow bone cavity (Fig. 4). Other suggestive
radiographic findings include suggestion of ovarian or uterine enlargement
and displacement of other soft tissue structures by an enlarged uterus or eggs.
374 BOWLES et al
Fig. 4. Osteomyelosclerosis on a radiograph. These radiodense changes seen within the femurs
of the bird are seen commonly before and during egg laying.
Coelomic ultrasound often will reveal an egg and may help identify
a soft-shelled or nonshelled egg that may have been difficult to identify on
radiographs. Again, there may be several eggs visible within the coelom.
Follicles may be visible on the ovary, indicating the potential for further
ovulation and egg formation.
A hematologic analysis and serum chemistries are useful to identify any
predisposing and secondary diseases. A complete blood count may reveal
a leukocytosis with a relative heterophil in the presence of concurrent
inflammatory or infectious process. Serum chemistries may demonstrate el-
evated aminotransferase and creatinine phosphokinase caused by skeletal
muscle enzyme leakage from tissue damage, or as a result of reduced food
consumption and a hypermetabolic state. Hypercholesterolemia and hyper-
globulinemia are supportive of ovulation. Elevated total and ionized
calcium and may be indicative of calcium mobilization in a reproductively
active bird. Conversely, hypocalcemia may be observed if the hen has
been consuming a calcium-poor diet or has been laying excessive numbers
of eggs, resulting in depletion of calcium stores [42–44].
Therapy varies with history, severity of clinical signs, and diagnostic test
results. Supportive care should include elevated environmental temperature,
parenteral calcium, fluid therapy, and nutritional support. Broad-spectrum
antibiotics are indicated if an infectious etiology is suspected or if the integ-
rity of the oviduct may be compromised. Analgesics often are indicated.
Supportive care alone is often enough to facilitate oviposition, although
the hen should be monitored closely for deterioration of condition, which
may require further intervention [42–44].
Prostaglandin and hormonal therapy may be used to induce oviductal
contractions. This may result in expulsion of the egg if the contractility of
the oviduct is sufficient; the uterus is intact; the egg is actually within the
oviduct, and there is no obstruction such as a neoplastic mass, granuloma,
or egg adhered to the oviduct. Studies performed in poultry have found that
prostaglandin E2 (PGE2) and prostaglandin F2alpha (PGF2alpha) bind at

specific receptor sites in the uterus and vagina. The uterine myometrium
appears to preferentially bind PGF2alpha, because it contains low-affinity
and some high-affinity binding sites for PGE2, and specific high-affinity
for PGF2alpha. Prostaglandin F2alpha binds at the shell receptor sites to
cause a time- and dose-dependent mobilization of cellular calcium in the
presence of extracellular calcium, thereby causing uterine muscle contrac-
tion. It has been demonstrated in vitro that PGE2 is itself ineffective in
calcium ion mobilization, but will enhance PGF2alpha-induced calcium
mobilization. This suggests that PGE2 may potentiate the ability of PGF2-
alpha to cause uterine contraction. In the vagina, high-affinity binding sites
for PGE2 predominate. It is possible that a high PGE2 concentration in the
vagina is needed to saturate high-affinity binding sites and block PGF2-
alpha-binding sites. This allows relaxation of the uterovaginal sphincter
and vagina. Because fewer PGE2 high-affinity binding sites are present in
the uterus, they are not likely to interfere with PGF2alpha binding and
may potentiate the action of PGF2 alpha. When an egg is present in the
uterus, injections of PGF2alpha and PGE2 will cause the concentration of
arginine vasotocin (AVT) to increase in systemic circulation; however,
PGF2alpha is the more potent stimulator of AVT release. It is suggested
that prostaglandins stimulate uterine contractions, which in turn stimulate
the release of AVT from the neurohypophysis, and that AVT probably
acts synergistically with PGF2alpha to increase uterine contractions. Oxyto-
cin and AVT appear to specifically affect the uterus, inducing powerful
contractions. It is important to note that PGF2alpha, oxytocin, and AVT
do not cause relaxation of the uterovaginal sphincter while inducing
oviductal contractions. This may result in reverse peristalsis, dilation of
the uterovaginal sphincter, severe pain, and rupture of the uterus. Therefore,
before use it is important to determine if the uterovaginal sphincter is indeed
open. In addition, prostaglandin and hormonal therapy require exogenous
calcium to be effective. As many of these patients are severely hypocalcemic
because of either malnutrition or chronic egg laying, supplemental calcium
may be required before administration of these medications [42–44].
PGE2 gelg may be applied to the uterovaginal sphincter, at a dose of 0.1
mL per 100 g bird. PGE2 causes relaxation of the uterovaginal sphincter
while causing oviductal contractions, and it may be applied topically, thereby
decreasing the incidence of systemic side effects. These contractions may expel
the egg within 15 minutes. Contact with PGE2 gel may cause altered menses
and induce spontaneous abortion in women. Therefore, it is important to
flush any excess from the cloaca after egg expulsion, and precaution staff
and clients regarding contact with any stool and/or urine produced. Prosta-
glandin F2alpha, oxytocin, and AVT also will cause powerful uterine con-
tractions. Prostaglandin F2alpha is administered parenterally, rather than
locally, and is more likely to cause systemic reactions such as hypertension,
bronchoconstriction, and general smooth muscle stimulation [42–44].
376 BOWLES et al
If supportive care and medical therapy fail to induce oviposition, then

