Common Avian Emergencies

The critically ill avian patient

The most commonly presented avian emergency is that of the critically ill bird. Most often these are birds are found on the bottom of the cage with little if any history of prior signs of illness. The symptoms, visual examination, and initial diagnostics will often establish the direction of treatment and specific diagnostic tests. The following are common problems grouped by system. The patient that presents with only depressed mentation, and severe dehydration must be pursued aggressively until some clue is found to justify its condition. A diagnosis for the birds state of decompensation gives the patient the greatest chances for survival.

Hypocalcemia syndrome

African Grey parrots (Psittacidae), both Timneh and Congo sub-species, are rarely affected by a hypoglycemia syndrome (although there appears to be a decrease in it’s frequency in our practice, perhaps due to increased awareness of nutritional needs). Young birds 2 to 5 years of age are most commonly effected. Signs may range from incoordination to status epilepticus. Hypocalcemia should be on the differential diagnosis of any grey parrot with neurological signs. Grey parrots (Psittacidae) presented in seizure should be treated presumptively with intravenous calcium gluconate as well as with diazepam.

Respiratory emergencies

Difficulty breathing is a common complaint in birds presented for emergency or critical care. After administering oxygen or establishing an airway and adequate ventilation, a thorough evaluation of the animals respiratory tract must be performed to determine the cause of the problem. Character of respiration may be helpful in making a diagnosis and appropriate treatment. Primary pulmonary disease (pneumonia, pulmonary congestion or hemorrhage), upper airway obstruction and abdominal disease that interferes with the filling of air sacs may all present as respiratory distress.

Pulmonary disease may result from a variety of causes including heart disease, fungal, bacterial, viral and parasitic pneumonia or pneumonitis, and airborne toxins. Symptomatic treatment should include oxygen, antibiotics, and other supportive therapy such as diuretics. The use of bronchodialators and corticosteroid are controversial. Nebulization of medication and or humidification will benefit some patients.

Upper airway obstructions are common avian emergencies. Inhaled foreign bodies (e.g., millet seeds inhaled by cockatiels), fungal and bacterial granuloma at the syrinx and glottal papillomas may result in near total to total obstruction. These patients present with a history of acute onset of dyspnea, often with no previous sign of disease. Initial evaluation of respiration may show open mouth breathing, inspiratory and/or expiratory stridor, very often with a musical squeak-like respiratory sounds originating at the glottis or syrinx combined with cyanosis are suggestive of upper airway obstruction. The cyanosis and signs of distress may become evident with any stress or restraint. The decision of what point to intercede and intubate the air sac should be based on whether the patient can tolerate diagnostic and therapeutic care without becoming cyanosis. If cyanosis with or without restraint, intubation should be considered.

Bleeding and blood loss

The sight of blood strikes fear in all bird owners and is a common emergency presentation. Hemorrhage may result from numerous causes including trauma, infectious disease, metabolic and nutritional causes, and neoplasia. Trauma is the most common cause of hemorrhage. The majority of the birds bleeding due to minor trauma can be easily treated. Bleeding blood feathers, fractured or avulsed toenails and beaks, and traumatized wing tips make up the majority of these cases. Bleeding blood feathers must be pulled. Even if the bleeding has stopped, it may resume if the tip of the growing feather brushes a perch, or is groomed by the bird. If the feather appears to be gone but continues to bleed, look or palpate for a remnant of the feather shaft in the follicle (BE GENTLE!). Once the feather is pulled do not put hemostatic agents in the follicle! The bleeding will usually stop if the follicle is pinched closed for 60-90 seconds. If the hemorrhage continues try gluing the follicle closed with a drop of tissue cement in the opening of the feather follicle. Bleeding toenails may be cauterized with a mild styptic such as ferric sub-sulfate or the quick may be covered with a thin layer of tissue cement. Broken beaks are occasionally difficult to stop bleeding. This is particularly true with slab-type fractures of the tip of the upper beak or rhinotheca (common with cockatoos and African Grey parrots (Psittacidae). These fractures may be difficult to diagnosis due to blood spreading from the tip of the beak to the tongue, giving the appearance that the origin of the hemorrhage is elsewhere in the oral cavity. The bleeding will often stop if the broken surface is filed or ground smooth. This also appears to make the broken tip less irritating to the bird. The tip of the beak may be cauterized with hemostatic powder if needed.

