Antidepressant Toxicity

Antidepressant toxicity in dogs is a serious poisoning condition that occurs when dogs ingest human antidepressant medications, representing one of the most frequently reported medication-related toxic exposures in veterinary emergency medicine. With millions of people taking antidepressants daily, these medications are commonly found in households, making accidental ingestion by pets unfortunately common. The major classes of antidepressants that cause toxicity in dogs include selective serotonin reuptake inhibitors such as fluoxetine and sertraline, serotonin-norepinephrine reuptake inhibitors including venlafaxine and duloxetine, tricyclic antidepressants like amitriptyline, and monoamine oxidase inhibitors. Each class produces distinct toxic syndromes, though all can cause serious neurological and cardiovascular effects requiring emergency veterinary intervention.

The mechanism of antidepressant toxicity varies depending on the specific medication class involved but generally relates to excessive accumulation of neurotransmitters in the brain and body. Selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors cause serotonin syndrome by preventing the reuptake of serotonin, leading to dangerous accumulation that affects nervous system function, body temperature regulation, and muscle control. Tricyclic antidepressants have multiple mechanisms including blocking sodium channels in the heart, causing potentially fatal cardiac arrhythmias, as well as anticholinergic effects and norepinephrine reuptake inhibition. The diverse mechanisms across antidepressant classes mean that clinical presentation and treatment approaches vary significantly based on which type of medication was ingested.

The impact of antidepressant toxicity on dogs ranges from mild sedation or agitation to life-threatening seizures, cardiac arrhythmias, and death. Signs can develop within thirty minutes to several hours of ingestion depending on the medication formulation and amount consumed. Extended-release medications pose particular risks as they can cause delayed and prolonged toxicity. The severity depends on the specific drug, the dose ingested relative to the dog's size, whether the medication was immediate or extended release, and how quickly treatment is initiated. Small dogs ingesting even a single pill may experience severe toxicity, while larger dogs may tolerate small accidental exposures with only mild effects.

Treatment for antidepressant toxicity is available and can be successful when veterinary care is sought promptly, though management can be challenging due to the varied toxic mechanisms involved. There is no specific antidote for most antidepressants, making treatment primarily supportive with decontamination, seizure control, cardiac monitoring, temperature regulation, and intensive nursing care. Some tricyclic antidepressant toxicities respond to sodium bicarbonate administration for cardiac effects. The prognosis depends heavily on the amount and type of medication ingested and the time to treatment. Pet owners should understand that any suspected antidepressant ingestion warrants immediate veterinary evaluation, as the unpredictable nature of these toxicities means even seemingly small exposures can rapidly become dangerous.

The primary cause of antidepressant toxicity in dogs is accidental ingestion of human medications, which occurs with alarming frequency given the widespread use of these drugs in the population. According to poison control data, antidepressants consistently rank among the top ten most common toxic exposures reported in dogs. The prevalence of antidepressant use means these medications are present in millions of homes, often stored in locations accessible to curious pets. Dogs commonly access these medications by chewing through pill bottles, consuming pills dropped on the floor, getting into purses or bags containing medication, or accessing weekly pill organizers that are easier to open than original containers.

Accidental ingestion scenarios account for the vast majority of antidepressant toxicity cases in dogs. Many people take their antidepressants in the morning or evening at home, times when dogs are often nearby and alert to anything that might be food. Pills can easily be dropped and roll under furniture where dogs can find them later, or dogs may catch falling pills mid-air before owners can react. Medication stored on nightstands, bathroom counters, or kitchen tables is readily accessible to dogs who can reach these surfaces. Some dogs have learned to open certain cabinet types, and determined chewers can make short work of plastic pill bottles regardless of childproof caps.

Intentional administration by owners represents a less common but still significant cause of antidepressant toxicity. Some pet owners who take antidepressants themselves may assume that giving their anxious dog a portion of their medication would be helpful and safe. This dangerous misconception fails to account for the vast differences in drug metabolism between humans and dogs, as well as the narrow margin of safety for these medications in canines. While some antidepressants are used therapeutically in veterinary medicine, the doses are carefully calculated and monitored, and human formulations are often inappropriate due to strength and release characteristics.