manual manipulation may be necessary. Massaging the abdomen and
vaginal opening may relax the vaginal sphincter and allow passage of the
egg. It may be helpful to infuse lubricants into the cloaca to moisten the
urodeum and vagina. Careful digital pressure applied to the cranial portion
of the egg and directed caudally may encourage movement through the
distal oviduct and cloaca. Using a cloacal speculum, the vaginal opening
of the oviduct can be dilated by inserting a blunt probe (ie, lubricated
cotton-tipped swab) that is advanced gently in a twirling motion. Potential
complications may include retroperistalsis of the egg out of the oviduct into
an ectopic position within the coelom, rupture of the egg, oviductal trauma,
oviductal laceration, and displacement of the egg or fragments out of
the uterus and into the ceolom. If fertilization may have occurred and
the egg may be fertile, it may be incubated if successfully removed intact
[42–44].
Ovocentesis may be performed to facilitate passage of an egg. Aspiration
may be performed through the cloacal opening if the egg is located distally,
or transcelomically if the egg is positioned more cranially. The egg is manip-
ulated so that it is visible through the cloaca, and a needle is inserted into the
egg through the cloaca. The contents of the egg are aspirated into a syringe,
while the shell is collapsed manually and the pieces expelled through the
cloaca. If the egg cannot be visualized through the cloaca because of a
more cranial location, transabdominal ovocentesis may be performed. The
egg is manually placed directly against the abdominal wall so that other ab-
dominal organs are displaced and not damaged during aspiration. A needle
is inserted through the skin and abdominal wall into the egg. The egg
contents are aspirated into the syringe while the egg is collapsed manually.
The eggshell remnants are expelled through the cloaca, either naturally or
with clinical assistance. It is important to confirm radiographically that
these eggshell pieces have been expelled completely. If these pieces are not
expelled within a reasonable amount of time, approximately 36 hours, it
may be necessary to irrigate the oviduct through the cloaca or laparotomy
approach. A salpingohysterectomy may be performed if egg remnants are
retained and the hen is not required for breeding. Some clinicians advocate
flushing the uterus postoviposition with saline, chlorhexidine, or iodine to
remove any shell fragments and decrease the incidence of metritis. Oviductal
rupture, resulting in an ectopic egg, shell fragments, or yolk coelomitis, is
a possible complication of ovocentesis [42–44].
Medical therapy to reduce reproductive hormone levels and reproductive
activity should be used to temporarily prevent further egg production.
Surgical removal of an egg is required in cases of ectopic eggs and dystocia,
including oviductal rupture, oviductal torsion, or mechanical obstruction,
or if medical treatment is not successful. If surgical intervention is necessary,
bacterial culture and sensitivity and histopathology should be performed on
oviductal tissue samples. Salpingohysterectomy may be considered to
prevent further reproductive complications, and any predisposing and

secondary diseases should be corrected [42–44].
Cloacal and oviductal prolapse

Cloacal prolapse may occur secondary to chronic straining from mastur-
bation, egg laying, space-occupying abdominal masses, and inappropriate
weaning and social behavior. Physical examination will reveal prolapsed
tissue through the vent that may be intermittent or persistent. Careful clean-
ing, irrigation, and lubrication of prolapsed tissue are a necessity. Affected
tissue should be examined for necrosis, and any adhered egg should be re-
moved. Cytology and bacterial culture and sensitivity should be performed
on prolapsed tissue to aid in antibiotic therapy. A complete blood count,
serum chemistries, radiographs, ultrasound, and endoscopic examination
of the ceolom and cloaca are useful to determine any other predisposing
cause. Chronic reproductive-associated behavior and straining secondary
to masturbation may respond to pharmacologic therapy such as leuprolide
acetate, and/or environmental manipulation to decrease reproductive stimuli.
Cloacopexy and the use of temporary stay sutures may be helpful in
temporary or permanent reduction. Those procedures interfere with move-
ment of the cloaca, however, and may alter defecation and micturition.
Ventplasty may decrease the vent opening and prevent further prolapse if
the vent has become flaccid. Clomipramine hydrochloride administration
anecdotally has been reported to contract the vent orifice and assist in the
resolution of prolapse of the cloaca. Salpingohysterectomy with partial
ovariectomy or orchiectomy may be beneficial in those patients refractory
to medical therapy. Broad-spectrum antibiotics should be initiated, pending
bacterial culture and sensitivity, because primary and secondary bacterial
infections are common [42–44].
Oviductal prolapse may occur secondary to any condition that causes
chronic, excessive abdominal straining such as physiologic hyperplasia,
egg laying or dystocia. An intraceolomic, space-occupying mass also may
induce prolapse of the oviduct. Predisposing factors may include abnormal
or soft-shelled eggs, malnutrition, obesity, salpingitis, and cloacitis. Typi-
cally, the uterus protrudes through the cloaca, often with a partial prolapse
of the vagina and cloaca [42–44].
Rapid management is necessary to prevent necrosis of these tissues. Any
egg that may be present should be removed, and all exposed tissues cleaned,
irrigated, and kept well moistened to prevent desiccation. Topical anti-
inflammatories such as dimethyl sulfoxide may be applied; any lacerations
should be repaired, and all tissues should be replaced gently. Temporary
stay sutures may be indicated to aid in preventing recurrence, as prolapse
of the oviduct may recur, and repeated replacement often is required.
Bacterial culture and sensitivity of the prolapsed tissue should be performed
to aid in appropriate antibiotic therapy. Complete blood count, serum
chemistries, radiographs, ultrasonography, and laparoscopy should be
378 BOWLES et al
included in a complete diagnostic evaluation to identify any predisposing

and secondary disease conditions. Treatment should be directed at clearing
any bacterial infection, preventing further prolapse. It also is important to
decrease reproductive hormone levels to prevent further egg formation,
decrease the size of oviductal tissue, and allow the reproductive tract to
rest. Broad-spectrum antibiotics and antifungal medication should be initi-
ated while bacterial and fungal cultures are pending. Salpingohysterectomy
may be considered to prevent recurrence, or in cases of severe uterine dam-
age. Predisposing factors should be corrected to prevent recurrence and sec-
ondary diseases addressed [42–44].
Neurologic disease
Head trauma is common in free-flying birds. Seizures are common in pet
birds because of heavy metal intoxication, hypoglycemia (neonates and
raptors), or idiopathic epilepsy (cockatiels). Infectious disease such as pro-
ventricular dilatation disease (PDD) and paramyxovirus also may cause
neurologic signs as weakness and ataxia. Weakness and falling off the
perch can be seen in African gray parrots with hypocalcemia syndrome.
The etiology is controversial and may be primary vitamin D3 deficiency.
Neoplasia, egg yolk embolism, and other nonviral infectious diseases
have been reported to cause neurological signs [45]. Sarcocystis spp. have
been reported to cause ataxia and weakness. Infection has been reported
in over 60 species of birds, with Old World psittacines apparently more
susceptible [46]. One of the authors (Lichtenberger) has seen a chronic
case of sarcocytis in a cockatoo in Wisconsin that presented with weakness
and ataxia.
Signs of neurological disease include seizures, ataxia, paresis or paralysis,
head tilt, circling, and blindness. A neurological examination should be
performed to confirm if there is a neurological abnormality and to localize
the lesion. An excellent review of the neurological examination has been
written [46]. The basic neurological examination consists of observation,
cranial nerve examination, postural reactions, and spinal reflexes. The bird
initially is evaluated in the cage for mentation, posture, and gait. Seizures
and abnormal behavior (changes in personality) are a function of the cere-
brum. Change in consciousness is a function of the brainstem and cerebral
cortex. The cranial nerves (CN) are evaluated as follows:
Evaluation of menace test (CN 2 and 5)
Evaluation of papillary light reflex (CN 2 and 3)
Detection of strabismus (CN 3, 4, and 6)
Evaluation of palpebral reflex (CN 5 and 7)
Determination of beak tone (CN 5 and 7)
Observation of oculocephalic or physiological nystagmus (CN 8 with CN
3, 4, and 6 responsible for eye movements)
Postural conscious proprioception is performed by placing the leg in an

