Cheyenne, a 5.5 year old, 28.5 kg, female spayed Husky was referred to the Veterinary Emergency and Specialty Center of New England (VESCONE) for azotemia on April 2nd, 2003. She has a history of zinc responsive dermatitis and was treated on 3/29/03 with IV zinc when her topical zinc ointment was not resolving her condition. Within 24 hours of the IV zinc administration, she became lethargic, anorectic and started vomiting profusely. She was then seen at another referral hospital where she was placed in IV fluids and diuresed for 24 hrs. She received pepcid and amoxicillin. Her urine output was possibly decreased. Her blood work is as follows:
HCT- 42%, CBC WNL
Creat 7.1 mg/dl
BUN 72
K+ 2.9 mg/dl
SAP 151
ALT 144
Albumin 2.6 g/dl
Globulin 2.1
Phosphorus 3.2
Urinalysis showed 1+ Ca+ Oxalate crystalluria, no protein
Cheyenne was taken home after 24 hours, taken to her regular DVM 24 hrs later where her bloodwork was repeated and unchanged, and she was again placed on IV fluids (rate unknown). Her urine output (UO) was 80cc over the day. She was then transferred to VESCONE for further diuresis and management of her renal failure.

Physical Exam and Diagnostic Procedures

On physical exam, Cheyenne was inappetant, depressed, slightly pale, mildly tachycardic at 130 bpm, a Grade 2/6 low-pitched systolic murmur was asculted bilaterally. She was panting with a temperature of 100.6, lungs were clear. We could not palpate a bladder, she had just urinated.
Her initial blood pressure (BP) was 130mmHg, initial in-house Chemistry panel/venous blood gas were as follows:
All else was normal except for:
Albumin 2.5
BUN 91
Creatinine 9.0
K+ 3.7
HCT –28%
TS –4.4
Blood for leptospirosis, tick serology and a zinc level was sent to Antech. All titers were negative and her blood zinc level was slightly above normal at 2.3 2-3 days after her IV zinc was given. Normal serum zinc levels are .7-2 ppm, with zinc levels above 10ppm in cases of zinc toxicity. We did not have any initial zinc levels from her RDVM or other referral hospital where she was initially treated.

Treatment

Upon admission a jugular and peripheral catheters were placed, central venous pressure to assess hydration and BP were measured three times daily, as well as IV plasmalyte was started at 70cc/hr.
12.5mg Pepcid IV SID and 700 mg Ampicillin IV TID was started. Her centrl venous pressure (CVP) was 14cm H2O, which indicated overhydration. Thoracic radiographs showed a mildly increased interstitial pattern, a slightly wide vena cava, and mild LV enlargement. Ultrasound revealed hyperechoic cortices, smooth and with good blood flow, with a possible faint rim of hypoechogenicity at the outer cortex, suggesting fluid accumulation.
Negligible amounts of urine was produced the first 8hrs. She was now in oligouric renal failure. We then sedated her with propofol; 4mg/kg IV followed by isoflurane gas and placed a 10Fr. Foley urinary catheter. A lasix constant rate infusion (CRI ) was started to promote urine production, at 6mg/hr IV in plasmalyte. A bolus of lasix was given first, 2mg/kg IV. Her fluids were increased to 150cc/hronce she started to produce urine and her CVP reduced to below 10cm H20.
Over the next 7 days we monitored her renal values, electrolytes, CVP, BP and urine output. We controlled her nausea most with pepcid, Amphogel even with her persistent anorexia, and carafate. Her fluids were increased to 150cc/hronce she started to produce urine and her CVP reduced to below 10cm H20.
Her temperature was consistently 99 degrees, HR 100 bpm, and she was still not eating for the first 24-72 hrs.
With the intensive fluid therapy and lasix, her UO improved to equal her intake of fluids, but her renal values and electrolytes remained elevated. Her creatinine slowly came down to its lowest value of 5.6, BUN to 55. The phosphorus remained high at 10.8, despite Amphogel orally as a phosphate binder. She became hyponatremic at 111g/dl and had 2 seizures, and we switched her IV fluid crystalloid to .9% isotonic saline. She improved on the saline and was much more alert, with her final NA+ at 134 MMOL/L.
After 5 days in the hosp, with intensive diuresis, all but her renal values had normalized. Dialysis was again discussed with her owner and declined. She was sent home on oral carafate, pepcid, and to follow up with her regular DVM for subq fluid therapy – 300cc twice daily. He was to follow up in 5-7 days, for a recheck exam, blood pressure, and bloodwork. If her values were not improving or worsening, she was to return toVESCONE for additional diagnostics: coagulation panel, and a renal biopsy to rule out other causes of her renal failure.
Over the next few weeks, despite our predicted poor prognosis, she started to eat and her renal values reduced to completely normal. This dog has no residual clinical signs or abnormal lab values, and she is doing very well.

Discussion

The most common forms of zinc toxicity are in the form of ingestion of coins or products that contain zinc such as Desitin ointment. The ASPCA Animal Poison Control Center has reported 18 presumptive cases of zinc toxicity between January of 1998 and December of 2000. To this date, there are no known documented cases of zinc toxicity when given zinc intravenously. Cheyenne was being treated originally with topical zinc for her dermatosis. The most common clinical signs reported by the ASPCA were anemia, depression, vomiting, hemolysis, and hemoglobinuria. The renal effects included azotemia, and PU/PD.
The exact mechanism of zinc mediated renal injury is not known. This can occur secondary to anemia, hypoxia, or hemoglobinuria which Cheyenne did not have an overwhelming evidence of, as well as possible direct injury to the renal tubular epithelium. This is similar to renal injury from other heavy metal toxicoses.
Increased pancreatitis and liver enzyme activity can be seen with zinc toxicity but are not commonly reported. Death can occur from severe anemia or multiorgan failure. Measuring plasma or urine zinc levels can be helpful when trying to diagnose toxicosis.
Treatment involves removing the inciting agent, any metal (pennies) foreign bodies seen either surgically or by emesis induction if the patient is stable. Stabilization with fluids, blood products if needed, oxygen, gastroprotectants such as carafate, pepcid, and metoclopromide to control vomiting. Pepcid will reduce gastric acidity thereby reducing zinc absorption. Activated charcoal is not recommended, as it is ineffective in adsorbing zinc.
Monitoring should include monitoring electrolytes, BUN, creatinine, BP, urine output, hydration, temp, and mm color
Chelation is considered controversial. The zinc concentrations in the blood will decrease over time if the inciting agent is removed. Chelating may increase gastrointestinal absorption and is potentially nephrotoxic.