Risk factors for antidepressant toxicity relate to medication storage practices, household composition, and canine behavior patterns. Homes where multiple family members take different medications present higher risk due to increased opportunities for exposure. Extended-release formulations are particularly dangerous because they contain larger total doses designed for gradual release, and when chewed, the entire dose can be absorbed rapidly. Dogs with strong food drive, counter-surfing habits, or history of getting into forbidden items face increased exposure risk. Young dogs who explore with their mouths and older dogs with cognitive changes affecting judgment are also at elevated risk.

The toxic dose varies significantly between different antidepressant classes and specific medications. For selective serotonin reuptake inhibitors, toxic effects in dogs can occur at doses of five to ten milligrams per kilogram for some medications, while tricyclic antidepressants may cause severe toxicity at much lower doses. A single pill of certain antidepressants can be life-threatening to a small dog. Because pet owners typically cannot determine safe versus dangerous doses, and because individual sensitivity varies, any known or suspected antidepressant ingestion should be treated as potentially serious requiring veterinary evaluation.

Early warning signs of antidepressant toxicity in dogs often appear within one to four hours of ingestion, though extended-release formulations may cause delayed onset of symptoms. Initial signs frequently include restlessness, agitation, or the opposite extreme of sedation and lethargy, depending on the specific medication and dose involved. Vomiting commonly occurs in the early stages as the gastrointestinal tract responds to the medication. Some dogs may exhibit excessive vocalization, panting, or pacing as early neurological effects develop. These initial signs can be subtle and may not immediately suggest poisoning to owners unfamiliar with the condition, potentially delaying critical treatment.

Common symptoms of antidepressant toxicity reflect the neurological and gastrointestinal effects of excessive neurotransmitter activity. Gastrointestinal signs including nausea, vomiting, diarrhea, and drooling are frequently observed across all antidepressant classes. Neurological signs are prominent and may include dilated pupils, disorientation, vocalization, hyperactivity or depression, incoordination, and tremors. Dogs may appear anxious, exhibit unusual eye movements, or seem unable to settle. Heart rate abnormalities are common, ranging from rapid heart rate with SSRIs and SNRIs to potentially dangerous arrhythmias with tricyclic antidepressants. Body temperature elevations can occur, particularly with serotonergic medications.

Behavioral changes in antidepressant toxicity can be dramatic and disturbing for owners to witness. Affected dogs may alternate between extreme agitation and sudden sedation, appearing confused about their surroundings. Some dogs become unusually vocal, whining, barking, or howling persistently. Others may exhibit compulsive behaviors such as circling, head pressing, or repetitive movements. Fear responses may be exaggerated, with dogs startling at normal stimuli or hiding. Social behavior often changes markedly, with previously friendly dogs becoming withdrawn or normally calm dogs becoming hyperactive. These behavioral manifestations reflect the disruption of normal neurotransmitter function in the brain.

Physical signs of antidepressant toxicity provide important diagnostic information and indicate toxicity severity. Dilated pupils that respond poorly to light are characteristic of many antidepressant toxicities. Hyperthermia, or elevated body temperature, develops in serotonin syndrome and can become dangerously high. Muscle rigidity, tremors, and twitching reflect neuromuscular irritability. The gums may appear bright red due to elevated body temperature and cardiovascular changes, or pale if shock is developing. In tricyclic antidepressant toxicity, cardiac signs predominate with irregular heart rhythms detectable on examination. Rapid or labored breathing may indicate the body's attempt to cool itself or compensation for cardiovascular compromise.

Symptom progression in antidepressant toxicity can be rapid, with dogs deteriorating from mild agitation to life-threatening seizures within hours. Serotonin syndrome, caused by SSRIs, SNRIs, and some other antidepressants, follows a characteristic progression from mild signs of anxiety and restlessness to moderate signs including tremors, hyperthermia, and hyperreflexia, to severe signs including high fever, muscle rigidity, seizures, and cardiovascular collapse. Tricyclic antidepressant toxicity may progress from initial anticholinergic signs to dangerous cardiac arrhythmias and seizures. Extended-release medications can cause prolonged toxicity lasting twenty-four to seventy-two hours or longer.

