Flight Trouble: To Trim or Not to Trim

Clinical Case Challenge: Schatzi (Cockatiel)

Prepared by:
Jennifer Graham, DVM, Dipl. ABVP (Avian / Exotic Companion Mammal), Dipl. ACZM
Zoological Companion Animal Medicine


Shatzi, an 8-year-old male cockatiel, presented to his referring veterinarian with a recent history of lethargy, watery droppings and decreased appetite. According to the owner, the bird had recently been taken into a local pet store for a nail trim. The bird ate a varied diet including some pellets, nutriberries, vegetables, and fruit. Physical examination revealed that the bird was bright, alert, and responsive.

Fecal examinations including Gram’s stain and wet mount were within normal limits. Blood work was submitted and revealed elevated blood glucose (420 mg/dL; reference, 180-350 mg/dL), AST (617 U/L; reference, 20-350 U/L) and CPK (1327 U/L; reference, 50-400 U/L). Radiographs were obtained (Figures 2 and 3). The rDVM submitted samples for Chlamydia testing and started the cockatiel on azithromycin while awaiting results of diagnostic testing.

Untitled2Based on results of blood work and radiographs, what are your differentials? What do you recommend as the next step?

Whole Body Ventrodorsal and Lateral Radiographic Projections

Untitled1Treatment and Outcome

Shatzi presented to the Foster Hospital for Small Animals at Cummings Veterinary Medical Center at Tufts University for evaluation when the owner felt he wasn’t responding to antibiotic therapy. The referring veterinarian was astute to consider chlamydia as a differential since the bird had recently been to a pet store and was exposed to birds with unknown disease status. Fortunately, Shatzi’s chlamydia tests were negative, and blood work and radiographs were not suggestive of infectious disease. During Shatzi’s visit(s) to Foster Hospital, the Zoological Companion Animal Medicine team recognized that he was unable to fly, which was unusual given he was a flighted bird who flew whenever given the chance. Upon closer inspection, it was noted the bird’s wings were trimmed. After further discussion with the owner it became apparent the bird’s wings had likely been trimmed during a recent grooming visit at a local pet store; however, the owner was not aware this had happened. Since the grooming visit, the owner had noticed that Shatzi was lethargic and had been experiencing watery stools. Upon further questioning, the ZCAM team suspected that the elevated AST and CPK (which can be consistent with muscle enzyme elevation) were caused by Shatzi attempting to fly and repeatedly crashing to the ground. In addition, the veterinary team suspected the watery droppings and elevated blood glucose were consistent with a stress response (diabetes mellitus, while rare in birds, is usually associated with substantially higher glucose elevations than noted in this case). Since radiographs and CBC were unremarkable, it was recommended that while Shatzi adjusted to his wing trim the antibiotics would be discontinued, and the owner would provide a padded environment. Shatzi has recovered well. Through astute observation, interpretation of the lab test results, physical examination and questioning of the owner, the ZCAM veterinarian was able to diagnose and associate the side effects with Shatzi’s recent wing trimming.

Although wing trimming has traditionally been considered a ‘routine procedure’; there are potential risks, which need to be considered. Improper wing trims have been associated with feather picking, traumatic keel injuries, phobias, and even death. Many of the resulting problems can take weeks or months to develop and wing trim may not be suspected as the cause.

Wing trimming in bird:

Flight in birds

It is important to understand the function of the feathers of the wing to provide an appropriate trim.The wing can provide lift and thrust for the bird, much like the propeller and wings of an airplane. The four outermost primary feathers (primaries number 10-6) are primarily responsible for thrust power. The inner wing, along with shoulder muscles, provides lift. The inner primary feathers (primaries number 5–1), secondary feathers, and tertiary feathers also help to provide lift. Different types of wing feather trims provide varying results, depending on the body type of the bird. Clipping only the outer flight feathers will result in a reduction of thrust, while clipping the inner primary feathers reduces lift. Unilateral or asymmetrical clipping of the feathers results in an imbalanced delivery of lift or thrust.

