HISTORY

A 5 month old female, sexually intact Labrador Retriever was referred for ingestion of paintballs, approximately 5-7 hours prior. Abdominal radiographs already obtained at the referring veterinarian showed: a large amount of circular masses with soft tissue opacity in the stomach, along with a small metallic wire (latter was on the bag of paintballs). She had been treated with 1 liter of intravenous lactated ringers and 500 mg of Soludelta cortef IV. She was observed to urinate green urine. Poison control was consulted and she was referred for continued care. The dog did not have any prior medical nor surgical problems.

PHYSICAL EXAMINATION

On presentation she was hypothermic at 98.4 degrees Fahrenheit. She had muddy/grey mucous membranes with a slow capillary refill time. Her heart rate was 120 bpm and her pulses were strong and synchronous. Her respiratory rate was 24 bpm and her respiratory effort was normal. She weighed 20.3 kg. She had green material in her oral cavity and a digital rectal examination revealed bright green diarrhea. Her abdomen was mildly distended and tense on palpation. She urinated green urine on presentation. She was non-ambulatory and obtunded on presentation with a minimal gag reflex. Her pupils were miotic. Her heart and lungs ausculted normally.

DIAGNOSTICS AND TREATMENT

She was normotensive at 160 mm Hg. A complete blood count, chemistry screen, venous blood gas and coagulation profile revealed the following abnormalities:
Metabolic acidosis (bicarbonate = 18.6 mM, pH = 7.286)
Hypernatremia 165.9 mM
Hypokalemia = 3.48 mM
Elevated alkaline phosphatase (164 U/L) and hyperphosphatemia (10.7 mg/dl) -> these attributed to age of patient
Poison control was again consulted on the case now that the above bloodwork was obtained. The dog was started on 0.45% sodium chloride with 20 mEq/L potassium chloride at a twice maintenance rate. The dog was intubated (intravenous propofol was titrated to effect to facilitate this) and an orogastric tube was placed. Gastric lavage was performed with warm water, and a large amount of green fluid with collapsed paintballs (soft and looked like dog kibble) were evacuated. She was given warm water enemas. She recovered uneventfully from anesthesia, and was extubated, but remained obtunded.
Her electrolytes were monitored. Bloodwork six hours after presentation demonstrated a worsening of hypernatremia (175.6 mM), worsening of metabolic acidosis (bicarbonate =16.1 mM, pH = 7.181), and now present hemoconcentration and elevated total solids (49% and 7.6 mg/dl, respectively on presentation; now 53% and 8.4 mg/dl, respectively). She remained obtunded. She was given a 500 ml intravenous bolus of 0.45% sodium chloride and her CRI was increased to three times maintenance. The warm water enemas were continued.
Eight hours after presentation bloodwork illustrated stabilization of the hypernatremia (16.7 mM) and metabolic acidosis (bicarbonate = 16.7 mM, pH = 7.216). The PCV was now 48% with a total solids of 7.0 mg/dl. At this point she was ambulatory but ataxic, and was wagging her tail. Warm water enemas were continued.
Fourteen hours after presentation, bloodwork demonstrated improvement in her hypernatremia (155.3 mM), and her metabolic acidosis (bicarbonate = 18.6 mM, pH = 7.248). Her PCV and total solids were 50% and 7.8 gm/dl, respectively. At this point she was drinking and eating well. Clinically, her attitude and gait were normal. Her intravenous fluids were later tapered and she was discharged 24 hours after presentation to VESCONE.

DISCUSSION

Paintball ingredients can vary depending upon the manufacturer but can consist of the following: polyethylene glycol, glycerol (glycerin), gelatin, sorbitol, dipropylene glycol, mineral oil, dye, ground pig skin, and water.
The most common clinical signs are vomiting, ataxia, diarrhea, and tremors. These can occur as early as one hour after ingestion. Other clinical signs include: tachycardia, weakness, hyperactivity, hyperthermia, polydipsia, blindness, depression, and coma. The toxic dose of paintballs is not known.
Laboratory abnormalities typically involve acidosis and electrolyte disturbances, of which hypernatermia is the most common. Hyperchloremia and hypokalemia are also possible.
While the exact mechanism of the hypernatremia is not known, it is suspected to be secondary to an alteration in water balance. Polyethylene glycol, glycerol and sorbitol are osmotically active and promote the influx of water into the lumen of the gastrointestinal tract.
It is thought that the rapidity of hypernatremia, rather than the magnitude, is more significant in affecting neurologic clinical signs. Even small elevations in sodium as low as 5 mEq/L can cause neurologic effects, if the change is acute enough. Hypernatremia results in the movement of water out of the brain cells by osmosis. A loss of brain volume can ensue with subsequent tearing of meningeal vessals. Hypernatremia can cause cerebral vessals to swell and rupture.
This is in contrast to a more gradual onset of hypernatremia (i.e. over 24-48 hours) where idiogenic osmoles are produced. Fluid balance is maintained longer and neurologic signs may not be seen until sodium is elevated by 20 mEq/L.
Treatment of paintball toxicosis follows basic toxicology principles: limit exposure, symptomatic and supportive care.
Once ingested, the osmotically active paintball toxins can act quickly in the gastrointestinal tract. Induction of emesis should be attempted within one hour of ingestion. As neurologic signs can be common and severe, it is very important that animals be evaluated before induction of emesis is considered. The dog described above had severe neurologic signs. The advantages and disadvantages of light anesthesia and gastric decontamination were considered with respect to this. As paint balls were radiographically evident in the stomach, gastric decontamination was performed.
Warm water enemas may help with passage of the paint balls through the gastrointestinal tract, and may help counter the electrolyte imbalances induced by the osmotically active toxins. Due to the suspected mechanism of action, activated charcoal would not be of much benefit. Activated charcoal with sorbitol would be contracindicated.
Obtain baseline bloodwork and monitor electrolytes every few hours until hypernatremia and any clinical signs have resolved. For asymptomatic patients with normal bloodwork, monitor for a minimum of four hours.
Treat hypernatremia with half-strength saline. Rates of 2-3 times maintenance, or more, may be necessary. This is in contrast to the treatment of more chronic hypernatermia (i.e. over 24-48 hours). Here if idiogenic osmoles aren’t allowed to dissipate, cerebral edema may result. Thus a slower fluid rate should be used.
Supplemental potassium can be used for hypokalemia. Metoclopramide can be used for vomiting. Muscle tremors and seizures can be treated with diazepam. Provide thermoregulation and other supportive care as needed.
Although paintball toxicosis is potentially fatal, most animals will recover in 24 hours with appropriate symptomatic and supportive care.

REFERENCES

ASPCA Animal Poison Control Center, 886-426-4435.
Donaldson, CW. Paintball toxicosis in dogs. Veterinary Medicine 2003: 995-997.