Successful therapy of coumatetralyl rodenticide induced pericardial effusion with pericardiocentesis in a dog

Abstract

A 5-year-old, intact male, golden retriever was presented with an acute onset of lethargy and respiratory distress. The dog was diagnosed as having rodenticide intoxication with pericardial effusion. Pericardiocentesis was successfully performed and was followed with a blood transfusion. This case suggests that rodenticide intoxication might cause pericardial effusion in dogs.

Although rodenticide intoxication is one of the most common poisonings reported, concerns about its cardiac effects have not been a focus in veterinary medicine. There is only 1 case report of pericardial effusion secondary to the ingestion of anticoagulant rodenticide in a dog (1).

Anticoagulant rodenticides include first and second generation compounds. Coumarins such as warfarin, dicoumarol, and coumatetralyl, and indanediones such as valone and pindone belong to the first generation. The second generation compounds include brodifacoum, diphacinone, and bromadiolone. The second generation rodenticides are far more toxic and have a longer duration of action compared with the first generation (2–4). Fatal internal bleeding can be caused by lethal doses of anticoagulants such as brodifacoum, coumatetralyl, or warfarin.

This report describes a dog with a pericardial effusion associated with coumatetralyl rodenticide intoxication that was successfully treated with pericardiocentesis and standard management.

Case description

A 5-year-old, intact male, golden retriever weighing 30 kg was presented with an acute onset of lethargy and respiratory distress. The owners reported that they had spread several pieces of bread with rodenticide in their backyard about 3 d before clinical signs started. The dog was found at the backyard in lateral recumbency. The owners brought the dog with a bottle of the rodenticide which was identified as coumatetralyl. On physical examination, the dog was lethargic and had a temperature of 39.0°C, labored tachypnea (54 breaths/min), and tachycardia with a heart rate of 150 beats/min. There were no petechiae or ecchymoses on the mucous membrane and skin. Although there were no heart murmurs, mild muffled heart sounds were detected. A complete blood (cell) count (CBC) demonstrated a mild leukocytosis with a stress leukogram and moderate regenerative anemia with moderate thrombocytopenia (Table 1). The serum biochemical analyses revealed a mild azotemia, marked elevation of creatinine kinase (CK), and increased aspartate aminotransferase (AST), hypoalbuminemia, and hypoproteinemia (Table 2). The heartworm antigen and microfilaria tests were negative. The dog’s serum cardiac troponin I (5.42 ng/mL; reference range: 0.0 to 0.7 ng/mL) and creatine kinase isoenzyme MB (28.36 U/L; reference range: 0.3 to 2.9 U/L) were markedly increased. The coagulation panel abnormalities included prolonged prothrombin time (PT) (32.6 s; reference range: 7.5 to 10.5 s), activated partial thromboplastin time (APTT) (37.2 s; reference range: 8.0 to 11.8 s), increased concentration of fibrin degradation products (FDP) (between 10 and 30 μg/mL; reference range: < 5 μg/mL), and elevated D-dimers (> 5.0 μg/mL; reference range: < 0.5 μg/mL) (Table 3). Moderate thrombocytopenia was confirmed on both a blood smear examination and a CBC panel. The radiographic findings showed signs of a pleural effusion with an interlobar fissure on the right lateral view and air bronchograms around the heart base (Figure 1A). The cardiac silhouette was obscured and the right lung field had increased opacity on the dorsoventral view (Figure 1B). The initial electrocardiographic findings revealed a sinus tachycardia with mild variation of the QRS complexes and ST segment depression; however, no significant electrical alterations were seen. Pleural effusion and pericardial effusion presenting as an echo-free space between the epicardium and the pericardial sac were confirmed on the echocardiographic examination with ECG gating (Figure 2). There were no anatomical or functional abnormalities of the heart except for the pericardial effusion.

Table 1.