Hemorrhage secondary to more significant trauma, such as lacerations of major vessels, hematoma, or fracture of the liver, spleen or kidney is immediately life threatening. The first goal is to recognize the hemorrhage. This is not a problem when trauma results in external hemorrhage. The greater challenge is to recognize internal blood loss. The hemorrhage must be slowed or stopped and restorative therapy initiated in order to prevent the bird from bleeding out and support vital organ function. The rate that blood is lost from the circulation is the determining factor in its mortality. Losing 20% to 25% blood volume over several minutes may be fatal where the same volume lost over several hours is not. Generalized clinical signs of blood loss include pallor of skin, nails and mucous membranes, delayed capillary refill time, increased cardiac and respiratory rates, thin appearance to blood visible in peripheral veins (median ulnar and jugular), generalized weakness, fear, and dyspnea, especially with restraint. More specific signs of hemorrhage depend on the location of the hemorrhage but may include bruising, distention and/or discoloration of the abdomen, and coolness of isolated limbs.

Timely diagnosis may make the difference between life and death in these cases and should be aggressively pursued. If hemorrhage is unapparent in an animal with a history of recent trauma, serous ongoing internal hemorrhage should be assumed to be ongoing until proven otherwise the patient should be hospitalized for several hours for observation.3 External hemorrhage is not difficult to diagnose. Volume of blood loss may be estimated with the aid of history, blood on the cage or carrier floor papers or in the materials used to wrap the patient prior to presentation. Diagnosis and/or assessment of blood volume loss is much more difficult with internal hemorrhage. Patients presented with a history of trauma along with signs of hypovolemia or hypotension should be assumed to have sustained internal hemorrhage. Hemorrhage into the bird’s abdomen and into bone and muscle compartments are the most common in the authors experience. Discoloration or bruising of the abdominal wall, especially along the ventral midline and caudal on the ventral abdomen, may give a clue to hemorrhage. Radiology and endoscopy may aid in locating the site. Removing the feathers from a traumatized limb or the trunk area may aid in locating hemorrhage in those locations. Bruised or swollen areas should be evaluated for an increase in the size of the swelling or diameter of the limb. Definitive location of internal hemorrhage may require exploratory surgery.

These cases must be treated by a veterinarian, preferable one familiar with avian patients. Treatment must be initiated early and progress rapidly if the patient with significant hemorrhage is to survive. Direct pressure should be applied in those situations where it will not interfere with respiration. Clamp or suture vessels that are readily accessible. In some cases, the application of elastic bandage wraps to produce counterpressure to pelvic limbs may be possible to increase systemic vascular resistance and venous return to the heart. The resulting influx of blood acts as an “autotransfussion” of blood pooled in the limbs. The degree of stress created by wrapping the limbs must be weighed against the benefits of increasing blood pressure. Counterpressure pneumatic “garments” are not available for avian patients and counterpressure may not be applied to the abdomen to avian trauma patients due to their need to expand abdominal air sacs for respiration. An intraosseous or intravenous catheter should be placed for the rapid administration of fluids to restore systemic pressures. Whole blood, plasma, colloid plasma expanders, hypertonic (7.5%) saline or crystalloid solutions have been recommended. Fluids should be continued until systemic pressures are at or slightly greater than normal. The single heterologous blood transfusion has been shown to be safe and anecdotally demonstrated to be efficacious.30,31 Studies of radio-labeled (51Cr) red blood cells administered as either homologous or heterologous transfusions have suggested the half-life of the transfused cells to be substantially shorter than previously thought. These studies imply that heterologous transfusions (blood from different species) may be of little or no benefit and homologous transfusions (from a bird of the same species) of only limited benefit.