When to trim and when to avoid trimming:

Many owners wish to have free-flighted birds in their home and as seen with Shatzi, trimming the wings led to an inability to fly. Flying is certainly the best exercise for birds and leads to improved muscle tone and cardiac health. However, any bird that is not trimmed is potentially ready to engage in free flight at any time. This increases the chance that the bird may be startled and fly into a predator’s grasp or onto a hot kitchen stove. Owners, who refuse wing trimming ,should be willing to assume the risks associated with housing a flighted bird. Although an owner assumes their bird would never fly away, accidents happen.

A young bird should not be trimmed before it is allowed to fledge. Ideally, weaned birds should be allowed to take short flights to ‘get used’ to flying and improve coordination. Most reputable breeders are aware of this and allow the bird to fledge before giving a conservative trim to avoid escapes. Gradual is best, and the trim can be modified during the first veterinary visits for best results.

Goals of wing clipping and types of trims

Wing clipping is most often used to prevent escape and to control mobility. Trimmed birds rely more on their owners than non-trimmed birds for transportation, and behavioral problems can be improved by limiting mobility in some instances. Cosmetic appearance after the trim is important when trimming display birds and to some owners.

Care must be taken to avoid causing the avian patient injury during handling. Excessive restraint may result in a fearful patient and create behavior problems at home. Trimming feathers too drastically can also cause a bird to be more prone to falling and result in injury.

There are many opinions on how to trim wings.

  • Unilateral wing trims were recommended in the past but have now been found to be unacceptable as they can result in injury.
  • A bilateral and symmetric wing trim is best.
  • In a ‘cosmetic trim’, the outer 2-3 remiges are not cut while several are cut behind these to result in an aesthetically pleasing trim. If an owner prefers a ‘cosmetic trim’, advise them that it is possible for the bird to damage the outer 2-3 remiges that are left behind. If an owner has no preference, taking these outer remiges may be a safer alternative.

Tips on Trimming a Birds Wings

  • When performing trims, carefully extend the wing, never restraining the wing by the tip to avoid iatrogenic humeral fractures.
  • Use blunt tip scissors with rounded edges and carefully identify each shaft of the primary wing feather at its base.
  • Cut the feather at the base, where it is just a bare quill, taking care to not cut the overlying covert feathers. Since each individual feather is identified before clipping, there is no chance of inadvertently cutting a blood feather, an active, growing feather with a blood supply. Blood feathers are easy to identify by its thickened, soft, purplish shaft and should never be cut. Additionally, if a blood feather is seen, a non-trimmed feather should be left on either side of it to avoid injury to the exposed feather. Using this type of trim, varying numbers of primary feathers are taken, depending on the body type of the bird. Most often, just five feathers can be taken and allow the bird to gently glide to the ground. Strong flyers or light-bodied birds (such as cockatiels and budgies) may need the outer seven primary feathers clipped on each wing (I have had to trim all 10 primaries on some determined cockatiels!).
  • If possible, test-fly the bird after removing five feathers to make sure that it can glide to the ground, and not gain any lift or maintain horizontal flight for any length. It’s better to be conservative in the amount of feathers clipped at first and have the owner return with the bird for additional clipping, as necessary.
  • Both wings should be clipped symmetrically.
  • Trim only primary feathers. Heavier bodied birds such as Amazon parrots or African greys may need only 2-3 feathers trimmed in this manner.

Alternatively, just the last inch or two of the outer primary feathers may be trimmed. With this trim, lift is reduced gradually. This is a nice trim to use on heavy-bodied birds or young birds after they have fledged and before receiving a more aggressive trim. Avoid trimming the feather at mid-shaft level. The edges of the remaining feathers are just the right length to poke into the side of the bird’s body and cause discomfort that can lead to feather picking and mutilation

