- Toxicities are relatively rare in pet birds, with lead toxicity being the most common poisoning reported in companion birds.
- Lead can affect all major organs, particularly the brain, kidney, and gastrointestinal tract.
- Injectable calcium EDTA is the initial chelating agent of choice for heavy metal toxicity.
- Consider organophosphate or carbamate poisoning in birds with non-specific signs of illness, crop stasis, dyspnea, and/or neurologic signs including a prolapsed nictitating membrane.
Poisonings are relatively uncommon in companion bird emergency medicine, but these conditions do occur and can involve a wide assortment of toxins. In principal, treatment in birds is the same as for other animals. First, stabilize the patient presented with abnormal clinical signs. Establish an airway, initiate respiration, and address cardiovascular needs. Administer fluids to maintain circulatory volume and pressure, and support renal function. Address seizures or other central nervous system problems and support general metabolism. Halt further exposure to the toxin and prevent or delay absorption by bathing soiled birds, lavaging crops, and administering absorbents or cathartics. Use specific antagonists or antidotes when available if a safe dosage is known, and begin treatments that may facilitate toxin removal, such as diuresis.
Heavy metal toxicity
Heavy metal toxicity is the most common form of poisoning reported in avian medicine.
Lead is ubiquitous in the environment, and parrots seem to be attracted to its malleable nature. Common sources of lead include:
- Caulking products
- Costume jewelry
- Curtain weights
- Fishing weights
- Foil from wine bottles
- Glass lamps and windows
- Solder in electronic appliances
- Some large cities with old water systems may have lead in the drinking water.
Lead adversely affects every system to which it is distributed, with the neurologic, hematopoietic, gastrointestinal, renal, and immunological systems most often involved. Clinical signs may vary with species, dose, and duration of exposure. Signs may also be vague and nonspecific.
- Central and peripheral neurologic signs include dull mentation or somnolence, wing droop, ataxia, muscle fasciculations, and occasionally seizures.
- Lead can also damage erythrocytes leading to premature destruction and subsequent biliverdinuria (yellow-green to green-black coloration of urine and urate). Disruption of heme formation leads to anemia, polychromasia, and anisocytosis. In Amazon parrots (Amazona spp.), and occasionally other species, hemoglobinuria (“chocolate milk”-to-red colored urates) may occur (Fig 1).
- Many birds with lead toxicity are also polyuric due to renal tubular damage caused by both lead and hemoglobin.
- Gastrointestinal signs, such as anorexia, regurgitation, and ileus, result from both local effects of lead on the gastrointestinal tract and neurological pathology.
Diagnosis of lead toxicity relies on imaging and laboratory testing.
- Radiographs may or may not show metal in the ventriculus or elsewhere in the gastrointestinal tract. Other radiographic changes such as proventricular dilation may be caused by ileus.
- Hematological effects of lead include mild to severe anemia and abnormal red cell morphology such as polychromasia, hypochromasia, or anisocytosis.
- Biochemistry panel may show elevations in lactase dehydrogenase, aspartate transaminase, creatine phosphokinase, and uric acid.
- Blood lead levels greater than 20 µg/dL (0.20 ppm) suggest lead toxicity, and levels greater than 50 µg/dL are diagnostic. Delta-aminolevulinate dehydratase (ALAD) levels have also been used to diagnose lead toxicity in waterfowl and occasionally caged birds. ALAD is inhibited by lead.
Initial treatment of lead toxicity consists of supportive care along with chelation therapy.
- Administer fluids (subcutaneous, intravenous [IV], or intraosseous depending on the degree of dehydration and volume of polyuria), provide supplemental heat, and control seizure activity.
- Chelation of circulating lead forms nontoxic complexes that are excreted in bile or by the kidneys. As circulating lead is removed, this in turn leads to equilibration of lead from tissue and bone and further chelation. Calcium ethylene diaminetetraacetate or CaEDTA (Calcium disodium versonate, Riber Laboratories) is the treatment of choice for initial therapy. D-penicillamine may be added and has the advantage of oral administration.
- Cathartics, such as sodium sulfate (Glauber’s salt) or magnesium sulfate (Epsom salts), have also been recommended to precipitate lead in the gastrointestinal tract.
- Large lead objects, such as fishing sinkers, or other large fragments, may be removed using a rigid laparoscope or even a flexible endoscope in large species, once the patient is stabilized. Surgical removal is indicated only as a last resort.
