Originally Posted by TeddyBear1992
You should be alright if it was only a few.
Here is an article on dogs and paintball toxicosis.[/url]
Here is what the article says:
Toxicology Brief: Paintball Toxicosis
Paintballs, which are used in “capture the flag” and other games, are sold online and in many sporting goods stores in packages of up to 2,000. Most paintballs are slightly more than a half-inch in diameter, making them small enough to be swallowed easily. While ingestion of small numbers of paintballs (less than one per 10 lb of body weight) is considered to pose a low risk of adverse effects, most dogs tend to ingest very large amounts.1
PAINTBALLS AND PETS
Paintballs are gelatin capsules filled with dyed liquid. They are designed to be fired from a paintball gun and break open on impact, marking their target with their contents. Although paintball “paint” is nontoxic, many of the ingredients, such as polyethylene glycol, dipropylene glycol, glycerol, and sorbitol, are osmotically active when ingested, meaning that they act to draw free water from the body into the gastrointestinal tract. Ingestion of these substances can result in a fluid shift that can cause increased plasma osmolarity, hypernatremia, metabolic acidosis, and neurologic signs. Although some of these compounds can be used therapeutically in dogs, large amounts can be unsafe. Since 2002, the ASPCA Animal Poison Control Center has received more than 300 calls regarding paintball toxicosis in dogs, cats, and ferrets. The overwhelming majority (98%) of these cases involved dogs.
The most common clinical signs of paintball toxicosis are vomiting (64%), ataxia (34%), and diarrhea (27%). Other reported signs include tremors (20%), lethargy, polydipsia, hyperthermia, depression, weakness, and acidosis.1
Clinical signs can be seen in as few as 30 minutes after exposure but generally occur within 2 to 4 hours. The severity of clinical signs depends on the number of paintballs ingested, the weight of the animal, and the timeliness and effectiveness of decontamination.2 The number of paintballs that must be ingested to cause clinical signs is unknown and may depend on the individual patient. In one case reported to the Animal Poison Control Center, a 90-lb Labrador retriever showed clinical signs after ingesting only 15 *paintballs.3
Hypernatremia and other electrolyte imbalances are common laboratory findings. The exact mechanism that results in hypernatremia is unknown, but it is suspected to be related to hypotonic fluid loss caused by the shift of body water into the intestinal lumen. Signs of hypernatremia include a serum sodium level higher than 160 mEq/L, vomiting, diarrhea, polydipsia, muscle weakness, tachycardia, seizures, disorientation, tremors, behavior changes, coma, and death.3,4
Emesis should be induced within 1 hour of paintball exposure to reduce the risk of signs in an asymptomatic animal and if no contraindications to emesis exist.3 Because activated charcoal does not bind to the paint ingredients, it is not beneficial in these cases. In addition, activated charcoal that contains sorbitol is contraindicated because it will draw even more free water into the gut, worsening the hypernatremia and neurologic signs.3,4
Serum electrolyte concentrations should be monitored every 2 to 4 hours and any imbalances corrected; the patient’s acid–base status should be monitored and corrected as necessary; and thermoregulation should be provided.2,3 Tremors and seizures should be controlled with a muscle relaxant (e.g., diazepam, methocarbamol) and vomiting controlled with an antiemetic (e.g., metoclopramide). Potassium chloride may be supplemented if the serum potassium level is low, but the potassium level should not exceed 0.5 mEq/kg/hr. If the serum potassium level is raised too quickly, fatal hyperkalemia may develop.5
Fluid Therapy in Hypernatremia
Fluid and electrolytes should be replaced in hypernatremic animals, but care should be taken when setting initial fluid rates. Treatment with fluid replacement varies depending on whether the hypernatremia developed quickly (acute) or over 24 to 48 hours (chronic).6 The type and severity of clinical signs are thought to be more related to how fast the serum sodium level rises than to the change in the sodium concentration itself.3 In pa*tients with acute hypernatremia, signs may be noted when the serum sodium level exceeds 160 mEq/L, whereas signs in patients with chronic hypernatremia may not be noted until the level exceeds 175 mEq/L.3 This is because in patients with chronic hypernatremia, the brain can compensate over time and maintain its own fluid balance by producing intracellular solutes that hold the space of the lost water and prevent the brain from shrinking when there is fluid loss.3,6 If fluids are replaced too quickly in an animal with these solutes present in the brain, cerebral edema may develop.3,6
When treating patients with acute hypernatremia, intravenous fluids should be given at a rate of 1.5 to two times the maintenance dose using 5% dextrose in water or 2.5% dextrose in 0.45% saline.3,6 Warm-water enemas may be given at a rate of 3 to 5 ml/lb to help stimulate movement of the paintballs out of the GI tract and can be repeated every 1 to 2 hours initially if sodium levels continue to rise.2,6 The colon has a good absorptive surface, and enemas may also help to decrease the serum sodium level by giving the body another source of water to absorb. The frequency of enemas varies depending on the sodium level and response to therapy.
When treating patients with chronic hypernatremia, extreme caution should be taken in calculating a fluid rate. The free water deficit should be calculated first, and no more than 50% of that volume should be replaced over the first 24 hours.6 The other 50% should be given over the next 24 to 48 hours.6 The fluid rate will be very low for these animals because the sodium level should not be lowered at a rate any faster than 0.5 mEq/L/hr.3,4,6 Enemas are contraindicated in these patients as well.6
As in any case, good nursing care is imperative in patients presenting with paintball toxicosis. Symptomatic and supportive care should continue until all clinical signs resolve, usually within 24 hours.4 The patient should be monitored closely and kept clean, dry, and warm, especially if it is unconscious. Vital signs, intravenous catheter placement, and fluid rate should be monitored as well, and whether the patient is able to drink water on its own should be noted. The patient should also be monitored for signs of fluid overload, such as pitting edema or moist lung sounds.
ROLE OF THE TECHNICIAN
Technicians play an important role in these cases because they are usually the first team members to see the patient on presentation. Getting an accurate history, including the time of exposure, amount of paintballs ingested, and any clinical signs, dictates where the treatment process will begin. Also, it is important to stay on top of the treatment schedule, monitor the patient for clinical signs, and recheck the blood work for changes and response to therapy. Client education is also key, since owners can be warned about other potentially toxic substances that they may have in their homes. Most labels for paintballs list them as nontoxic, so owners may be lured into a false sense of security. It should be explained to clients that while the individual ingredients alone may be nontoxic, ingestion of a large number of paintballs may cause serious and life-threatening signs.
The author thanks Brandy Sobczak, DVM, Camille DeClementi, VMD, Mindy Bough, CVT, and Sharon Gwaltney-Brant, DVM, PhD, DABVT, DABT, all of whom are affiliated with the ASPCA Animal Poison Control Center, Urbana, Illinois, for reviewing this column and offering suggestions and comments.
1. ASPCA Animal Poison Control Center Case Database: Unpublished data, Urbana, IL, 2002–2006.
2. Bough M: Paintballs. NAVTA J 2006 (spring):27.
3. DiBartola SP: Fluid Therapy in Small Animal Practice, ed 2. Philadelphia, WB Saunders, 2000, pp 52–59.
4. Donaldson C: Paintball toxicosis in dogs. Vet Med 98(12):995–997, 2003.
5. Plumb DC: Plumb’s Veterinary Drug Handbook, ed 5. Ames, IA, Blackwell Publishing, 2005, pp 645–646.
6. Sobczak B: Paintball Toxicosis. Toxicology Short Course presented by the University of Illinois College of Veterinary Medicine and ASPCA Animal Poison Control Center. Unpublished presentation, 2006.