Radiation exposure at airport security
On 3 May 2025, Mimi, a three-month-old female Maine Coon kitten weighing approximately 1.69 kg, was transported in a soft-sided carrier through Toronto Pearson International Airport. During security screening, the carrier was mistakenly placed onto the conveyor belt of a baggage X-ray scanner intended exclusively for luggage, contrary to Transport Canada and CATSA policies prohibiting the X-ray scanning of live animals. Security personnel reassured the owners that the scan was “like one chest X-ray,” but no quantitative information about beam energy, dose, scan duration, or number of exposures was provided. It remains unknown whether the carrier was scanned more than once or remained within the beam path for longer than a single pass. No dosimeter was present at the time of exposure, and no post-incident dose reconstruction has been made available.
Baggage scanners typically use higher‑energy X‑rays than many diagnostic units in order to penetrate dense luggage. For a very small animal in close proximity to the source, near‑whole‑body irradiation of all organs is likely, as minimal tissue thickness exists to attenuate the beam. While regulatory agencies generally assert that such systems operate at doses well below thresholds of deterministic harm for adult humans, those assurances do not explicitly account for juvenile, 1–2 kg animals, nor for the possibility of repeated or prolonged exposures. Mimi appeared outwardly well immediately after the scan and tolerated her subsequent flight home without overt distress.
Initial decline and first hospitalization
Over the ensuing weeks, Mimi’s owners noted a change in her behavior and appetite. Around 30 May 2025—approximately four weeks after the X‑ray exposure—she developed vomiting and lethargy, with reduced playfulness and decreased overall activity. These signs fluctuated but did not fully resolve. By 23 June 2025, she was sufficiently unwell to warrant presentation to a veterinary hospital.
On admission, Mimi was markedly icteric, with pale mucous membranes, tachycardia, and lethargy. Laboratory testing revealed:
- Packed cell volume (PCV) 12% (severe anemia)
- Total bilirubin 40 µmol/L (marked hyperbilirubinemia)
- Regenerative response with reticulocytes approximately 116.2 k/µL
- Normal FeLV/FIV testing
- No evidence of external or internal hemorrhage
- No known toxin exposure
This constellation—severe regenerative anemia, hyperbilirubinemia, and clinical jaundice in the absence of hemorrhage—met standard clinical criteria for immune‑mediated hemolytic anemia in cats (Stockham & Scott, 2008; Voges & Dowgray, 2022). Coombs testing was not performed, but Mimi’s response to immunosuppression further supported IMHA as the correct working diagnosis.
She was started on dexamethasone. Over the subsequent days, her PCV rose from 12% to 14% at discharge on 26 June 2025, and to 22% in the days following discharge. Her appetite and activity clearly improved at home. This trajectory is consistent with effective immunosuppressive control of hemolysis and adequate bone marrow regenerative capacity.
During this first admission, a barium contrast study of the esophagus and upper GI tract was performed. Imaging showed a diffusely dilated esophagus with delayed transit but successful passage of contrast into the stomach—findings consistent with megaesophagus, without evidence of complete obstruction. This was an important early marker of neuromuscular dysfunction predating Mimi’s later catastrophic decline.
Interim improvement and second decline
Following discharge, Mimi’s owners observed a marked and sustained clinical improvement. For the first 5–6 days, her gastrointestinal symptoms were fully resolved: she had four normal bowel movements per day, exhibited no constipation or gas, and ate approximately four cans of food daily with strong appetite and energy. She gained weight rapidly and appropriately, increasing from her discharge weight of 1.3 kg to approximately 1.85 kg—a 42.3% increase in body weight within one week—and was bright, interactive, and behaving like a normal kitten. Her jaundice also fully resolved during this period, consistent with effective suppression of hemolysis and improvement in bilirubin clearance.
In late June, after several days of complete post-discharge stability, Mimi began to show early signs consistent with evolving refeeding-syndrome physiology. Following a period of rapid caloric intake and a 42% increase in body weight within one week, her gastrointestinal motility slowed, with mild ileus, reduced appetite, and decreased stool output, reflecting early phosphate depletion and thiamine utilization outpacing supply. Importantly, megaesophagus-related symptoms were not clinically apparent at home during this time, and she had previously demonstrated full normalization of gastrointestinal function.