Changes in the complete blood count in a dog with a pericardial effusion caused by rodenticide intoxication

	Day 0a	Day 1	Day 2	Day 3	Reference
WBC (×103/μL)	18.38	16.02	19.58	20.2	6–17
RBC (×106/μL)	3.99	4.31	5.89	6.23	5.5–8.5
Hb (mg/dL)	9.4	9.8	13.7	13.9	12–18
PCV (%)	25	28	38	40	37–55
MCV (fL)	65	64	65	64.1	60–74
MCH (pg)	23.5	22.8	23.3	22.3	19.5–24.5
MCHC (%)	36.3	35.3	36	34.8	31–36
Platelet (×103/μL)	61	64	112	111	200–500

^aAnalysis was done before the blood transfusion therapy; WBC — white blood cell; RBC — red blood cell; Hb — hemoglobin; PCV — packed cell volume; MCV — mean corpuscular volume; MCH — mean corpuscular hemoglobin; MCHC — mean corpuscular hemoglobin concentration.

Table 2.

Serial profiles in the serum biochemistry in a dog with a pericardial effusion caused by rodenticide intoxication

	Day 0a	Day 1	Day 2	Day 3	Reference
BUN (mg/dL)	76.5	33	15.1	7.2	9.2–29.2
CRSC (mg/dL)	2.1	0.8	0.8	0.7	0.4–1.4
AST (U/L)	424	470	399	180	17–44
ALP(U/L)	187	307	941	611	47–254
LDH (U/L)	570	275	140	89	20–109
CK (U/L)	> 2000	> 2000	> 2000	> 2000	49–166
TP(g/dL)	4.4	4.5	6.2	5.9	5.0–7.2
Albumin (mg/dL)	2.4	2.4	3.3	3.1	2.6–4.0
NH3 (μmol/L)	104	53	ND	ND	16–75

^aAnalysis was done before the blood transfusion therapy. BUN — blood urea nitrogen; CRSC — creatinine; AST — aspartate aminotransferase; ALP — alkaline phosphatase; LDH — lactic dehydrogenase; CK — creatine kinase; TP — total protein; NH₃ — ammonia; ND — not done.

Table 3.

Changes in coagulation parameters over time after vitamin K1 therapy in a dog intoxicated with rodenticide

	Day 0a	Day 1	Day 3	Reference
PT (seconds)	32.6	12.4	10.0	7.5–10.5
APTT (seconds)	37.2	18.2	9.8	8.0–11.8
FDP (μg/mL)	10 ~ 30	< 5	< 5	< 5
D-dimer (μg/mL)	> 5.0	1.7	< 0.5	< 0.5

^aAnalysis was done before blood transfusion therapy. PT — prothrombin time; APTT — activated partial thromboplastin time; FDP — fibrin degradation products; ND — not done.

Figure 1.

Right lateral (A) and dorsoventral (B) thoracic radiographs of a 5-year-old, intact male, golden retriever that was presented with respiratory distress. There is a patchy alveolar infiltrate on air bronchograms (arrow heads) around the heart base area (A). An obscure cardiac silhouette and increased opacity (thin arrows) are noted at the right lung field in the dorsoventral view (B).

Figure 2.

Four chamber long axis views as imaged before and after the pericardiocentesis with ECG guide. Echocardiography of the dog showed a pericardial effusion (white arrows) at the initial presentation (A). The pericardial effusion was significantly reduced after therapeutic pericardiocentesis (B).

The initial therapy for 1 d consisted of vitamin K1 (Kaywan; Eisai Co., Tokyo, Japan), 2 mg/kg body weight (BW), subcutaneously, BID, ampicillin (Ampi-1, Dongwon Pharm., Sungnam, Korea, 20 mg/kg BW, intravenously, BID), oxygen supplementation, and normal saline infusion maintained at a consistent rate. A pericardiocentesis was performed at the right hemithorax with the dog in the left lateral recumbent position during preparation of fresh whole blood transfusion. The right lateral thorax was shaved and surgically prepared over the right hemithorax (sternum to mid-thorax, the 2nd to 8th intercostals spaces). A puncture site was locally anesthetized with 2 mL of 2% lidocaine (Lidocaine HCl; Huons Co., Hwaseong City, Korea) after the optimal intercostal space was found by echocardiographic guide. The costochondral junction of the 5th intercostal space was punctured using a 16 gauge over-the-needle catheter (with 2 additional side holes) and 100 mL of hemorrhagic pericardial fluid was removed. The retrieved fluid was analyzed and the results were similar to those of the CBC from blood samples (Table 4). Ventricular tachycardia suddenly developed following the pericardiocentesis. The ventricular tachycardia, however, immediately resolved after administration of a 2% solution of lidocaine hydrochloride (Huons Co.), 2.2 mg/kg, BW, intravenously, once. Then, cryoprecipitate (Korea Animal Blood Bank, Soksho, Korea), 1 mL/kg BW, intravenously and a fresh whole blood transfusion (total 160 mL) were administered to restore the blood volume and various coagulation factors.