Clinical Case Challenge

Prepared by: Orla Mahony, MVB, DACVIM, DECVIM

Case Description

Harry, a 9-year-old male castrated FIV positive, DSH cat, presented to the Internal Medicine Service at the Foster Hospital for Small Animals at Cummings School of Veterinary Medicine at Tufts University for a 5-month history of diabetes mellitus. An abdominal ultrasound had shown a hydronephrotic right kidney, an enlarged left kidney and changes suggestive of chronic pancreatitis. Fluid aspirated from the kidney had shown no evidence of infection or neoplasia. His blood work findings were consistent with iris stage 2, kidney disease (high normal creatinine) and mild anemia. He was receiving between 25 and 30 units of PZI insulin daily and was eating a low carbohydrate, high protein canned food. He was treated with flovent (fluticasone) inhaler as needed for wheezing. His owner was doing home glucose monitoring multiple times daily and adjusting his dose of insulin accordingly. Physical examination revealed a big cat (6.9kg) that had gained 0.5kg weight in the past 5 months. Snoring had been noted recently. His paws and legs were large but appeared unchanged to his owner. He had mild stomatitis, and unilateral renomegaly. Thoracic auscultation was normal.

Harry’s insulin dose is extraordinarily high. Doses above 1.5-2 U/kg/injection of insulin are suggestive of insulin resistance. What are your differential diagnoses for insulin resistance in cats? What further tests would you consider, and what treatment options would you recommend?


Unregulated diabetes in cats can be caused by problems with insulin handling and administration. It is important to make sure that the owner can mix, draw up and administer the insulin dose correctly using the appropriate insulin syringe. 40-U/ml syringes are required for U40 insulin such as PZI. The expiration date should be checked and it is worthwhile to replace the insulin before doing further tests. Often the duration of action is too short especially if using NPH or vetsulin in cats. Dose increases may only result in rapid decreases in blood sugar and/or hypoglycemia with rebound hyperglycemia (somogyi). It is important to perform a serial glucose curve after adjusting the insulin dose to make sure this is not happening. A switch to a longer acting insulin such as PZI, insulin glargine or detemir might be beneficial.

Insulin resistance can also occur secondary to any underlying disease that results in elevation of the counter regulatory hormones: catecholamines, glucagon, growth hormone and cortisol. Examples include chronic infection (urinary tract infection, dental disease), chronic inflammation (pancreatitis), hyperthyroidism, acromegaly, hyperadrenocorticism and functional adrenal tumors. Drugs associated with insulin resistance include glucocorticoids and progestagens (megestral acetate).

An extensive work up by Harry’s veterinarian had identified potential causes of insulin resistance, including kidney disease, chronic pancreatitis, FIV infection and intermittent use of an inhaled corticosteroid. Hyperthyroidism and urinary tract infection had been ruled out. Harry’s owner had no issues with insulin administration and was successfully performing serial blood sugar curves. PZI insulin is long acting and the bottle had been replaced with no change in glucose control. Before referral, Harry had an insulin-like growth factor 1 (IGF-1) concentration measured. It was high at 578 nM/L (range 12-92nM/L).

Although Harry had many underlying conditions that could contribute to insulin resistance, acromegaly is a condition that is associated with extreme insulin resistance and often necessitates high insulin doses for control. The screening test for acromegaly is IGF-1. Growth hormone stimulates IGF-1 secretion by hepatocytes in the presence of insulin and, therefore, is best tested after cats have been on insulin and are not newly diagnosed. Concentrations may be elevated in diabetic animals, but levels above 100nM/L are suggestive of acromegaly and warrant further investigation.

Figure 1: Transverse T1-W post contrast image of the brain at the level of the pituitary.  The pituitary is enlarged, with a non-contrast enhancing nodule (arrow).

Figure 1: Transverse T1-W post contrast image of the brain at the level of the pituitary. The pituitary is enlarged, with a non-contrast enhancing nodule (arrow).

At the time Harry was evaluated, a commercial growth hormone assay was available. Harry’s level was 16.9ng/ml and values >10 are believed to be consistent with acromegaly. Harry was scheduled for an MRI that showed a large pituitary tumor (Figure 1). Follow up abdominal ultrasound showed no change in the hydronephrotic right kidney, renal values were stable, and a repeat urine culture was negative. Acromegaly was considered the predominant cause of Harry’s insulin resistance.