abnormal position to evaluate the bird’s ability to correct it. Visual placing
can be performed by asking the bird to step up to or from a perch, as normal
motor tracts and motor cortex are required for this reaction. The patellar
reflex can be performed on each leg. Hyper-reflexia demonstrates an upper
motor neuron lesion (UMN), while hyporeflexia demonstrates a lower
motor neuron (LMN) lesion. A pinch stimulus to the end of the wing eval-
uates the withdrawal reflex (brachial plexus integrity), while pedal reflex is
demonstrated by pinching the toe. An intact vent reflex demonstrates
integrity of the pudendal nerve. Evaluation of deep pain is reserved for birds
showing evidence of spinal cord disease [46].
Collection of cerebral spinal fluid has been reported by means of an
approach into the atlanto–occipital joint under general anesthesia; however,
this procedure is difficult and not recommended because of high risk of
puncture of the venous sinus [46]. CT and MRI also can be performed [46].
Diagnostics and treatment

Head trauma
Head trauma is common in birds, and this frequently occurs without
direct observation by the owner. Many pet birds can become injured in their
enclosures, or when they are not observed outside an enclosure. If MRI and
CT are not available, practitioners must rely on history and clinical signs for
diagnosis and treatment options. With the exception of fracture, radio-
graphs are usually unrewarding. The mainstay of head trauma treatment
is oxygen and maintenance of a normal blood pressure. The bird is to be
kept in an incubator with heat and oxygen. Analgesics are provided if the
bird is excitable or restless in the cage. Seizures are controlled with pheno-
barbital or potassium bromide (follow seizure protocol). In traumatic brain
injury, it is documented that systemic hypotension in the face of intracranial
hypertension (vascular bleed or mass) results in perpetuation of secondary
neurology injury, and therefore worsened outcome. Hypotension is treated
with small-volume fluid resuscitation (0.9% sodium chloride bolus IO or IV
at 10 mL/kg until indirect systolic blood pressure is 90 to 120 mmHg). The
small-volume resuscitation is used to bring the blood pressure to normal and
to avoid hypertension and risk of disturbing the intracranial clot. Cortico-
steroids are controversial and no longer used in human or small animal
medicine. The authors recommend that steroids not be administered to
birds. Complications from steroids are immunosuppression, GI ulceration,
and delayed healing. Mannitol can be considered only in the bird showing
worsening of neurological status (ie, stupor to comatose).
Spinal disease
Paresis indicates the presence of reduced motor function in the limbs.
Paralysis indicates complete loss of motor movement in the pelvic limbs.
380 BOWLES et al
The most common etiology is trauma. The clinician should rule out a path-
ological fracture caused by hypocalcemia in chronic egg layers. Other causes
include neoplasia, degenerative disease (psittacine poliomyelomalacia),
nutritional deficiencies (vitamin E, thiamine, riboflavin, pyridoxine), and
inflammatory disorders including proventricular dilatation disease (PDD)
and polioencephalomyelitis of rainbow parakeets. Other etiologies include
aspergillosis, toxicities including heavy metal, organophosphates, botulism
and tick paralysis, and vascular disease (fibrocartilaginous embolic myelop-
athy). Diagnostic tests include blood work, radiographs, MRI, and CT.
Treatment for spinal trauma is almost always supportive, but can involve
bandage support, or in select cases, surgery [47–50]. The neck can be stabi-
lized using a rigid support bandage made out of tongue depressors, plaster,
and/or bandage material.
Corticosteroids are controversial in human and small animal medicine.
Supportive care is required for weeks, including nutrition and analgesia.
Seizure
The possible differentials for seizures include a toxin exposure, trauma,
hypoglycemia, hypertension, or hypocalcemia. Idiopathic epilepsy has been
diagnosed in peach-faced lovebirds, red-lored Amazons, double-headed
Amazons, and mynah birds.
The work up for a bird presenting with seizures should include a complete
physical examination and evaluation of blood glucose, calcium, and PCV/
TP. When the patient is stable, consider CBC and complete biochemistry
panel, radiographs, and heavy metal screening. Indirect systolic blood pres-
sure should be measured. Ideal levels are less than 200 mm Hg after the
seizure is controlled.
Any bird presenting in status epilepticus (seizure repeated at brief inter-
vals for 30 minutes or more without complete recovery of consciousness be-
tween individual attacks) should be treated with an injection of midazolam
(0.25 mg/kg intramuscularly) and therapy directed toward the underlying
cause, if known. When seizures cannot be controlled with the use of mida-
zolam, one of the authors (Lichtenberger) has used a phenobarbital load as
described: anesthetize the bird with isoflurane or sevoflurane. Most birds
will stop seizuring under general anesthesia. Administer phenobarbital
intramuscularly every 15 minutes at 4 mg/kg intramuscularly for a maximum
of two doses. Perform blood work, measurement of blood pressure, and
radiographs while the bird is under anesthesia Recover the bird in a warm
oxygenated incubator with the head elevated. Phenobarbital is continued
at a daily oral maintenance dose (2 mg/kg by mouth) for 12 hours after
the phenobarbital load.
Heavy metal. Metal intoxication includes ingestion of lead, zinc, or other

poisonous metallic substances. The bird may present with a history of inves-
tigating or ingesting foreign objects, but many cases of heavy metal toxicity
occur without history of known exposure. Common sources include drapery