Table 4.

Results of analysis of the retrieved pericardial fluid from a dog with a pericardial effusion caused by rodenticide intoxication

	Pericardial fluid	Reference
WBC (×103/μL)	9.95	6–17
RBC (×106/μL)	6.75	5.5–8.5
Hb (mg/dL)	16.3	12–18
PCV (%)	45.69	37–55
MCV (fL)	68	60–74
MCH (pg)	24.1	19.5–24.5
MCHC (%)	35.6	31–36
Platelet (×103/μL)	49	200–500

WBC — white blood cell; RBC — red blood cell; Hb — hemoglobin; PCV — packed cell volume; MCV — mean corpuscular volume; MCH — mean corpuscular hemoglobin; MCHC — mean corpuscular hemoglobin concentration.

The dog was monitored for 3 d following the pericardiocentesis and the vitamin K1 treatment (2 mg/kg BW, orally, BID) was continued along with normal saline fluid therapy at a maintenance rate. There was marked improvement during hospitalization based on the CBC, serum biochemistry, ECG, and echocardiographic examination. The coagulopathy panels were re-evaluated at 1 d and 3 d after the vitamin K1 therapy and blood transfusion. The PTs were 12.4 s and 10.0 s, respectively. The APTT were 18.2 s and 9.8 s each. The FDP remained within the normal range. D-dimers were 1.7 μg/mL and < 0.5 ug/mL each (Table 3). The dog was discharged on the 4th day with a prescription for limited activity and vitamin K1 (2 mg/kg, orally, BID) for 14 d. Follow-up 15 d after discharge showed that the dog had remained stable.

Discussion

A pericardial effusion is a potentially life-threatening problem; it causes an increase in the intrapericardial pressure resulting in varying degrees of hemodynamic compromise (5). The common causes of pericardial effusion in the dog include peritoneopericardial diaphragmatic hernia, congenital cysts, infectious pericarditis, right-sided heart failure, uremia, left atrial rupture, idiopathic pericardial effusion, cardiac neoplasia, and hemorrhage secondary to neoplasia (6). Pericardial effusion caused by rodenticide intoxication has been rarely reported in the veterinary literature. Petrus and Henik (1) reported successful pericardiocentesis in a dog that had ingested brodifacoum rodenticide; they drained the pericardial fluid into the pleural space without retrieving it for cytologic analysis. In our case, hemorrhagic pericardial fluid without clots was removed from the pericardial space and analyzed.

The rapid and appropriate emergency management involving pericardiocentesis may have contributed to the initial stabilization of the intoxicated dog in this case. The ventricular tachycardia associated with the pericardiocentesis was likely due to irritation of the myocardial surface by the catheter during the procedure and resolved after administration of 2% lidocaine hydrochloride. Despite this complication, these arrhythmias are usually self-limited following the retraction of the needle or catheter (7).

In human medicine, anticoagulants, such as warfarin, have been used for prevention and therapy of coronary artery diseases and previous reports have described the development of pericardial effusions associated with this anticoagulation therapy in humans (8–10). Despite strong evidence favoring a causative role of anticoagulation in the genesis of late cardiac tamponade from intrapericardial bleeding (11,12), there is not a clear answer to the question of whether anticoagulant treatment promotes development of pericardial effusion (13).

Cardiac biomarkers (cTnI and CK-MB) were significantly increased in this dog. According to the study by Shaw et al (14), dogs with pericardial effusion had significantly higher serum levels of cTnI than did normal dogs. