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“Charlie”: 3 year old MC Poodle, 31.8kg
Presentation: collapse and labored breathing
History: 48 hours prior to presentation, “Charlie” ingested 5 Nutballz energy bars, each containing 9gm of Xylitol, as well as another bar 24 hours later. The day prior to presentation, the owner reported that Charlie was lethargic, however eating normally. He was drinking more water. He had one episode of vomiting that evening. The day of presentation, he had urinated in the house and would not eat. Charlie went to his regular veterinarian that afternoon. Blood work had been sent to an outside laboratory. Radiographs did not show an obvious obstruction. He was treated conservatively (SQ fluids, reglan, etc) and sent home. After the initial visit, the owner thought Charlie seemed brighter, but still not himself. That evening, the owner found him in lateral recumbency. He was unresponsive and was having labored breathing. Charlie was rushed to VESCONE.
Presentation:
T: 103.8; HR 200, RR: 60 with moderate effort
Pale to white mm; >3 sec
Comatose/weak - with dilated pupils, minimal light and palpabral response. No menace response. He had been drooling and clear nasal discharge (bilateral) was noted.
Tachycardia, weak femoral pulses
Tachypnea with increased respiratory effort
Soft, non-painful abdominal palpation; frank blood found on rectal exam
Non-ambulatory; rigidity and weak reflexes found in all four limbs
Problem list:
Collapse
Tachycardia
Tachypnea
Febrile
Weak
CN deficits
hematochezia
History of vomiting, lethargy, polydipsia and inappropriate urination
Rule outs:
Shock (hypovolemic, cardiovascular)
Xylitol toxicity
Other toxin exposure
Sepsis
Hemorrhagic gastroenteritis
Infectious disease
Metabolic disease
Endocrine disease
Inflammatory (pancreatitis, etc.)
Neurologic (seizures etc.)
Treatment:
On presentation, Charlie’s blood glucose was 23 and his blood pressure was not measurable by Doppler. His EKG showed a sinus tachycardia. A one-liter bolus of LRS was given along with 10 cc of LRS/50% dextrose intravenously. A CBC, biochemical profile, blood gas, coagulation profile and lactate were collected after the initial bolus. His blood pressure at this time was 50mmHg. He was given a second liter bolus of LRS. After the second bolus, his heart rate dropped to 140 and both his blood pressure and blood glucose were 70. He was started on 5% dextrose drip and was given a hetastarch bolus. Charlie became more responsive and was attempting to pick up his head.
Approximately 45 minutes after presentation, Charlie became unresponsive and comatose. His heart rate and respiratory rate increased and effort was labored. His blood pressure was less than 50mmHg and his blood glucose was 300. The dextrose drip was stopped. Charlie was given a third litter bolus of LRS and an additional hetastarch bolus. He began to seizure, and was given intravenous valium. He then went into respiratory arrest shortly after. CPR efforts were started; he was intubated and frothy red foam was found in the back of his throat. Petechia was noted around his catheter sites. Soon after, he went into full cardiac arrest. Resuscitation measures were successful and his cardiac and respiratory function returned. Because of the critical and declining nature of Charlie’s condition, the owner declined further CPR measures.
30 minutes after initial CPR, he suffered a second cardiac arrest, and could not be resuscitated.
Results of blood work collected after the initial bolus upon entry:
PT/PTT: out of range
CBC: low platelet count on automated counter
Profile: low ALT (36), TP (4.9), Globulin (2.2); elevated T.Bil (2.0), BUN (35), Cre (1.3),
PCV: 49
Lactate: HI
Blood gas: metabolic acidosis (7.008) with low bicarbonate (8.5)
A necropsy was performed. The lungs were grossly normal. There was black fluid found in the trachea. The heart was small and the serosal surface was covered with petechia. The abdominal cavity contained a large amount of bloody fluid. There was marked hemorrhage extending from the mid jejunum to cecum region. There was grayish-red discoloration of the entire intestinal tract. There were blood clots and petechia seen in the messentry and in the omentum. The stomach and major portions of the intestines were open and all were filled with sersangiouis fluid. The liver, spleen and kidneys looked grossly normal
Tissue was obtained and submitted for histopathology.
Abnormal findings included:
1. Severe and diffuse acute hepatic necrosis
- Chronic idiopathic inflammatory bowel disease
- Protein casts found in renal tubules.
- Congestion and focal areas of atelectasis in the lungs
Discussion:
Xylitol is not a commonly seen toxin in companion animals. It is a 5 carbon sugar alcohol and is approximately as sweet as sucrose. It exists naturally in low concentrations in fruit and vegetables. It is mostly used as a sweetener in many sugar-free candies and gums, either alone or in combination with other sugar-alcohols and/or aspartame. Unlike glucose, xylitol does not require insulin to enter cells.
In humans, xylitol causes negligible to small increases in blood glucose and insulin levels. In dogs, however, xylitol exposure causes rapid and dose-dependent rise in insulin levels with a concurrent drop in blood glucose levels. Dogs that ingest a significant amount of gum or products containing xylitol may develop a sudden drop in blood glucose level resulting in depression, loss of consciousness, and possible seizures. It is also possible for xylitol to cause liver failure in dogs, though this has not been proven. The mechanism of toxicity is still not known. The current thought is that liver failure may be associated with prolonged hypoglycemia.
The oral minimum toxic level has yet to be established. In the literature, an IV dose of 0.2-0.4 g/kg can cause hypoglycemia in the dog. Xylitol is well absorbed. It is suspected that the oral toxic dose is similar to the IV dose.
Treatment for xylitol toxicosis includes emesis, provided that emesis can be performed shortly after ingestion and before clinical signs develop. A dog can show signs of hypoglycemia in as little as 30 minutes of ingestion. Frequent small meals or oral sugar supplementation may be used to manage dogs not showing signs. For dogs showing clinical signs, IV dextrose, via bolus, followed by dextrose as a constant infusion, should be used to control moderate to severe hypoglycemia. Hypokalemia, likely secondary to insulin-induced movement of potassium into cells, should be treated if significant (<2.5). Treatment should continue until blood glucose normalizes. It may take a up to 48 days for symptoms to resolve. Symptomatic treatment and prevention of other problems (DIC, renal failure etc) is also recommended. Prognosis is guarded to poor, depending on the severity. Other differentials for xylitol toxicosis are insulin overdose, oral hypoglycemic agents, pancreatic tumor, juvenile hypoglycemia, and idiopathic causes.
With the increased appearance of xylitol-sweetened products in the US, xylitol toxicosis in dogs may become more common, and should be considered in patients with profound hypoglycemia with no other obvious/detectable cause.
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