Anemia

As with bleeding, a bird presented with signs of anemia must first be evaluated to determine the cause of the anemia, the degree of blood loss as well as the site or the reason new cells are not being produced. Gastrointestinal bleeding, genitourinary bleeding along with hemolysis may be difficult to diagnosis. Hematochezia (red blood in the stool), typically from lesions in the lower GI tract, and melena (black tar-like digested blood), associated with gastritis, enteritis and ulcers of the gastrointestinal tract, GI foreign bodies, primary and secondary coagulopathies and hepatopathies. Cloacal bleeding may be associated with severe cloacitis, cloacal or uterine prolapses, papillomas, and other cloacal masses, and egg laying. Heavy metal poisoning (see lead or zinc poisoning) and chlamydiosis may result in hemolysis or bone marrow depression anemia.

Bite Wounds

Scratches and bite wounds very often lead to a fatal septicemia if not treated aggressively. The patient should be evaluated for its overall condition and treated appropriately for blood loss or hypotension. The extent of wounds should be evaluated. If the patient’s condition allows, wounds should be thoroughly flushed and fractures stabilized. Aggressive antibiotics should be begun early in treatment. Piperacillin or cefotaxime combined with amikacin or tobramycin are a good choice and should be continued for a minimum of 5 days is indicated in these cases. If septicemia is suspected treatment for septic shock should be instituted (intravenous fluids, rapid acting steroids, and intravenous bactericidal antibiotics).

Fractures

Fractures should be splinted as soon as the birds condition is stable to prevent further complication. Simple bandaging techniques may be employed to provide adequate stabilization until definitive treatment is possible. Fractures of the distal wing, including the radius and ulna, carpus, and manus, may be immobilized with a figure-8 bandage. Humeral fractures, shoulder luxation and fractures of the shoulder girdle should be splinted to the birds body utilizing a figure-8 bandage followed by wrapping the limb to the body in such a manner as to support the limb but not restrict respiration or interfere with the birds legs. The opposing wing should be left out of the wrap. Fractures of the leg below the stifle may be immobilized with an Altman tape bandage or a modified Robert Jones bandage with or without an acrylic half cast. Fractures of the femur require a Spica splint if they are to be splinted externally until surgical repair can be accomplished. See chapter TT on Hospital techniques.

Burns

Burns are not uncommon in avian medicine. Most common burns result from contact with hot liquids, water (scalds) or cooking oil, electrical burns from chewing on electrical wires and from being fed hot formula in pre-weaning bird. Burns resulting from entrapment in burning buildings or inside containers (chick incubators with burning bedding) are not as common but are much more difficult to treat with the complication of smoke inhalation.

The burns of avian patients may be classified by their severity, superficial, partial thickness and full thickness burns. Superficial burns, where only epidermis is effected, resulting in transient erythema and desquamation of epidermis and the site is highly sensitive or hyperesthetic. Clinical signs include hyperemia, desquamation, and pain. Partial thickness burns are those where the burn depth extends to the mid-dermis. Loss of epidermis is complete, capillaries and venule in the dermis are dilated, and congested, and they exude plasma. The site may be painful (especially feet, legs and facial skin), but sensitivity is decreased. Clinical signs include exudation, pain and decreased sensitivity. Change in ease of feather pulling (as noted with hair in mammals) may not be effected due to the depth of the feather follicle. Full thickness burns, result coagulation of epidermis and dermis so that they are no longer vital. Severe edema of the subcutis develops from the increased permeability of deep vessels and necrosis of the damaged tissues occurs, resulting in dry, leathery eschar. Feathers may be easily pulled if the burn is deep and scaled skin may peel easily. Clinical signs include necrotic tissue without sensation, subcutaneous edema, little or no pain and feathers that are easily pulled. Other signs of burns may include respiratory signs from smoke inhalation and carbon monoxide poisoning, hypovolemia and hypotension (“shock”) may be present in animals with severe burns, dehydration from loss of fluids, anorexia, and polyuria secondary to stress or inability to eat in the case of crop burns.

Diagnosis is typically made based on history and clinical signs. Smoke exposure should be expected in situations where smoke accompanied the burn, especially in an enclosed space or involved materials with a likelihood of producing toxic fumes. A through physical examination may revel the involvement of other organs. If greater than 50% of the body surface is involved in the burn with partial or full thickness burns the prognosis is grave and the client may want to, consider euthanasia. It is important to advise the client that the condition of the patient may become much worse before it improves. Look for signs of hypovolemia or hypotension. Evaluate for signs of infection and pain. Diagnostics testing should include radiographs, in cases exposed to smoke, to evaluate pulmonary injury. Hemogram, serum electrolytes are indicated in severe or extensive burns.
Initial observation and evaluation should include evaluation to determine the level of therapy required for the extent and depth of the burn. Birds with severe or extensive burns need emergency treatment. Dyspneic birds often have laryngeal edema and upper airway excretions benefit from an air sac tube and oxygen. An intraosseous catheter should be placed and the bird treated for shock. An initial bolus of fluids using Lactated Ringer’s solution or some other balanced crystalloid electrolyte solution. A short-acting glucocorticosteroids such as hydrocortisone Na succinate or Prednisolone Na succinate may be given. Systemic bactericidal antibiotics, such as Piperacillin, should be initiated in patients with severe burns that may complicated by infection or any burn that will not be treated in the hospital environment.

If the burn is recent, treating the site with cold water or compresses to minimize coagulation and minimize the extent of the burn and decrease the burn depth by dissipating heat. Continue cold compresses period of 20-30 minutes after the time of the burn. Body temperature must be monitored during this procedure, especially in very small patients. Superficial burns should be gently cleansed using saline with 5% povidone iodine (Betadine) or chlorhexadine (Nolvasan, ) solution. Partial and Full thickness burns should be gently cleansed and necrotic tissue and any foreign material removed daily then treated topically with a water soluble antibiotic dressing such as silver sulfadiazine. The lesions may be covered with a sterile dressing or left uncovered based on the likelihood of contamination and injury by the patient. This procedure is very painful and should be performed under general anesthesia. Early surgical intervention may shorten the course of therapy of some small partial and full thickness burns.

Burned birds should be monitored for blood loss and loss of body proteins. Plasma or colloidal fluids may be required in patients where total solids and hence osmolality drops below 1.0 g/dL. Renal function should be monitored by number of droppings and urine volume, uric acid and serum electrolytes. Continued fluids and judicious use of diuretics is indicated in birds with decreased urine output. White blood cell counts are commonly increase within 24 to 48 hours and persist for 5 to 10 days (in the authors experience). Pain medications (analgesics) are indicated in cases where the bird is in pain (see above).

Complications most likely to occur include circulatory collapse, decreased renal function (oliguria), renal failure and sepsis. Circulatory and renal complications are most likely to occur within the first 24 to 48 hours. This emphasizes the need to monitor hydration (PCV and TS) and renal function (uric acid, electrolytes and urinalysis). Infection is a common cause of death in birds surviving the initial injury. The most common agents cultured from the burns of avian patients has not been reported but is assumed to be the same opportunists that infect the burns of mammals, Pseudomonas, Streptococcus, Proteus and Candida. Prevention of burn sepsis involves early wound cleansing and closure when indicated; topical antibiotics, isolation of the patient in a clean, or if possible sterile, environment and maintaining sterility of the burn site. It is similarly important to monitor the patient’s WBC and note any discharge or odor from the lesion. Wet dressings should be changed often using sterile technique and early initiation of parental antibiotics if evidence of infection develops. Other potential complications include pneumonia, complications of scaring or difficulties of healing, especially in areas where tissues move.

Crop burns

Crop (thermal) burns in young birds and chemical burns in adult birds are not unlike other burns. Superficial burns may result in the chick refusing food and lead to secondary bacterial and fungal (yeast) infections. Partial thickness and full thickness burns may be identified early by edema of the tissue overlying the crop. Many partial thickness burns will result in the formation of an eschar that will later open to a fistula. Full thickness burns may result in the death of the chick. Partial and full thickness crop burns should be treated as any other burn.

Poisonings

Poisonings are not common presentations in avian emergency medicine, but do occur and involve a wide assortment of toxins. In principal the treatment of poisonings in birds are same as for other animals. That is treat the patient, not the toxin.31,32 The patient presented with abnormal clinical signs should first be stabilized, an airway established, and respiration initiated if necessary. Cardiovascular needs should be addressed. In general, fluids should be administrated to maintain circulatory volume and pressure and support renal function. Seizures or other problems involving the central nervous system should be addressed, and body systems and general metabolism supported. Further exposure should be prevented and further absorption prevented or delayed. Soiled birds should be bathed, crops may be lavage and absorbent or cathartics administered. Specific antagonists or antidotes are available for a few toxins and should be used in those instances when a safe dosage is known. Lastly treatments that may facilitate the removal of the toxin, such as diuresis, should be instigated.
Zinc and Lead Poisoning / Heavy Metal Toxicity

Heavy metal toxicity is the most common form of poisoning reported in avian medicine. Lead is ubiquitous in the environment, and psittacine birds (parrots (Psittacidae) seem to be attracted by the malleable nature of the metal. Common sources of lead exposure in pet and aviary birds include: curtain weights, leaded glass lamps and windows, fishing weights and lead shot, lead solder in electronic appliances and costume jewelry, lead foil from wine bottles, lead in paint, putty and caulking products and linoleum. Some large cities with old water systems may have high levels of lead in the drinking water that may lead to accumulated lead toxicity. Sources of zinc include: Galvanized cage wire, staples and nails and food containers, zinc containing products such as zinc oxide and US pennies. Other metal toxicities reported in birds include copper, iron, mercury and arsenic.32

Lead Poisoning

Lead is a systemic, heavy metal poisoning that adversely effects every body system to which it is distributed. Abnormalities and clinical signs may vary with species, and dose and duration of exposure. Signs may be vague and nonspecific causing lead poisoning to be added to many lists of differential diagnosis. Neurologic, hematopoietic, gastrointestinal, renal and immunological systems are most often involved. Central and peripheral nervous system signs include dull or poorly responsive mentation, wing droop, incoordination, muscle twitches and seizures. Central nervous signs are the result of perivascular edema, increase in cerebrospinal fluid, necrosis of nerves, and changes in neuronal metabolism. Peripheral neuropathy results from competition for calcium at neuronal junctions acutely and in more chronic cases, lead induced demyelination.34 Frequently symptoms are associated with the central nervous system. Incoordination, poor balance, muscle twitches or fasciculation, and (occasionally) seizures may result. Many of the clinical signs and laboratory findings result from lead damage to red blood cells leading to premature destruction. The anemia, polychromasia and anisocytosis is secondary to disruption of the formation of heme. The premature destruction of RBC’s results in biliverdinuria (yellow-green to green-black coloration of urine and urate). In amazon parrots (Psittacidae), and occasionally other species, hemoglobinuria which presents as a classic “chocolate milk”-to-blood colored dropping, may occur.35 With or without CNS signs lead should be suspected in these patients. Many birds with lead toxicity are polyuric. Polyuria results from renal tubular damage caused by both the lead and hemoglobin. Gastrointestinal signs include anorexia, regurgitation, gastrointestinal stasis or ileus including proventricular dilatation. Gastrointestinal signs are the result of both local effects of the lead on the gastrointestinal tract and neurological pathology.

Radiography may or may not show metal in the ventriculus or elsewhere in the gastrointestinal tract. Other changes may be those related to ileus. Laboratory changes hematological effects of lead include mild-to-severe anemia, changes in red cell morphology, including margination of hemoglobin, polychromasia, hypochromasia, and anisocytosis. See chapter HH on hematology. Serum chemistries may show elevations of LDH, AST, CPK and uric acid. Blood lead levels greater than 20 ?g/dL (0.20 ppm) is suggestive of lead toxicity, levels greater than 50 ?g/dL are diagnostic. Delta-amino levulonic acid dehydratase (ALAD) is inhibited by lead. ALAD levels have been used to diagnose lead toxicity in waterfowl and occasionally in cage birds. See chapter on Toxicology.

Initial therapy consists of supportive therapy along with chelation. Supportive fluids SQ, IV or IO, depending on the degree of dehydration and volume of polyuria, thermal support, anti-seizure medication if needed, make up the supportive care. Chelation of circulating lead forms nontoxic complexes that are excreted in the bile or by the kidneys. Removal of circulating lead leads to equilibration of lead from tissue and bone for further chelation. Calcium disodium versonate (CaEDTA) is the treatment of choice for initial therapy.32,35 D-penicillamine (PA) may be added to the therapy and has the advantage of oral administration.32, 36

Other therapeutics, Diethylene triamine pentaacetic acid (DTPA) and Dimercaptosuccinic acid (DMSA) have been investigated as treatments for lead intoxication but lack the experience of use of CaEDTA and PA, and DTPA requires a special FDA permit. Therapies to remove metal fragments from the gastrointestinal tract have been suggested but have not proven successful. Cathartics, such as sodium sulfate (Gluuber’s salts) or magnesium sulfate (epsom salts), have been recommended to precipitate lead in the gastrointestinal tract. Large lead object, such as fishing sinkers, or other large fragments, may be removed using a rigid or (in large species) flexible endoscope, once the patient is stabilized. Surgical removal is indicated only as a last resort.

Zinc

Zinc toxicity is similar to lead and the combination of lead and zinc toxicosis is not uncommon. Zinc toxicity differs in pathology and clinical signs in that the kidneys, liver, and pancreas are target organs for zinc. Often poisoned psittacines present with generalized weakness and no other signs. Tentative diagnosis may be made based on history and the presence of metal in the gastrointestinal tract on radiographs. Definitive diagnosis is made based on blood or tissue levels greater than 200 ?g/dL and 75 ?g/dL respectively, although clinical signs may not be noticed until levels are as high as 1000 ?g/dL. Samples should be submitted in plastic containers as the rubber stoppers may leach zinc from the sample giving a false low result. Treatment for zinc toxicosis is the same as for lead. In the author’s practice, zinc intoxication carries a poorer prognosis than lead.

Other metal toxicity

Iron and copper toxicity are not common in avian medicine.

Pesticides: organophosphates and carbamates

Pesticides seen most often in avian emergency and critical care include insecticides, and rodenticides. The most common insecticides are organophosphates including diazinon, dichlorvos, dieldrin, dursban, and malathion and carbamates (carbaryl). Intoxication generally results secondary to ingestion through contamination of food or water, although secondary poisoning of wild insectivorous species may occur. Pathology and clinical signs result from binding of the insecticide to and inhibition of aetylcholenesterase (AChE) and the resulting accumulation of acetylcholine (ACh) at ganglia and neuromuscular junctions. Organophosphate bonds are irreversible but carbamate bonds are slowly reversible. Signs include anorexia, weakness crop stasis, ataxia, muscular twitching, prolapsed nictitans, increased respiratory secretions, dyspnea, bradycardia and death. Tentative diagnosis is based on history of exposure, clinical signs and response to therapy. Bradycardia not responsive to atropine at 0.02 mg/kg given IV is suggestive, but not established in avian medicine. Definitive diagnosis is based on cholinesterase assay from blood, plasma, or serum, paired with an analogous subject.

Specific therapy includes atropine, for carbamate and organophosphate toxicity. Pralidoximechloride (2-Pam) is effective early in organophosphate toxicity and should be given in cases that are presented soon after ingestion and continued providing that there is a positive response. 2-Pam is contraindicated in carbamate toxicity and has been reported to be toxic in raptors.
Anticoagulant rodenticides

First generation (warfarin) and second generation (brodifacoum and bromadoline) rodenticide intoxication or suspected intoxication caused by both primary and secondary exposure (carnivorous birds) are not uncommon presentations. These agents are vitamin K antagonists that deplete and block the synthesis of prothrombin, accessory factors VII, IX, X. As noted earlier, extrinsic clotting factors are not important in avian patients, and low levels of factor VII may decrease the effects of these products. Clinical signs include depression, anorexia, feather follicle and subcutaneous hemorrhage, petechial hemorrhages of oral and cloacal mucosa and bleeding from nares. Many of these patients will present with no history of exposure and no specific symptoms. Once hemorrhage is noted the prognosis is grave.

Treatment involves Vitamin K supplementation and, in critical cases, fresh whole blood transfusions. Vitamin K1 is administered by injection until stable then given SQ, IM or PO daily33 or fed in the diet at a rate of 800 g/kg of food. IM administration has been reported to result in hematoma formation in dogs with clinical signs of coagulopathy. This problem has not been reported and may or may not result in birds. Supplementation of menadione (K3) is not effective in counteracting anticoagulants. Due to increased potency and slower metabolism (at least in mammals) of the second generation agents, it may be necessary to administer vitamin K for several weeks to control bleeding.