weights, stained glass windows, gunshot, pennies, linoleum, galvanized cage
metal, and other sources including contaminated drinking water. Many
older homes have lead paint or water pipes. Physical signs are often vague
and may include polyuria and polydipsia, regurgitation, diarrhea, green
urates, ataxia, lethargy, or stupor, and seizure. Amazon parrots commonly
present with hematuria or hemoglobinemia. Radiographs may reveal metal-
lic objects in the GI tract or the metal may already have been digested
and/or passed. Blood lead and plasma zinc levels may be elevated; however,
in suspected cases chelation therapy is initiated before receiving these results
in the critically ill bird [1,46,51]. The hemogram may be completely normal,
but might reveal anemia and erythrocytic ballooning (red blood cells that
show bulges in the normal elliptical shape and often accompanied by areas
of hypochromasia). Basophilic stipling is not seen in birds. Treatment
includes fluid therapy, antiemetics, nutritional support, chelation, and
anticonvulsants when indicated. Chelation options include calcium EDTA,
D- penicillamine, and succimer (30 mg/kg by mouth every 12 hours for 14
days made by a compounding pharmacy at 25 mg/mL suspension). Inject-
able calcium EDTA offers a benefit of parenteral therapy, particularly in
those patients that are regurgitating or those that may not absorb oral
D- penicillamine effectively [1]. Barium sulfate or activated charcoal may
help move lead particles through the digestive tract.
Proventricular dilatation disease (PDD). PDD is a disease of unknown eti-

ology, but circumstantial evidence suggests one or more viruses cause it. Nu-
merous clinical reports document spread of the disease through a collection,
and therefore it is likely contagious. Clinical manifestations of the disease
are the result of lymphoplasmacytic inflammation of the nerves of the GI
tract and brain, spinal cord, and peripheral nerves [1]. The disease is seen
most commonly in macaws, cockatoos, African greys, Amazon parrots,
and conures, although all species are susceptible. Clinical signs include re-
gurgitation, severe weight loss, anorexia, passing of whole seeds in the stool,
weakness, ataxia, and other neurological signs. PDD should be a differential
diagnosis with any bird with CNS disease. The onset of PDD is seen at 3 to 4
years, but birds as young as 10 weeks and as old as 17 years have been docu-
mented. Radiographs often reveal a dilated proventriculus, and barium
contrast studies reveal slow transit. Confirm definitive diagnosis with crop
or proventricular biopsies. Not all birds with PDD have crop lesions, so fail-
ure to find lesions in a biopsy does not rule out the disease. The biopsy must
contain a blood vessel (nerves travel with blood vessels). Treatment involves
supportive care and nutrition. Celecoxib (10 mg/kg every 24 hours) has been
advocated as a treatment, although no controlled trials have been done.
Hypocalcemia syndrome. Hypocalcemia occurs commonly in parakeets,

lovebirds, and cockatiels that are chronic egg layers (see chronic egg laying).
382 BOWLES et al
Large quantities of circulating calcium can be taken up by the shell gland dur-
ing egg formation. An important predisposing cause is an unsupplemented
all-seed diet. Clinical signs include tremors, weakness, and seizures. Chronic
egg layers commonly present with multiple pathological bone fractures. An
ionized calcium less than 1 mg/dL or total calcium less than 8 mg/dL is often
suggestive of hypocalcemia. Total calcium should be interpreted with
caution, because a hypoalbuminemia can lower the total calcium falsely. It
is always ideal to use measurement of ionized calcium. The clinician should
keep in mind that birds require exogenous vitamin D3 (100 IU/300 g every
7 days). Calcium is given (50 to 100 mg/kg intramuscularly). Change diet
to allow for supplemental calcium. Sunlight or UV light should be supplied.
A syndrome of hypocalcemia and associated clinical signs has been
described in African gray parrots. It appears to be caused by an abnormal
calcium and vitamin D3 metabolism. The birds should be treated with IV
or intramuscular calcium, vitamin D3, and exposure to full-spectrum UV
lighting. Dietary improvement should be initiated.
Gastrointestinal disease
Chlamydophilosis
This disease will be discussed under GI disorders, although respiratory
and GI signs are common. Chlamydophilia psittaci infections can occur in
almost any species of caged birds. Clinical signs vary from mild respiratory
sinusitis, rhinitis) or GI signs (diarrhea, regurgitation, yellow-green urates)
to severe multisystemic signs [52]. Doves, pigeons, and cockatiels carry the
disease without showing clinical signs except when stressed. A suspected
case of chlamydiosis is defined as a bird with compatible clinical signs
that is linked to a person or another bird that had chlamydiosis, a subclinical
infection with a single high serological titer (ie, high elementary body agglu-
tination or EBA in psittacines for anti-IgM; serum, cloacal, or choanal
positive polymerase chain reaction [PCR] assays; complement fixation or
CF anti-IgG for doves and pigeons; solid-phase enzyme-linked immunoas-
say [ELISA]-positive test which is not available in the United States) [44].
The PCR test has the advantage of identifying an early infection as early
as 5 days from oral cavity, 10 days from the cloana and 15 days from the
blood. No test is 100% sensitive. Supportive care initially is started with
heat and fluids. Nutritional support is recommended. No protocol ensures
safe treatment of complete elimination of infection in every bird. Doxycy-
cline is presently the drug of choice for treating birds with avian chlamydio-
sis. There are numerous protocols recommended depending on the situation
(ie, flock treatment, oral medication, or water treatments). The authors rec-
ommend that sick birds be treated with an injectable form of Vibramycin SF
IV (European formulation that can be imported through www.NOIVBD.nl,
[email protected]) and given at 75 to 100 mg/kg intramuscularly every
5 to 7 days for the first 4 weeks and then every 5 days for two more treat-
ments. The injectable tetracycline formulation labeled for IV use in people
can be used IV in birds. The bird can be given the initial dose IV and
then continued on oral doxycycline medications [45].
Vomiting and regurgitation

Differentiation must be made between behavioral and pathological regur-
gitation. Behavioral regurgitation usually is directed at an object (mirror) or
the owner. Birds also can vomit with the stress of traveling or after anesthe-
sia. Pathological vomiting or regurgitation can lead to life-threatening
dehydration, starvation, electrolyte imbalance, and aspiration pneumonia.
It is difficult for an owner to differentiate passive regurgitation versus active
vomiting. Most clinicians use the terms interchangeably. Often food mate-
rial is adhered to the feather on the head or nares. Decreased body condition
must be attributed to a specific disease. Birds that have a history of vomiting
or regurgitation may suffer from aspiration pneumonia or sinusitis. Etiology
includes neonates with crop stasis (improper formula temperature and
consistency), dietary indiscretion (toxins, plants, spoiled food), infections
(PDD, bacterial, fungal, gastric yeast), goiters in budgerigars, chlamydio-
philia, heavy metal intoxication (lead or zinc), or metabolic (hepatopathy,
sepsis, pancreatitis). Fecal and esophageal/crop cytology and culture/sensi-
tivity should be performed to reveal primary or secondary pathogens (see
discussion under diagnostic testing). CBC count, chemistry panel, heavy
metal testing, plasma EPH, and chlamydiophila testing may be useful
also. Radiographs may identify foreign body, dilated proventriculus, ileus,
or organomegaly, but must be performed with care in birds with GI motility
disorders to prevent regurgitation and aspiration. Fluoroscopy or barium
series can identify delayed gastric empty time or an obstruction. Ultrasound
and biopsy can identify liver disease, masses, or intestinal disease further.
Toxin plants can cause serious burns or systemic signs. Contact the poison
control center for recommendations for treatment. Treatment for heavy
metal intoxication was discussed previously in the neurological disease
section. GI obstructions are treated with fluids until stable. Surgical explor-
atory in recommended. Appropriate antibiotics and/or antifungal medica-
tions are indicated. Metoclopramide (Reglan,) or cisapride (compounding
pharmacies, 0.5 mg/kg by mouth three times daily) may assist improve
crop motility and control regurgitation, but should not be used in cases of
GI obstruction. No studies have been performed in birds for dosing,
pharmacokinetics, or toxicity for either cisapride or metoclopramide [33].
Delayed emptying of the crop (crop stasis) may occur with any illness that
causes debilitation and may not indicate a localized problem. Crop stasis in
neonates is common and may be secondary to poor husbandry or improper
feedings. A complete blood count, chemistry panel, and electrolyte levels
should be performed to assess hydration, leukocyte count, metabolic, and
384 BOWLES et al
electrolyte abnormalities [46]. Soften impacted material with warm water.

Massage material and the fluid; then withdraw the material out into a large
bore red rubber tube. This procedure is moderately stressful and must be
done with care in debilitated birds. Thickened ingesta may cause prolifera-
tion of bacteria and yeast and contribute to dehydration and infection.
The birds are treated with fluid therapy and nutritional support with tube
feedings. Antibiotics (ie, trimethoprim sulfadiazine at 30 mg/kg by mouth
twice daily) and antifungal therapy (nystatin at 100,000 to 300,000 IU/kg ev-
ery 12 hours by mouth for 7 to 14 days) are given when large numbers of
gram-negative bacteria and yeast are seen on crop smears. The owner should
be instructed on proper feeding methods [33].
Diarrhea
Differentiation of diarrhea into large and small bowel disease is difficult
with the exception that small bowel disease is more likely in the presence of
with melena, and large bowel/cloacal disease in the presence of frank blood.
Etiology of diarrhea is diet change or indiscretion, infections (avian gastric
yeast, chlamydiophila, gram-negative bacteria, yeast, virus), protozoan
(Giardia, cryptosporidium) toxins (plants, zinc or lead), systemic disease,
GI foreign body, or neoplasia. The clinician must differentiate between
true diarrhea and watery stool caused by polyuria. Malnutrition, especially
hypovitaminosis A, predisposes a bird to GI disease.
The presence of blood in the stool can have several causes. Cloacal pap-
illomas (primarily South American birds) can cause frank bleeding into the
cloaca. Hematuria is seen commonly with zinc and lead toxicity (Amazons
and cockatiels). Cloacal trauma and irritation can cause presence of blood
in stool.
Medications and stress can cause stool changes. The stool should be
evaluated with a Gram’s stain, direct cytology, and culture of abnormal
findings. Cloacal mucosa is examined for papilloma and trauma. Provide
supportive care and treat for suspected infections, yeast, and protozoan
parasites as necessary. Radiographs are recommended for toxin, foreign
body, and systemic disease. Treat for underlying cause.
Renal disease
Kidney disease is common in avian species. Most studies have been done
on chickens or other nonpet birds. Many retrospective studies and case
reports support the conclusion that renal diseases are clinically significant
in many species of birds (S. Echols and H. Gerlach, personal communica-
tion, 2006).
Birds have many of the same kidney functions as is seen in small animals,
including renal regulation of water by means of electrolyte balance, endo-
crine function (production of active form of vitamin D and
erythropoietin-like substance production), and osmoregulation (arginine va-