Sources of zinc include galvanized cage wire, zipper teeth, staples, hardware (screws, nails, nuts and bolts), zinc containing products such as zinc oxide, and coins. The kidneys, liver, and pancreas are target organs for zinc.
Poisoned psittacine birds often present with only generalized weakness. Tentative diagnosis may be based on history and the radiographic presence of metal in the gastrointestinal tract. Definitive diagnosis requires blood or tissue levels greater than 200 µg/dL and 75 µg/dL respectively. Clinical signs may not be noticed until levels are as high as 1000 µg/dL. Submit samples in plastic containers as rubber stoppers may leach zinc from the sample giving a falsely low result. Treatment for zinc toxicosis is the same as for lead, although in my experience, zinc intoxication carries a worse prognosis than lead.
Other metal toxicities
Other metal toxicities reported uncommonly in birds include copper, iron, mercury, and arsenic.
Maleffects from organophosphates and carbamates such as diazinon, dichlorvos, dieldrin, dursban, malathion and carbaryl have been reported in birds. In companion birds, intoxication generally results from consumption of contaminated food or water, although secondary poisoning of wild insectivorous species may also occur. Pathology results from binding of the insecticide to and inhibition of acetylcholinesterase and the resulting accumulation of acetylcholine at ganglia and neuromuscular junctions. Organophosphate bonds are irreversible but carbamate bonds are slowly reversible.
Clinical signs include:
- Crop stasis
- Muscle twitches
- Prolapsed nictitans
- Increased respiratory secretions
Tentative diagnosis is based on history of exposure, clinical signs, and response to therapy. Bradycardia non-responsive to atropine (0.02 mg/kg IV) is suggestive, but not an established diagnostic test in birds. Definitive diagnosis is based on a cholinesterase assay from whole blood, plasma, or serum, paired with an analogous subject.
Specific therapy for carbamate and organophosphate toxicity calls for atropine. Pralidoxime chloride (2-PAM) is effective early in organophosphate toxicity and should be given in cases that are presented soon after ingestion. Continue 2-PAM providing there is a positive response. Pralidoxime is contraindicated in carbamate toxicity.
Intoxication caused by both primary, and in carnivorous birds, secondary exposure to first generation (warfarin) and second-generation (brodifacoum and bromadoline) rodenticides is seen in avian patients. Anticoagulant rodenticides are vitamin K antagonists.
Many patients present with no history of exposure and non-specific clinical signs such as depression and anorexia. Additional signs may include feather follicle and subcutaneous hemorrhage, oral and cloacal petechial hemorrhages, and epistaxis, however, once bleeding is noted the prognosis is grave.
Provide fresh whole blood transfusions to critical cases. Administer injectable vitamin K1 until the patient is stable then given subcutaneous, intramuscular, or oral vitamin K daily or feed at a dose of 800 g/kg food. Menadione (K3) supplementation is not effective in counteracting anticoagulants. In mammals, it may be necessary to administer vitamin K for several weeks to control bleeding due to increased potency and slower metabolism of second generation rodenticides.
Bromethalin is a highly potent rodenticide that acts by uncoupling oxidative phosphorylation in the mitochondria of the central nervous system leading to decreased production of adenosine triphosphate. Clinical signs of bromethalin toxicity in small animals include ataxia, depression, extensor rigidity, opisthotonus, lateral recumbency, and vomiting. High doses may induce muscle fasciculations, hind limb hyperreflexia, seizures, hyperesthesia, depression, and death. There are no definitive antemortem tests, although consistent clinical signs, a history of exposure, irregular electroencephalographic measurements, and fundiscopic findings suggestive of cerebral edema may all support a diagnosis. There is no specific antidote for bromethalin poisoning, and prevention of absorption is of the utmost importance. Treatment is most successful in dogs and cats when emesis is induced and activated charcoal with a saline cathartic is given immediately. Since bromethalin and its metabolites enter hepatoenteric cycle, charcoal should be continued for 48-72 hours. Treatments with osmotic diuretics and steroids have also been utilized with less success. The predominant necropsy lesions in dogs involve the brain. Bromethalin or its metabolite, desmethy-bromethalin, can be detected in liver, fat, kidney, and brain samples, which should be frozen and wrapped in aluminum foil.