Emergency symptoms requiring immediate veterinary intervention include seizures, which may occur as a single event or progress to continuous seizure activity known as status epilepticus. High body temperature exceeding 104 degrees Fahrenheit represents a medical emergency requiring active cooling. Cardiac arrhythmias, evidenced by an irregular or abnormally fast heart rate, collapse, or weakness, indicate cardiovascular toxicity requiring immediate intervention. Loss of consciousness, inability to stand, severe muscle rigidity, or respiratory distress all warrant emergency care. Any dog with known or suspected antidepressant ingestion should be evaluated by a veterinarian immediately, as the unpredictable progression of these toxicities means early intervention is essential for the best outcomes.

Initial examination of a dog with suspected antidepressant toxicity begins with rapid assessment of vital signs and neurological status while gathering critical history about the exposure. The veterinarian will immediately evaluate heart rate and rhythm, respiratory rate and effort, body temperature, and level of consciousness. Physical examination focuses on pupil size and responsiveness, muscle tone and presence of tremors, and signs of seizure activity. Simultaneously, the veterinary team will gather information about which medication was ingested, the strength per tablet, estimated number of pills consumed, time since ingestion, and whether the medication was immediate or extended release. Having the medication bottle available greatly aids in identification and dose estimation.

Diagnostic tests in antidepressant toxicity primarily focus on assessing organ function and identifying complications rather than confirming the specific toxin. An electrocardiogram is essential, particularly when tricyclic antidepressant ingestion is suspected, to identify cardiac arrhythmias that require intervention. Blood work including a complete blood count and chemistry panel evaluates overall organ function and establishes baseline values for monitoring. Blood glucose is checked as some antidepressants can cause hypoglycemia. Blood pressure monitoring helps identify cardiovascular effects. Body temperature monitoring is critical for identifying and managing hyperthermia. Specific drug levels are not typically available for rapid turnaround but may be submitted for retrospective confirmation in some cases.

Differential diagnosis involves distinguishing antidepressant toxicity from other conditions causing similar neurological and cardiovascular signs. Other toxicities that may present similarly include stimulant medications such as ADHD drugs, illicit drug exposure including methamphetamine or cocaine, certain pesticide exposures, and mycotoxin ingestion from moldy food. Non-toxic conditions to consider include idiopathic epilepsy, infectious encephalitis, metabolic disturbances such as hypoglycemia or hepatic encephalopathy, and heat stroke. The clinical presentation combined with known or suspected exposure history typically allows differentiation, though treatment may need to proceed based on clinical suspicion while waiting for confirmation.

Diagnosis confirmation relies primarily on the combination of consistent clinical signs and known exposure history, as specific laboratory confirmation is often impractical in the emergency setting. The characteristic constellation of agitation or sedation, dilated pupils, tremors, hyperthermia, and tachycardia strongly suggests serotonin syndrome from SSRI or SNRI ingestion. Cardiac conduction abnormalities on electrocardiogram, particularly QRS widening, are highly suggestive of tricyclic antidepressant toxicity. Response to treatment can also provide diagnostic confirmation, with improvement following appropriate supportive care supporting the suspected diagnosis. Serial monitoring of vital signs, electrocardiogram, and laboratory values tracks response to treatment and identifies complications.

Emergency and immediate treatment for antidepressant toxicity prioritizes stabilization of life-threatening conditions while initiating decontamination when safe to do so. Seizure activity is controlled immediately with intravenous benzodiazepines such as diazepam, which also help reduce agitation and muscle rigidity associated with serotonin syndrome. Active cooling is initiated for dogs with hyperthermia, using cool water application, fans, and intravenous fluids. Cardiac arrhythmias from tricyclic antidepressant toxicity may respond to sodium bicarbonate administration, which helps stabilize cardiac membranes. Intravenous catheter placement and fluid therapy support cardiovascular function and drug elimination. If ingestion occurred recently and the dog is stable without seizures, decontamination through induced vomiting may be attempted, followed by activated charcoal to reduce further absorption.

Medical management of antidepressant toxicity is largely supportive, as no specific antidotes exist for most antidepressant classes. Benzodiazepines serve as the primary pharmacological intervention, controlling seizures, reducing muscle rigidity, and providing sedation for severely agitated patients. Cyproheptadine, a serotonin antagonist, may be administered for serotonin syndrome to help block excessive serotonergic activity, though its effectiveness is variable. Beta-blockers or other cardiac medications may be needed to manage persistent tachycardia. Sodium bicarbonate is specifically indicated for tricyclic antidepressant toxicity with cardiac conduction abnormalities. Intravenous lipid emulsion therapy has shown promise in treating lipophilic drug toxicities including some antidepressants by sequestering the drug in a lipid phase.