Acromegaly is the result of a growth hormone secreting tumor (hypersomatotropism) of the anterior pituitary gland. It is believed to occur in up to one quarter of diabetic cats and should be considered in any poorly regulated diabetic cat. An IGF-1 concentration over twice the high normal range is very suspicious, but the only way to confirm the diagnosis is with a CT or an MRI. Acromegalic cats commonly have upper airway stridor like Harry. They often gain weight and they may have big paws, a broad head and spacing between their teeth. A protruding tongue and prognathia may be observed. Many owners do not notice a change in their cat’s appearance. Weight gain occurs in over 50% of cats. Heart and kidney disease are common complications of acromegaly.


Options for management of acromegaly include radiation therapy and surgery. Conventional external beam radiation therapy involves 5 to as many as 20 small fractions of radiation over a three- to four-week period of time. Stereotactic radiosurgery involves 2 to 4 large fractions of radiation, delivered using sophisticated technology, to a precisely targeted area, minimizing damage to surrounding healthy tissue.

Hypophysectomy (surgical removal of the pituitary gland) is the treatment of choice in people and has been successfully performed in the Netherlands on cats. It requires considerable training and expertise to become proficient.

Drug therapy is commonly used in people and includes somatostatin receptor analogues, such as octreotide that block GH release from the pituitary. The only analogue shown to be effective in cats is pasireotide (Signifor®, Novartis) given bid or pasireotide LAR given once monthly. The long acting product is currently under investigation in people in the US, and may be an option for our patients in the near future, albeit an expensive one. In a UK study using pasireotide LAR in 12 acromegalic cats, 3 achieved remission. Gastrointestinal side effects occurred in 9 cats. Dosing may need to be individualized.

For many cats with acromegaly, insulin therapy is the only option. Insulin doses should be gradually increased to a level required to control their diabetes. These doses can be extremely high and should only be done with home blood glucose monitoring. Owner’s need to be advised that occasionally cats can become transiently sensitive, making high doses potentially unsafe. By the time of presentation to Tufts Harry was receiving over 30 units of insulin (PZI and regular insulin) divided three times daily.

Harry was entered into a stereotactic radiosurgery study at Colorado State University and received four fractions of radiation therapy. He was in diabetic remission 3 months later. Harry’s remaining functioning kidney deteriorated and he died of chronic kidney disease 2 years following his diagnosis of acromegaly.

Clinical Case Challenge

Oscar, a 10-year-old male castrated Yorkshire terrier, presented to the Tufts Foster Hospital for Small Animals at Cummings School Radiation Oncology Service for a several month history of nasal signs. Oscar’s owners initially noted increased sneezing and increased respiratory noise/congestion approximately six months prior that was non-responsive to treatment with steroids and antibiotics. Intermittent unilateral epistaxis was then noted approximately three months prior. This progressed to a mild but noticeable facial deformity approximately three weeks prior to presentation.

On presentation to Foster Hospital for Small Animals, physical examination revealed a mild facial deformity over the dorsal maxilla. There was no evidence of nasal, ocular, or aural discharge but no airflow was present from the left nare. Nuclear sclerosis was present bilaterally and retropulsion of both eyes was normal. Mild dental calculus was present. The mandibular lymph nodes were mildly enlarged but soft and symmetrical. Thoracic auscultation and abdominal palpitation were unremarkable.

Based on examination findings, what are your primary differential diagnoses? What further diagnostics would you consider, and what treatment options would you recommend?

Based on the clinical history of epistaxis and presence of facial deformity, neoplasia is the primary differential diagnosis. Adenocarcinoma is the most common nasal tumor in dogs. Additional neoplastic considerations include undifferentiated carcinomas, squamous cell carcinoma, fibrosarcoma, chondrosarcoma, osteosarcoma, and lymphoma. Non-neoplastic differentials are considered less likely, but include fungal infection (aspergillosis most common), other infectious rhinitis, or foreign body.

Figure 1. Contrast-enhanced, soft-tissue window CT image of the initial CT scan, displaying a large, destructive heterogeneously contrast-enhancing, left-sided nasal mass, extending into the right nasal cavity invading into the right size with destruction of the left nasal and maxillary bones.

Figure 1. Contrast-enhanced, soft-tissue window CT image of the initial CT scan, displaying a large, destructive heterogeneously contrast-enhancing, left-sided nasal mass, extending into the right nasal cavity invading into the right size with destruction of the left nasal and maxillary bones.

A diagnostic workup for nasal tumors includes obtaining a sample of cells, usually through a biopsy to establish a definitive diagnosis. Options for biopsy include transnostril core sampling, blind or rhinoscopy-guided pinch biopsy, nasal flushing or punch biopsy of facial deformities. The latter option was performed on Oscar and histopathology revealed nasal adenocarcinoma. Staging tests then helped to determine the extent of disease through the body as well as a dog’s general health. These tests included blood work with a complete blood count and serum chemistry profile, urinalysis, chest x-rays, abdominal ultrasound and aspirates of the regional lymph nodes (if enlarged). This information is used to develop the best treatment plan for an individual patient. Oscar’s blood work and urinalysis were unremarkable. An abdominal ultrasound revealed hepatic and splenic nodules. Ultrasound-guided fine needle aspiration of the hepatic nodules revealed moderate hepatocyte vacuolization, a suggestion of glycogen deposition, and fine needle aspiration of the spleen revealed reactive lymphoid tissue. The mandibular lymph nodes were aspirated and found to be reactive. Oscar subsequently underwent a CT scan of his head for radiation therapy planning and a thoracic CT scan to complete staging. The CT scan revealed a large (1.7 x 2.7 x 3.1 cm), destructive, heterogeneously contrast-enhancing, left-sided nasal mass, extending into the right nasal cavity invading into the right size (Figure 1). The mass was causing destruction of the left nasal and maxillary bones, the right and left aspect of the cribriform plate and the left palatine and frontal bones with extension into the left retrobulbar space. The left mandibular lymph node was mildly enlarged. There was no evidence of pulmonary metastasis.

Nasal carcinomas are the most common type of nasal tumor in dogs, accounting for ≥50-75% of all nasal tumors in dogs. Nasal tumors are relatively common in older dogs and long-nosed dog breeds seem to be predisposed. Nasal cancer is a progressive disease, that mostly affects dogs through space occupation, local destruction, and invasion of nearby tissues and can lead to clinical signs such as nasal discharge, nose bleeds, facial deformity, and occasionally neurologic deficits (such as seizures). Metastatic potential to other areas of the body is low with nasal carcinomas (<30% metastatic rate), but it can happen, and usually occurs in the lymph nodes and lungs, often later in the disease course.

Surgery is not typically recommended for nasal tumors in dogs due to the location of the tumor and inability to remove the entire tumor.

Definitive radiation therapy allows for the best control over future tumor growth with the average survival time being 1 to 1.5 years for most nasal tumors. This treatment plan typically involves 16-19 daily treatments (M-F) under a light plane of general anesthesia. There are some short- and long-term side effects associated with definitive radiation therapy. Short-term side effects typically arise midway through the treatment cycle and peak around the end or 1 week following completion of radiation therapy before healing. Short-term effects include: dry eye and/or conjunctivitis; erythema, hair loss, and dry or moist desquamation of the skin; and inflammation to the oral cavity and throat. We typically manage these short term side effects with oral antibiotics (if indicated), anti-inflammatory medications, pain medications, and topical eye medications. There is also a small risk of long-term effects from radiation therapy, which may develop several months to years after treatment has finished. These effects include: chronic nasal discharge/sneezing, dry eye, cataracts (typically begin to develop around 9-12 months post radiation), bone or soft tissue damage/cell death, and rarely (<3-5% incidence at 3-5 years post radiation) secondary tumor induction.

A less aggressive course of radiation, termed palliative radiation therapy, may also be considered. This treatment protocol typically involves either 6 once weekly treatments or 10 daily radiation treatments (M-F), but other protocols are also available. Palliative radiation generally decreases the number and severity of the potential short-term side effects mentioned above to a very mild level, if at all. This treatment plan is associated with a median survival time of approximately 6-10 months for nasal tumors.

Figure 2. Graphical representation of Oscar’s 3-D conformal radiation therapy plan. The target volume is represented by the red shaded region. The concentric colored lines represent the dose level as a percentage of prescription dose.

Figure 2. Graphical representation of Oscar’s 3-D conformal radiation therapy plan. The target volume is represented by the red shaded region. The concentric colored lines represent the dose level as a percentage of prescription dose.

Although radiation therapy is considered the gold standard for treatment of nasal tumors, chemotherapy can also be considered. There are two different chemotherapy options: conventional and non-conventional chemotherapy. Conventional chemotherapy for treatment of nasal tumors is typically intravenous therapy with a platinum agent, such as cisplatin or carboplatin. Reported response rates are low at approximately 30%. Non-conventional chemotherapy for treatment of nasal carcinomas includes use of the small molecule inhibitor, Palladia. There is little clinical research regarding response rates with Palladia treatment in nasal carcinomas but anecdotally it seems to have some efficacy.

Figure 3. Contrast-enhanced, soft-tissue window CT image of recheck scan at 7 months post radiation  therapy, displaying resolution of the previously described contrast enhancing soft tissue mass associated  with the nasal cavities but persistent loss of the left nasal and maxillary bones.

Figure 3. Contrast-enhanced, soft-tissue window CT image of recheck scan at 7 months post radiation therapy, displaying resolution of the previously described contrast enhancing soft tissue mass associated with the nasal cavities but persistent loss of the left nasal and maxillary bones.

In the case presented herein, after discussion with the owners, definitive radiation therapy was performed. Oscar underwent 16 daily radiation therapy treatments (Figure 2). Halfway through the radiotherapy course, the facial deformity was nearly completely resolved. Epistaxis also resolved. He experienced moderate inflammation to his skin and oral cavity secondary to the radiation therapy, which resolved by 2 weeks post radiation therapy. Oscar was subsequently monitored every 3 months via physical exam and thoracic radiographs. Repeat CT scan at 7 months post radiation therapy revealed complete resolution of the previously described contrast enhancing soft tissue mass associated with the nasal cavities (Figure 3). There was persistent right displacement of the nasal septum and loss of the majority of the left nasal turbinates, as well as persistent loss of the left nasal and maxillary bones, left palatine bone, and right and left cribriform plate.

Clinical Case Challenge: Animal Behavior Clinic

Digital StillCameraCase Description

A 2.5-year-old miniature dachshund named Otto, presented to the Animal Behavior Clinic at Cummings School of Veterinary Medicine at Tufts University for the sudden onset of aggression to his owners. The aggression consisted of growling, lunging, snapping and biting. Lifting him, attaching a leash and approaching him while resting triggered an aggressive response. He used aggression to guard valued resources, such as his food bowl, long-lasting treats and objects he had taken that did not belong to him. He growled or snapped when petted. He was more likely to attack when he was on an elevated level, such as a sofa or lap. The aggression was intermittent, giving the impression of unpredictability to the owners.

Otto’s referring veterinarian conducted a thorough physical examination. A CBC, chemistry and total T4 were within normal limits. Medical causes of behavioral changes secondary to hypothyroidism, hepatic insufficiency, painful conditions, such as IVDD or orthopedic issues were ruled out.

What is your diagnosis and what treatment would you recommend?


The correct diagnosis is conflict aggression, which is characterized by aggressive behavior directed toward owners in response to a perceived provocation. Triggers can be separated into three categories: resource guarding (e.g., resting places), postural interventions (e.g., lifting, petting, nail trims) and when owner takes on a leadership role (e.g., grabbing the collar, removing from furniture, reprimands, physical punishment). A dog with this problem may behave differently to different individuals in the family. The behavior may also appear unpredictable to owners because it is intermittent. For example, a dog may tolerate being picked up one day and not the next. However, close questioning reveals that there is generally a predictable set of triggers that at least sometimes, will lead to an aggressive response.

This diagnosis used to be called Dominance Aggression. However, our current understanding is that this form of owner-directed aggression is rooted in anxiety, not confidence. Conflict-aggressive dogs are temperamentally bold. However, their anxiety renders them impulsive and reactive toward members of their social group. Studies have shown that conflict-aggressive dogs have lower levels of the transmitter serotonin. (Çakiroǧlu 2007). This condition can be inherited genetically, as seen by its increased frequency in certain breeds, such as dachshunds, chihuahuas, Australian cattle dogs, and others (Serpell 2008). Insufficient early socialization can also predispose dogs to conflict aggression. While the seeds of conflict aggression are planted early in life, it usually manifests at social maturity (9 -24 months of age.)

Important differentials are Irritable Aggression, Fear Aggression and Rage Syndrome (partial complex seizures). Irritable aggression occurs when a dog has a painful medical condition that lowers his or her aggression threshold. Fear aggression is commonly directed at people outside of the dog’s inner circle of family and friends. Rage syndrome occurs in response to a trivial trigger or no trigger at all. It is prolonged and often accompanied by a pre- and postictal behavior change. Dogs may have multiple diagnoses.


Treatment consists of behavioral modification in which triggers of aggression are strictly avoided and steps are taken to improve the owner’s benign leadership position in the eyes of the dog. Changes in diet and exercise are also part of the treatment regimen.

Exercise and Diet:

The owners were instructed to provide Otto with an hour a day of aerobic exercise. They were also told to feed a diet low in protein and free of colorings and preservatives. Exercise and diets lower in protein may help to stabilize serotonin in the brain.


Neutering was recommended as it has been associated with a decrease in aggression. (Tsu 2010)

Avoidance of Conflict and Triggers of Aggression:

The list of triggers was discussed in depth with the owners, and strategies were developed to avoid them. It was explained to the owners that avoidance is therapeutic in that it prevents Otto’s continued sensitization to interactions that he does not like, thereby building trust. The owners were told to no longer permit Otto on laps or furniture and to leave him alone when he rested in his own bed. He should not be lifted up the stairs or into the car. He should not be given any chews or toys he would guard. If he had a stolen object, the owners were instructed to let him have it if it were not dangerous for him or valuable to them. If it were necessary to take it away from him, they were instructed to use a distraction technique such as ringing the doorbell or asking him to go for a walk, then picking it up when he left the room. They were instructed to decrease the frequency and duration of petting sessions. The owner developed a very clever leash and collar combination that could be slipped over his head and fixed onto him from a standing position.


The owners were instructed to strengthen their leadership position by having Otto obey a command before both of his twice daily meals and all food treats. Once his food was prepared, Otto was told one time to sit. If he obeyed, the food was put down instantly and the owner was to walk away. Otto was given 15 minutes to eat. All uneaten food was picked up to prevent guarding. If he did not obey the command to sit, his food was put away and he was not to be fed again until the next meal. If he anticipated the command by sitting before he was told, he was given a different command, such as down. The owners were also instructed to ignore demanding and attention-seeking behaviors.


Fluoxetine (Prozac) was prescribed at 1 mg/kg once daily. Fluoxetine is a selective serotonin reuptake inhibitor that stabilizes mood, increases confidence and decreases reactivity and impulsivity.


Weekly follow-up phone calls were instituted to check in about the program. Each episode of aggression was discussed in detail and the behavioral modification plan was adjusted. The dose of fluoxetine was adjusted once. Otto was neutered.


Three months after the consultation, aggression decreased from one episode per day to one per week. Six months after the consultation, aggression occurred less than once per month.


  1. Duffy D, Hsub Y, Serpell JA, Breed differences in canine aggression Applied Animal Behaviour Science, Volume 114, Issues 3–4, 1 December 2008, Pages 441–46
  2. Çakiroǧlu D, Meral Y, Sancak AA, Çifti G, Relationship between the serum concentrations of serotonin and lipids and aggression in dogs Veterinary Record 2007;161:59-61 doi:10.1136/vr.161.2.59
  3. Hsu Y, Liching Sun L, Factors associated with aggressive responses in pet dogs, Applied Animal Behaviour ScienceVolume 123, Issues 3–4, March 2010, Pages 108–123