On the morning of 6 July 2025, her bowel movements had still not resumed, and formed stool could be palpated in the colon. That same morning, she briefly played normally before experiencing a sudden neurologic collapse. A photograph taken at 11:04 a.m. documented her in marked neurologic distress: sternally recumbent with her head resting flat on the floor, limbs extended forward, body flaccid, ears laterally rotated, and eyes wide and unfocused. Despite being on a smooth wooden surface, she was unable to sit upright or maintain normal posture.
This presentation is medically consistent with early Wernicke’s encephalopathy, the neurologic expression of acute thiamine deficiency (Sechi & Serra, 2007), occurring in the context of developing refeeding syndrome (Mehanna et al., 2008). The abrupt loss of motor control represents central nervous system failure, not simple lethargy or fatigue.
Upon readmission later that day, Mimi was not jaundiced. The hyperbilirubinemia that developed subsequently occurred after admission, coinciding with progressive metabolic decompensation. Her generalized seizures occurred only after readmission, consistent with worsening thiamine deficiency and severe electrolyte instability. This sequence indicates that Mimi’s pre-admission collapse was an early neurologic manifestation of refeeding-associated thiamine depletion superimposed on a physiologic state already strained by prior illness and recent rapid caloric reintroduction
Second hospitalization: refeeding syndrome and metabolic collapse
On re-admission, Mimi was profoundly unwell. Her initial neurologic collapse occurred prior to any in-hospital laboratory testing, and the first bloodwork panel was drawn approximately seven hours after admission—and at least five hours after her metabolic seizure. This timing indicates that the documented abnormalities likely underestimate the degree of electrolyte and thiamine depletion present at the time of neurologic decompensation.
Key laboratory abnormalities included:
- Severe hypokalemia, with potassium values as low as 1.9–2.5 mmol/L on serial testing
- Hypophosphatemia, with phosphate levels in the critically low range and a rebound decline following a single IV bolus
- Hyponatremia and hypochloremia
- Borderline to mild hypocalcemia
- Strong suspicion of hypomagnesemia, not directly measured, but strongly supported by refractory hypokalemia, neuromuscular weakness, and clinical signs
- Rising total bilirubin, eventually reaching 27–29 µmol/L, despite earlier hematologic improvement
- Evidence of urinary tract infection, with documented bacteriuria and pyuria
These findings—particularly the combination of hypophosphatemia, hypokalemia, presumed hypomagnesemia, and delayed thiamine repletion—are hallmarks of refeeding syndrome with evolving Wernicke’s encephalopathy, occurring in a physiologically vulnerable juvenile cat.
Clinically, Mimi exhibited:
- Two witnessed seizures on the first day of readmission
- Post‑ictal obtundation and inability to lift her head (a classic sign of thiamine deficiency in cats)
- Progressive respiratory weakness and recumbency
- Worsening esophagitis and regurgitation, with aspiration risk
Mimi met widely accepted criteria for refeeding syndrome in a high‑risk animal (Mehanna et al., 2008; Whitby et al., 2019). She had experienced a period of reduced intake and weight loss, followed by rapid caloric reintroduction during her initial post‑discharge recovery. She then entered a second period of compromised intake prior to readmission. Her severe hypophosphatemia, hypokalemia, neurologic collapse, and rising bilirubin are classic for refeeding-related metabolic failure in the context of untreated thiamine deficiency and multi‑electrolyte depletion.
Critically, although the owner explicitly requested emergency stabilization with IV phosphate, IV thiamine, IV magnesium, and IV calcium immediately after Mimi’s seizures, the medical record confirms that:
- IV phosphate and IV calcium were eventually administered, but not systematically maintained.
- IV thiamine was never given at any time during the second admission.
- IV magnesium was never administered, despite textbook indications and refractory hypokalemia.
- Oral thiamine and oral magnesium were started late, in the final 24–36 hours of Mimi’s life.
Mimi survived approximately 56 hours after her initial seizures without receiving IV thiamine or IV magnesium. During this time, her neuromuscular and metabolic status progressively worsened until she suffered terminal collapse and died in hospital.
Necropsy findings
A full necropsy was performed at a regional diagnostic laboratory. Key findings included:
- Evidence of immune‑mediated hemolytic anemia (IMHA), confirming the working clinical diagnosis.