Surgical intervention is not part of standard antidepressant toxicity treatment, as this is a medical condition requiring pharmacological and supportive management rather than surgical correction. In extremely rare circumstances involving ingestion of large quantities of extended-release tablets very recently, surgical removal of a pill bezoar from the stomach might theoretically be considered, but this is exceptional. The focus remains entirely on medical stabilization, decontamination when feasible, and supportive care through the toxic period.

Supportive care forms the cornerstone of antidepressant toxicity treatment and may be required for twenty-four to seventy-two hours or longer depending on the medication involved. Continuous monitoring in an intensive care setting allows rapid response to complications. Temperature management through active cooling or passive monitoring continues until normothermia is stable. Intravenous fluids maintain hydration and support renal elimination of the drug. Bladder catheterization may be needed if urinary retention develops from anticholinergic effects. Nutritional support is provided once the patient stabilizes. Quiet, low-stimulation environments help minimize anxiety and reduce the risk of triggering seizures in sensitized patients.

Alternative and complementary treatments play a limited role in acute antidepressant toxicity management but may include muscle relaxants for severe rigidity not responding to benzodiazepines and antiemetics for persistent nausea. Once the acute crisis resolves, supportive supplements for liver health may be considered if hepatic stress occurred. Physical therapy may help dogs who experienced prolonged muscle rigidity or weakness. However, all complementary approaches are secondary to aggressive medical management during the acute toxic period.

Treatment decisions are guided by the specific antidepressant involved, estimated dose, clinical severity, and patient response. Dogs with mild toxicity from small SSRI exposures may be managed with monitoring and supportive care alone. Those with severe serotonin syndrome or tricyclic toxicity require intensive intervention with multiple medications and continuous monitoring. Extended-release medication ingestion necessitates prolonged hospitalization even if initial symptoms are mild, as delayed toxicity may develop. Cost of treatment can be substantial for severe cases requiring intensive care, and veterinarians work with families to provide appropriate care while discussing realistic expectations for outcome.

Recovery timeline from antidepressant toxicity varies based on the specific medication, dose, and severity of clinical signs. Dogs with mild toxicity from small exposures may recover within twelve to twenty-four hours with appropriate supportive care. Moderate toxicity typically resolves within twenty-four to forty-eight hours, though some residual sedation or mild neurological abnormalities may persist for several days. Severe toxicity, particularly from extended-release medications, may require three to five days of intensive hospitalization before the patient is stable for discharge. Dogs that experienced seizures or severe hyperthermia may show residual effects for a week or more as the nervous system recovers from the insult.

Post-treatment care following antidepressant toxicity focuses on supportive recovery and monitoring for delayed complications. After discharge, dogs should be kept in a quiet, low-stress environment to allow continued neurological recovery. Activity should be restricted initially, with gradual return to normal exercise over several days to a week. Appetite may be reduced following gastrointestinal upset and should recover progressively over a few days. Follow-up veterinary examination within one to two weeks confirms complete recovery and assesses any lingering effects. Dogs that experienced cardiac abnormalities may benefit from repeat electrocardiogram to confirm resolution.

Prognosis factors in antidepressant toxicity include the specific drug class, dose relative to body weight, time to treatment, severity of clinical signs at presentation, and presence of complications. Selective serotonin reuptake inhibitor toxicity generally carries a good prognosis when treated appropriately, with most dogs recovering fully. Tricyclic antidepressant toxicity is more dangerous due to cardiac effects, with worse prognosis if significant arrhythmias developed. Dogs that experienced status epilepticus or severe hyperthermia may have neurological damage affecting long-term prognosis. Prompt treatment before the development of severe complications significantly improves outcomes across all antidepressant classes.

Long-term outlook for dogs surviving antidepressant toxicity is generally excellent, with most patients returning to completely normal function. Permanent neurological damage is possible but uncommon when appropriate treatment was provided before prolonged seizures or severe hyperthermia occurred. Cardiac function typically returns to normal following tricyclic toxicity, though some dogs may require ongoing cardiac monitoring if significant myocardial damage occurred. Dogs that recover do not have increased sensitivity to future antidepressant exposure, but obviously must be protected from any possibility of repeat ingestion through rigorous medication safety practices.