sotocin, norepinephrine, aldosterone, rennin angiotensin, and prolactin).
The kidneys auto-regulate renal blood flow as in small animals between
blood pressures of 60 to 110 mm Hg. At mean arterial pressures less than
50 mm Hg, glomerular filtration rate decreases. Avian kidneys are different
from small animal kidneys in two significant ways: excretion of uric acid as
the end product of nitrogenous waste and the presence of the renal portal
system. The renal portal system shifts blood from the legs and coelomic or-
gans directly through the kidneys or into the vena cava through the action of
a valve under the control of the sympathetic (SNS) and cholinergic nervous
system. Stress, handling, and hypovolemia (any factors stimulating the SNS)
cause the valve to close, and blood is shifted directly to the vena cava and
central blood flow. For this reason, injection medication into the leg
muscles is unlikely to have negative consequences, as stress of restraint
and handling will cause blood flow to return to the heart, as is does in mam-
malian species [53].
The most common clinical signs of renal failure are polyuria and polydip-
sia. Dehydration, anorexia, and feather picking over the synsacrum also
have been noted. As renal failure progresses, oliguria and then anuria will
occur. The most diagnostic test is a persistently elevated uric acid in a nor-
mally hydrated bird. A pure urine sample is difficult to obtain (see urinalysis
in procedures). Other diagnostics are ultrasound, especially for diagnosis of
renal enlargement or neoplasia. Calcification of the kidney may be seen in
some cases on radiographs. A CBC and chemistry panel and other serology
should be done to rule out other diseases. Blood pressure is measured to rule
out hypertension. When the bird is stable, an endoscopic kidney biopsy
should be performed [53].
In the past, etiologies of renal disease in psittacine birds have been
extrapolated on information on renal disease in chickens and other nonpsit-
tacines. More information is forthcoming with the acceptance and increas-
ing frequency of renal biopsy of the psittacine kidney. Gout is reported
commonly and may be caused by reduced of the excretion of renal urates
or by increased dietary protein. There are two types of gout: visceral gout
with uric acid deposition on visceral organs, and articular gout with accu-
mulation of uric acid in the synovial tendon sheaths and joints. Nephritis
is a nonspecific inflammation of the kidney and may involve interstitium,
tubules, or glomerulus. Glomerulopathies are assumed to be immune-
mediated (specific etiologies such as fungal, viral, and bacterial agents),
but the exact cause is often unknown. In one retrospective postmortem
examination on cockatiels, 67% of the birds had glomerular atherosclerosis
[54]. In people, high cholesterol levels clearly are associated with the devel-
opment of atherosclerosis, but a link between high blood cholesterol levels
and atherosclerosis in psittacine birds has not been established [55]. Some
common diseases in birds potentially could interfere with cholesterol met-
abolism, such as hepatopathies, iron storage disease, amyloidosis, goiter,
386 BOWLES et al
and obesity, and thus contribute to atherosclerosis [56]. One of the authors
(Lichtenberger) belies that glomerulonephropathies are common in birds,
and changes may be secondary to another disease process and eventual
atherosclerosis and hypertension. Future studies are warranted evaluation
of cholesterol, low-density lipoproteins, and blood pressure measurements
in birds with renal disease.
There is a report on diet-induced renal disease of color variety psittacine
birds (S. Echols, unpublished data). The birds affected are color variety
cockatiels, lovebirds, budgerigars, and parrotlets that have consumed a pre-
dominantly pelleted diet. Lesions seen on kidney biopsy were tubular
nephrosis, which theoretically may be related to decreased water consump-
tion when consuming pelleted diets. The disease is reported to be reversible
by changing the diet to vegetables, fruit, and a small amount of seeds
(S. Echols, personal communication, 2006). More work is needed to confirm
this theory.
Other less common renal disease include nutritional, vitamin D toxicosis,
congenital, urolithiasis, and trauma. Renal neoplasia is common, especially
in the budgerigars. Renal carcinomas most frequently reported are kidney
tumor. The birds present after 5 years of age with one-legged lameness
and abdominal enlargement. Renal tumors may induce hypertension by
activation of the RAAS. Renal tumors are common in psittacine birds,
primarily parakeets [11]. An author documented hypertension (systolic
blood pressure O300 mm Hg) in two parakeets with renal tumors. The par-
akeets were treated with benazepril (0.5 mg/kg twice daily by mouth), which
lowered the systolic blood pressure to 110 to 130 mm Hg within 1 week. The
parakeets lived for 4 months.
Treatment for renal failure regardless of the cause will be to correct dehy-
dration, elevated uric acid, and electrolyte and acid-base imbalances. The bird
should be stabilized with heat and fluids as discussed elsewhere in this issue.
The bird with an elevated uric acid should be anesthetized and an IO catheter
placed. Radiographs, ultrasound, and other diagnostics are performed. Blood
pressure is measured. The bird is rehydrated as discussed elsewhere in this is-
sue. Immediately after rehydration, the uric acid is rechecked, and if still el-
evated, diuresis is initiated. The bird is continued on fluids at thee to four
times maintenance (3 to 4 mL/kg/h) for diuresis until uric acid value is normal
or near normal. The bird should be tube-fed if not eating as discussed else-
where in this issue. The tube feeding amounts can be calculated as part of
the total diuresis fluid amount to be given. When the bird is eating on its
own, fluids and tube feeding should be tapered by 50% per day. Oliguria
and anuria are treated when decreased to no urine production occurs after
rehydration. Lasix at 1 mg/kg intramuscularly can be given and fluids contin-
ued. If there is no urine production within 1 hour, prognosis is poor.
The consequences of glomerulonephropathies in small animals are a result
of immune-mediated (secondary to hepatopathies, heartworm disease infec-
tions, or chronic skin disease neoplasia) glomerular injury. After the
deposition of immune complexes, complement platelet aggregation, neutro-

phils, and activation of the coagulation system contribute to the glomerular
damage. There is reduced renal blood flow, proteinuria, hypertension, and
production of thromboxane, which causes vasoconstriction and platelet
aggregation. Arterial hypertension is seen in 80% of dogs with glomerular
disease. The coagulation system is activated, and pulmonary throm-
boembolisms are a common sequelae.
In dogs, treatment measures for glomerular disease are prophylactic treat-
ment of a thromboembolism with use of low-dose aspirin (0.5 mg/kg every
24 hours by mouth). The low-dose aspirin selectively inhibits thromboxane
(vasoconstrictor, platelet aggregation) without preventing the beneficial
effects of prostacyclin formation (eg, vasodilation, inhibition of platelet
aggregation). Omega-3 polysaturated fatty acids (as found in fish oil) may
suppress glomerular inflammation and coagulation by interfering with the
production of proinflammatory prostaglandins. Hypertension is treated
with benazepril (0.5 mg/kg). This is also beneficial for decreasing proteinuria.
No specific therapy is given for amyloidosis. Colchicine (0.03 mg/kg/d by
mouth) may delay or prevent amyloid fibril deposition and may decrease
serum amyloid A concentration. The authors recommend that glomerular
disease in birds be treated with omega-3 fatty acids, low-dose aspirin, and
benazepril (ie, for documented hypertension and/or proteinuria).
All other renal failure diseases must be treated appropriately depending
on underlying etiology. Bacterial nephropathy is treated with broad-spec-
trum antibiotics pending culture of the biopsied kidney tissue. Renal fibrosis
and amyloidosis are treated with colchicine. Articular gout is treated
with colchicine (0.03 mg/kg) and allopurinol. Articular gout lesions can
be opened aseptically to express the uric acid crystals and decrease painful
joints [11].
Hypertension
The definition of hypertension in birds is somewhat vague. A study of
normal conscious and anesthetized psittacine birds of different species reports
mean systolic indirect Doppler arterial pressures of 90 to 180 mmHg and 120
to 180 mmHg, respectively (Fig. 5). In an authors’ experience, systolic indirect
Doppler blood pressures greater than 200 mm Hg (in conscious and anesthe-
tized birds) are taken to indicate hypertension in birds [57]. In raptors, that
value may be higher. One of the authors (Lichtenberger) believes that
hypertension in anesthetized raptors is indicated by systolic indirect blood
pressure greater than 240 mm Hg.
Pathophysiology and clinical consequences