- Megaesophagus with marked esophagitis and chronic reflux injury.
- A chronic fibrotic jejunal “ring” consistent with a long‑standing, compensated intussusception or stricture.
- No evidence of acute small intestinal obstruction, perforation, or necrosis at the time of death.
- No neoplastic lesion to explain anemia or GI changes.
- No infectious process sufficient to account for the clinical picture.
The pathologist’s report emphasized the chronic jejunal lesion as a potential contributor and stated that Mimi’s “electrolytes were replaced appropriately.” As detailed elsewhere, this conclusion is incompatible with the documented absence of IV thiamine and IV magnesium and the persistence of severe electrolyte derangements in the days before death. For the purposes of this paper, the necropsy is most important in confirming three key points:
1. Mimi did indeed have IMHA.
2. She did have megaesophagus and esophagitis.
3. She did have a chronic, fibrotic intestinal lesion, not an acute obstructive event.
Taken together with her clinical course and radiation history, these findings support a unifying etiologic hypothesis rooted in the known delayed effects of ionizing radiation in rapidly dividing and neuromuscular tissues.
Radiobiologic Mechanisms Relevant to Mimi’s Case
Hematologic injury and immune-mediated hemolytic anemia
Ionizing radiation is well known to injure bone marrow hematopoietic stem and progenitor cells. In the hematopoietic subsyndrome of acute radiation syndrome, whole‑body doses on the order of 0.5–1 Gy in adult humans can precipitate declining blood counts over 1–3 weeks as existing circulating cells die and marrow fails to replenish them (MacVittie et al., 2015; Waselenko et al., 2004). At higher doses, pancytopenia and fatal infection or hemorrhage may occur. Juvenile animals are expected to have heightened susceptibility to these effects because their baseline marrow proliferation rate is higher and their reserve capacity is lower than in adults (Hall & Giaccia, 2012).
In Mimi’s case, the timing of her anemia—appearing roughly three to four weeks after the airport X‑ray exposure—falls squarely within the classic window for early marrow-related radiation effects. However, her hematologic picture was not that of pure marrow aplasia. Instead, she exhibited a strongly regenerative response, with reticulocytosis and rising PCV once steroids were initiated. This suggests that:
- Her hematopoietic stem cell compartment remained at least partially functional.
- Radiation may have contributed by altering red cell membrane antigens, promoting oxidative damage, or disrupting immune tolerance, thereby triggering immune-mediated hemolysis.
There is precedent in human and experimental literature for radiation-induced immune dysregulation and autoimmunity, including altered T‑cell subsets and increased autoantibody production after sublethal exposures (Hayashi et al., 2013). While feline IMHA is most often secondary to infections, neoplasia, or drugs (Voges & Dowgray, 2022; Weiss, 2010), no such triggers were identified in Mimi. Given the temporal relationship, the absence of alternative causes, and the pathologist’s confirmation of IMHA, it is reasonable to posit that Mimi’s IMHA was a delayed hematologic manifestation of her whole‑body X‑ray exposure.
Gastrointestinal radiation injury and chronic jejunal fibrosis
The small intestine is one of the most radiosensitive organs. Intestinal crypt stem cells divide rapidly and are highly vulnerable to DNA double‑strand breaks and vascular injury (Hall & Giaccia, 2012; StatPearls – Radiation Enteritis). High-dose whole‑abdominal irradiation produces acute GI syndrome with epithelial denudation and sepsis within one to two weeks. Lower dose or partial‑volume irradiation may not cause immediate catastrophic failure but can lead to chronic radiation enteropathy characterized by:
- Chronic submucosal and transmural inflammation
- Progressive fibrosis
- Obliterative endarteritis of submucosal vessels
- Localized strictures and rings
- Impaired motility and malabsorption
These changes can manifest weeks to months after the inciting exposure (Booth et al., 2012). In dogs and cats receiving therapeutic abdominal radiation, delayed intestinal strictures and obstructions are recognized complications, especially when doses per fraction are high or concurrent chemotherapy is given.
Mimi’s necropsy finding of a chronic fibrotic jejunal ring closely matches these descriptions. The lesion was fibrotic and well‑organized, with no evidence of acute necrosis. It behaved as a compensated, non‑obstructive segment during life—Mimi maintained normal stools, gained weight after her first discharge, and showed no signs of chronic obstructive vomiting in the weeks before readmission. The fibrotic ring may thus be understood as a delayed, localized expression of chronic radiation enteritis, anatomically silent but pathologically significant.
Importantly, nothing in Mimi’s history explains such a lesion other than radiation. She had no prior abdominal surgery, no documented GI foreign body, and no chronic inflammatory bowel disease diagnosis. In a three‑to‑five‑month‑old kitten, idiopathic chronic jejunal fibrosis is extraordinarily unlikely. Radiation injury offers a coherent mechanism: localized damage to a jejunal segment during the airport exposure, followed by progressive fibrosis and vessel narrowing, culminating in the chronic fibrotic ring observed at necropsy.
Neuromuscular injury and megaesophagus
Megaesophagus in cats is uncommon and is far more often secondary than idiopathic. Reported causes include neuromuscular junction disease (e.g., myasthenia gravis), generalized neuropathy or dysautonomia, severe esophagitis, chronic esophageal obstruction, and nutritional deficiencies such as thiamine deficiency (Platt, 2014; Wilmot & Washabau, 2017). In Mimi’s case:
- Myasthenia gravis was not demonstrated.
- No structural vascular ring anomaly was identified.
- Megaesophagus was documented by barium swallow during her first admission, weeks before the profound electrolyte disturbances of her second decline.
- Neurologic examination aside from post‑ictal changes and later ventroflexion was otherwise unremarkable for a global dysautonomia syndrome.
Ionizing radiation is known in human oncology and experimental models to cause both acute esophagitis and delayed esophageal dysfunction when the thoracic esophagus and regional nerves are irradiated. Chronic radiation effects can include fibrosis of the esophageal wall, damage to the myenteric plexus, and injury to vagal nerve fibers, all of which may impair peristalsis and sphincter control (Hall & Giaccia, 2012; Platt, 2014). These late injuries often emerge weeks to months after radiotherapy.
Given Mimi’s exposure to a penetrating X‑ray beam in a baggage scanner, it is plausible that her esophagus, vagus nerves, and esophageal neuromusculature received enough radiation to suffer subclinical injury. The appearance of megaesophagus by late June—roughly seven weeks after exposure—fits the expected timing of early delayed radiation neuropathy. This neuromuscular impairment then interacted with later metabolic stresses (thiamine deficiency, severe hypophosphatemia and hypokalemia) to worsen esophageal function and esophagitis, further compromising nutrition and increasing aspiration risk.
Radiation, malnutrition, and refeeding vulnerability
Although refeeding syndrome is not itself caused by radiation, radiation enteropathy contributes to malnutrition through pain, dysmotility, and impaired nutrient absorption. Mimi’s course illustrates this interaction vividly. After her first admission, she experienced periods of reduced intake, GI gas, constipation, and regurgitation. Her esophagitis and megaesophagus made feeding both uncomfortable and inefficient. These factors, combined with prior illness, left her in a depleted metabolic state with limited reserves.
When calories are suddenly reintroduced after undernutrition—particularly carbohydrate-rich calories—insulin secretion drives glucose and electrolytes (phosphate, potassium, magnesium) into cells. Serum levels fall, precipitating:
- Hypophosphatemia, impairing ATP generation and oxygen delivery
- Hypokalemia, leading to arrhythmias and muscle weakness
- Hypomagnesemia, worsening hypokalemia and destabilizing neuromuscular excitability
- Acute thiamine depletion, as thiamine is consumed in high‑throughput carbohydrate metabolism
This pattern defines refeeding syndrome (Mehanna et al., 2008; Whitby et al., 2019). Cats are especially dependent on adequate thiamine, and thiamine deficiency in cats is well known to produce neurologic signs, ventroflexion, and, in some cases, esophageal dysfunction (Platt, 2014; Merck Veterinary Manual).
Mimi’s severe hypophosphatemia and hypokalemia, seizures, encephalopathy, ventroflexion, and progressive inability to hold her head up are textbook manifestations of refeeding syndrome compounded by thiamine deficiency and absent magnesium replacement. Radiation did not cause the refeeding syndrome directly, but it set every precondition: intestinal injury, chronic nausea and regurgitation, compromised intake, and heightened metabolic demands related to healing.