Primary prevention of antidepressant toxicity requires rigorous medication safety practices in any household where these drugs are present. All antidepressants should be stored in secure, elevated locations inside closed cabinets or drawers that dogs cannot access. Original prescription containers with childproof caps should be used, though these provide limited protection against determined chewers. Weekly pill organizers, while convenient for humans, are easily opened by dogs and should be kept in secured locations. Medications should never be left loose on any surface, and any dropped pills should be retrieved immediately. Purses, travel bags, and overnight bags containing medications should be stored in closed closets rather than left on floors or furniture accessible to pets.

Owner education about the dangers of antidepressant toxicity helps prevent both accidental ingestion and misguided intentional administration. All dog owners in households with antidepressants should understand that these medications are toxic to dogs and should never be shared. The misconception that giving a portion of one's own medication to an anxious pet is helpful and safe should be clearly dispelled. Family members, guests, and visitors should be informed about keeping all medications away from pets. Understanding the rapidity with which symptoms can develop encourages immediate veterinary consultation rather than watch-and-wait approaches.

Safe alternatives for managing canine anxiety should be discussed with veterinarians to reduce any temptation to use human medications. Veterinary-prescribed medications at appropriate doses can address behavioral concerns safely. Behavioral modification, training, and environmental management provide non-pharmaceutical options for many anxious dogs. Pheromone products, anxiety wraps, and supplements formulated for dogs offer additional options. Having a plan in place for managing a dog's anxiety reduces the likelihood of inappropriate self-treatment attempts.

Health maintenance through regular veterinary care establishes a relationship that encourages owners to seek professional guidance rather than attempting self-treatment. Annual or biannual wellness examinations provide opportunities to discuss behavioral concerns and appropriate management options. Keeping emergency veterinary contact information readily accessible ensures owners know where to turn in crisis situations. Understanding that effective, safe veterinary options exist for anxious dogs removes any perceived need to resort to human medications.

Early intervention when suspected ingestion occurs dramatically improves outcomes in antidepressant toxicity. Owners should contact a veterinarian or poison control immediately upon discovering potential exposure, regardless of whether symptoms have appeared. Time is critical, as decontamination is most effective within the first hour or two of ingestion. Having poison control hotline numbers and emergency veterinary clinic contact information posted visibly enables rapid response. Any container that may have been accessed by a dog should be brought to the veterinary visit to aid in identification and dose estimation.

Daily management during recovery from antidepressant toxicity involves creating a calm environment conducive to neurological healing. Dogs should be kept in a quiet area of the home away from excessive activity, noise, and stimulation that might trigger residual neurological sensitivity. Regular, small meals help restore normal gastrointestinal function without overwhelming a potentially sensitive digestive system. Fresh water should always be available, and water intake should be monitored to ensure adequate hydration. Any prescribed medications should be administered consistently according to veterinary instructions. Short, calm leash walks for elimination are appropriate, with avoidance of strenuous activity until full recovery is confirmed.

Home environment modifications support safe recovery and prevent future incidents. All medications throughout the household should be inventoried and secured in dog-proof storage. This includes not only the medication that caused the current toxicity but all prescription and over-the-counter medications, vitamins, and supplements. Sleeping areas should be comfortable and easily accessible without requiring jumping or climbing. Non-slip surfaces help dogs with any residual incoordination navigate safely. The recovery area should be temperature-controlled to avoid heat stress in dogs whose thermoregulatory mechanisms may still be recovering.

Quality of life during antidepressant toxicity recovery is typically good once the acute crisis resolves. Most dogs are ready for calm interaction and gentle affection within a day or two of discharge. Mental stimulation through puzzle feeders, training exercises, and interactive toys can be gradually reintroduced as energy and interest return. Physical activity is increased slowly over days to a week, starting with short walks and progressing to normal exercise once the veterinarian confirms complete recovery. Most dogs return to their normal personalities and activity levels within one to two weeks.

Monitoring and ongoing care requirements focus on identifying any delayed complications or incomplete recovery. Owners should watch for return of any neurological signs including tremors, agitation, disorientation, or seizures, which would warrant immediate veterinary attention. Appetite, energy level, and behavior should progressively return to normal over several days. Any persistent abnormalities lasting beyond a week should be reported to the veterinarian. A follow-up appointment confirms complete recovery and provides opportunity to reinforce medication safety practices. Once recovery is complete, routine wellness care resumes without need for ongoing specialized monitoring.

Caregiver support during and after pet poisoning events addresses the emotional and practical challenges owners face. The stress of emergency veterinary care, worry about a beloved pet, and financial concerns can be significant. Open communication with the veterinary team about prognosis, treatment options, and costs helps owners make informed decisions. Family members should share caregiving responsibilities during the recovery period to prevent burnout. Support from friends, family, or online pet owner communities can provide emotional sustenance. Processing feelings of guilt over the accidental exposure is normal, and channeling that energy into improved medication safety practices is constructive.

Antidepressant toxicity can affect all dogs regardless of breed, as susceptibility is determined by the toxic mechanisms of these medications rather than breed-specific genetic factors. No breed has enhanced ability to metabolize antidepressants safely, meaning all dogs face equivalent risk when exposed to these medications. However, body size significantly influences the severity of toxicity from a given dose, with smaller dogs experiencing more severe effects from ingesting the same number of pills as larger dogs. A single tablet of many antidepressants can cause severe toxicity in toy breeds weighing under ten pounds, while a large breed dog might tolerate the same pill with only mild effects. This dose-to-weight relationship makes small breeds particularly vulnerable to serious poisoning.

Behavioral tendencies associated with certain breeds may influence exposure risk independently of any metabolic factors. Breeds known for scavenging behavior and strong food drive, including Labrador Retrievers, Beagles, and many terrier breeds, may be more likely to investigate and consume found pills. Breeds with a tendency to chew inappropriate objects may attack pill bottles with greater determination. Young dogs of any breed are typically more curious and prone to oral exploration than adults, increasing their exposure risk. Conversely, well-trained dogs with excellent impulse control may be less likely to consume unauthorized items, though no dog should be considered safe around accessible medications.

Screening recommendations for antidepressant toxicity differ from heritable conditions, as there is no genetic predisposition to identify. Prevention through environmental management and education is the only effective approach. Veterinarians should counsel all dog owners about medication safety during puppy visits and wellness examinations, with particular emphasis in households where antidepressants are present. Owners of small breeds should understand the heightened risk posed by even single-pill exposures. Following any ingestion, emergency screening through physical examination, electrocardiogram, and blood work assesses toxicity severity and guides treatment decisions regardless of breed.

Commonly co-occurring conditions with antidepressant toxicity develop as complications of the poisoning rather than existing alongside it. Serotonin syndrome is the primary toxic syndrome associated with SSRI and SNRI antidepressant ingestion, characterized by the triad of altered mental status, neuromuscular abnormalities, and autonomic dysfunction. Cardiac arrhythmias, particularly from tricyclic antidepressant toxicity, represent a life-threatening complication requiring specific intervention. Hyperthermia develops secondary to increased muscle activity and altered thermoregulation, potentially causing rhabdomyolysis and kidney injury if severe. Aspiration pneumonia can occur if vomiting and decreased consciousness result in inhalation of stomach contents. These complications underscore the need for intensive monitoring and aggressive treatment in significant exposures.

Conditions with similar symptoms to antidepressant toxicity include other poisonings and primary neurological disorders. Ingestion of stimulant medications such as ADHD drugs causes similar signs of agitation, tachycardia, and hyperthermia. Illicit drug exposure, including amphetamines or cocaine, can produce a nearly identical clinical picture. Certain pesticides, particularly organophosphates, cause neurological signs that may overlap. Heat stroke produces hyperthermia, neurological dysfunction, and cardiovascular stress resembling severe serotonin syndrome. Idiopathic epilepsy manifests with seizures that may be confused with toxic seizures. Accurate history and specific testing help differentiate these conditions, though treatment is often initiated based on clinical suspicion.

Potential complications from antidepressant toxicity extend beyond the acute poisoning event. Prolonged seizure activity can cause permanent neurological damage including memory deficits, personality changes, or ongoing seizure disorders. Severe hyperthermia may result in muscle breakdown, kidney failure, or disseminated intravascular coagulation. Cardiac damage from arrhythmias or prolonged cardiovascular compromise may have lasting effects in severe cases. Aspiration pneumonia requires prolonged antibiotic treatment and can be life-threatening in its own right. Fortunately, with appropriate early treatment, most dogs recover completely without permanent complications, emphasizing the importance of immediate veterinary care for any suspected antidepressant ingestion.