An increase in systemic vascular resistance (SVR) is the common denom-
inator in most hypertensive crises. This increase is mediated by increased
388 BOWLES et al
Fig. 5. Indirect blood pressure monitoring. Use of the Doppler indirect blood pressure monitor
in a bird.
levels of circulating catecholamines, increased alpha-adrenergic activity, and

activation of the renin–angiotensin–aldosterone system. The rise in arterial
pressure increases renal perfusion and induces a pressure naturesis. This is
important to remember, because most patients presenting with
hypertensive crises tend to have a relative hypovolemia. Baroreceptors are
stimulated by the resultant decrease in effective arterial circulating volume
and produce further increases in the alpha-adrenergic and beta-adrenergic
tone. This causes a further increase in blood pressure [58].
Most organs control perfusion by the process of autoregulation. Organ
blood flow can be maintained at a relatively constant level over a wide range
of perfusion pressures (usually 60 to 150 mm Hg). Target organ damage
occurs when systemic pressures exceed the usual autoregulatory range. This
may result in endothelial damage, platelet and fibrin deposition, ischemia,
fibrinoid necrosis, and/or hemorrhage. The eyes, brain, heart, and kidneys
are affected most commonly. Signs of organ damage may be the presenting
complaint in some patients with severe hypertension. The patients may pres-
ent for ocular lesions (ie, retinal hemorrhages, detachments, and/or papille-
dema), neurological signs (ie, confusion or seizures), cardiovascular signs
(ie, ventricular hypertrophy and congestive heart failure), or renal system
abnormalities (ie, glomerulonephritis) [58].
Etiology of hypertension
Primary or essential hypertension
Primary hypertension is common in people, and has been documented in
dogs, although the prevalence is extremely low. Its presence in other animals
and birds is unknown [58,59].
Renal disease. Renal failure is associated relatively commonly with severe

hypertension in dogs and cats (ie, 60% of renal failure patients), particularly
in patients with protein-losing nephropathy (PLN) [58,59]. The presence of

PLN and hypertension in birds is unknown. An author has treated a para-
keet with hypertension secondary to a renal tumor.
Atherosclerosis
Atherosclerosis denotes inner arterial wall thickening in association with
lipid deposition. Affected large arteries often appear grossly thickened, yel-
low-white, and have a narrowed lumen. Histological deposits of plaque con-
taining cholesterol, lipoid material, focal calcification, and lipophages
thicken the inner sections of arterial wall (intima and inner media). There
can be widespread involvement of arteries from many organs [60]. The dis-
ease in people commonly is associated with extensive plaque formation, ar-
terial calcification, or thrombosis [61].
Clinical diagnosis of atherosclerosis is difficult, and the prognosis for
animals with clinical signs related to stenosing atherosclerosis is poor. His-
tory of a high-cholesterol diet may be important and may lead to obesity.
Obesity in psittacine birds is common and occurs when birds are fed
a high-cholesterol and high-fat diet. Physical examination may reveal an
extremely obese bird. To an authors’ knowledge, no reports of obesity
and hypertension have been documented in the avian species. Blood
pressure measurement may be used to diagnose hypertension. Future studies
need to be performed in birds on high-fat, high-cholesterol diets. Blood tests
for cholesterol, low-density lipoproteins, and thyroid testing may be
warranted. ECG and echocardiography evaluation may detect primary or
secondary heart changes. Hypertension accelerates atherosclerosis because
of the high pressure changes in the artery [60].
Atherosclerosis is suspected strongly as being an inflammatory disease
developing in response to injury in the vessel wall in humans. Infiltration
of the mononuclear lymphocytes into the intima, local expansion of vascular
smooth muscle cells, and accumulation of extracellular matrix are believed
to be the pathogenesis of the inflammation. Previously determined risk
factors including hyperlipidemia and hypercholesterolemia are believed to
enhance leukocyte adhesion to damaged endothelium and reduce local
immune response. The role of inflammation in the development of psittacine
atherosclerosis has yet to be determined [60,61].
Possible risk factors for atherosclerosis include:
Obesity and decreased exercise

High-fat/cholesterol diet
Hypothyroidism
Exposure to stress factors as cold, cigarette smoke
Hypertension
Treatment for atherosclerosis includes reducing fat and cholesterol in the

diet, increasing exercise, ruling out hypothyroidism, and decreasing stress
390 BOWLES et al
factors such as exposure to cold and cigarette smoke. Blood cholesterol

reducing agents (eg, statins such as lovastatin) have not been used in birds.
Most human lipid-lowering drugs are not licensed for use in small animals
or birds. Certain drugs, however, have been used in birds, and there are
anecdotal reports of successful treatment. These drugs are to be used with
caution, and every effort should be made to monitor blood chemistry,
hematology, lipoprotein concentrations, and blood pressure [61].
Omega-3 fatty acids. These drugs reduce serum cholesterol and triglycer-
ide concentrations by decreasing the synthesis of very low-density
lipoprotein (VLDL) and low-density lipoprotein (LDL). There is
a liquid human product that can be used at 0.22 mL/kg body weight,
by mouth every 24 hours (Optomega). This drug has been used by the
authors for hyperlipidemia with hypertension in a parrot [61].
Chitosan. This is a fiber supplement made from shellfish that reportedly
binds lipids in the diet and decreases absorption of them. The drug is
given 30 minutes before meals and given separately from the omega
fatty acids by several hours. The drug is available in health food stores.
This drug has been used with apparent success in an eclectus parrot
with hyperlipidemia and hypertension (Lennox and Lichtenberger).
Niacin. This drug acts primarily to reduce hepatic triglyceride synthesis.
There is a new drug that has been used in cats and dogs (acipimox,
5 mg/kg by mouth every 24 hours).
Statins. These drugs are of less value for lowering triglycerides, but may
be effective in reducing cholesterol.
Arterial hypertension treatment is also a possibility for treating
atherosclerosis.
Antihypertensive medications
Unless evidence for hypertension-related organ injury is seen (eg, retinal
lesions, neurological signs, renal disease), the decision to initiate antihyper-
tensive therapy is not an emergency. The initial blood pressure should be
taken, and every effort should be made to minimize the risk that measured
elevations in blood pressure represent a transient white coat or stress effect,
rather than a sustained elevation in blood pressure [61].
The optimum endpoint for antihypertensive therapy has not been estab-
lished for dogs, cats, or birds with hypertension. In the absence of such in-
formation, treatment for arterial hypertension should be initiated cautiously
with the goal of reducing blood pressure by 25% over weeks in patients
without hypertension-related injury [61].
Angiotensin converting enzyme (ACE) inhibitors. Angiotensin converting

enzyme (ACE) inhibitors inhibit the conversion of angiotensin I to angio-
tensin II, and thus attenuate angiotensin-mediated vasoconstriction and
aldosterone release. These drugs also decrease glomerular efferent arteri-

olar vasoconstriction, and help reduce protein loss and inhibit the pro-
gression of glomerulosclerosis by lowering glomerular filtration pressure.
ACE inhibitors such as benazepril (0.5 mg/kg twice daily) have the po-
tential renoprotective benefits and are therefore appropriate options for
renal patients with hypertension [58]. In the authors’ experience, ACE in-
hibitors generally produce a relatively small reduction in blood pressure
in dogs and cats. Because of their beneficial role in altering intraglomer-
ular hemodynamics, proteinuria, and profibrotic effects of the intrarenal
rennin-angiotensin system, however, ACE inhibitors may have renopro-
tective effects even in the absence of achieving adequate blood pressure
control. Furthermore, in dogs with naturally occurring glomerulopathies,
enalapril significantly reduced proteinuria and may have been beneficial
in stabilizing renal function.
One of the authors (Lichtenberger) has measured a systolic blood
pressure in two parakeets with renal tumors at greater than 300 mmHg.
The birds was started on antihypertensive medication (Benazepril or enalap-
ril 0.5 mg/kg twice daily by mouth) and returned weekly for Doppler blood
pressure measurements [15]. Because of the stress level of the bird, he was
anesthetized under sevoflurane anesthesia for weekly blood pressure mea-
surements. Blood pressure was controlled in both birds for 4 to 6 months.
An Amazon bird presented for seizuring at an author’s (Lichtenberger)
clinic. The indirect systolic blood pressure was greater than 240 mm Hg.
The bird was started on benazepril 0.5 mg twice daily, and after 1 week
the blood pressure was 150 mm Hg. The bird is doing well 6 months later
without seizures and on benazepril. There are several other cases treated
by the authors (Lichtenberger and Lennox) for hypertension, with the
most common presenting complaint neurologic disease. (eg, seizures, ataxia,
weakness, and blindness).
Calcium channel blockers. Calcium channel blockers (CCBs) preferentially

antagonize preglomerular vasoconstriction, which theoretically should not
reduce glomerular hypertension. CCBs, however, appear to have additional
renoprotective properties. They may prevent renal injury by limiting renal
growth, by reducing mesangial entrapment of macromolecules, and by
attenuating the mitogenic effects of diverse cytokines and growth factors
(eg, PDGF, platelet-activating factor). In addition, CCBs inhibit the prolif-
eration of mesangial cells [58]. In the authors’ experience, CCBs have been
effective antihypertensive agents in dogs and cats with renal and cardiac dis-
ease [61]. Because it is usually highly effective, has few adverse effects, and
has a rapid onset, the long-acting dihydropyridine calcium antagonist amlo-
dipine is the antihypertensive of choice for most dogs and cats. Future stud-
ies are needed in birds for evaluation of amlodipine toxicity and dose
recommendations.
392 BOWLES et al
Summary
Acute respiratory distress, trauma, reproductive diseases, neurological
diseases, GI diseases, renal disease, and hypertension are the most common
syndromes affecting the pet bird that presents in an emergency situation.
Knowledge of these and other disease processes, indicated diagnostic test-
ing, and immediate treatment protocols are critical to provide efficient
and effective care to the pet bird in crisis.
References
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Harrison GJ, Harrison LR, editors. Avian medicine: principles and application. Lake Worth
(FL): Wingers Publishing; 1994. p. 382–416.
[2] Jenkins JR, et al. Avian critical care and emergency medicine. In: Altman RB, Clubb SL,
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Vet Clin Exot Anim 10 (2007) 345–394

Emergency and Critical Care of Pet Birds

1094-9194/07/$ - see front matter Ó 2007 Published by Elsevier Inc.

of thrombocytes should be documented also. Reduced numbers may be

Ionized calcium in normal individuals is maintained within a narrow

Phosphorus and glucose

Evaluation of feces and crop specimens

to be anesthetized, other diagnostic procedures and treatments may be

Computed tomography (CT)

Fig. 1. Intraosseous catheterization. Placement of an intraosseous catheter in proximal tibiotar-

Because of its potential irritation to the airways, a bronchodilator should

Common diseases and syndromes

Fig. 2. Nebulization technique. Nebulization using an ultrasonic nebulizer and mask.

in a warmed oxygenated incubator (oxygen ﬂow at 5 L/min delivers a oxygen

Five areas of the respiratory system

Pattern of breathing, respiratory sounds, and physical examination

pox [27,28]. Squamous metaplasia from nutritional hypovitaminosis A may

Large airway (glottis, trachea to the syrinx)

the neck. Overinﬂation of cuﬀed endotracheal tubes is potentially easier in a

Pattern of breathing, respiratory sounds, and physical examination

Etiology. The most common cause of large airway obstruction is foreign

with 100% oxygen. It should be noted that birds in extreme respiratory

Pattern of breathing, respiratory sounds, and physical examination

Etiology. Small airway disease includes exposure to inhalant respiratory

compounds in nonstick cookware or newly installed furnaces, smoke, aero-

nebulization (10 mL in 4 mL saline) by means of the endotracheal tube. This

Coelomic cavity disease (mass, ﬂuid, or organomegaly)

Pattern of breathing, respiratory sounds, and physical examination

Diagnostic tests and treatment

causes of a transudate are liver failure (eg, cirrhosis) or heart failure.

will require blood pressure measurements, radiographs, and an echocardiog-

Parenchymal disease (lungs and/or air sacs)

Pattern of breathing, respiratory sounds and physical examination

Wounds and open fractures

Punctures and small contaminated wounds can be left open to drain

Treatment for self-mutilation

External burn injuries

bandaging. A ﬁgure-eight bandage is applied to stabilize fractures of the ra-

prostaglandin E2 (PGE2) and prostaglandin F2alpha (PGF2alpha) bind at

If supportive care and medical therapy fail to induce oviposition, then

prevent further reproductive complications, and any predisposing and

Cloacal and oviductal prolapse

included in a complete diagnostic evaluation to identify any predisposing

Postural conscious proprioception is performed by placing the leg in an

Diagnostics and treatment

Heavy metal. Metal intoxication includes ingestion of lead, zinc, or other

occur without history of known exposure. Common sources include drapery

Proventricular dilatation disease (PDD). PDD is a disease of unknown eti-

Hypocalcemia syndrome. Hypocalcemia occurs commonly in parakeets,

Vomiting and regurgitation

electrolyte abnormalities [46]. Soften impacted material with warm water.

erythropoietin-like substance production), and osmoregulation (arginine va-

deposition of immune complexes, complement platelet aggregation, neutro-

Pathophysiology and clinical consequences

levels of circulating catecholamines, increased alpha-adrenergic activity, and

Renal disease. Renal failure is associated relatively commonly with severe

in patients with protein-losing nephropathy (PLN) [58,59]. The presence of

Obesity and decreased exercise

Treatment for atherosclerosis includes reducing fat and cholesterol in the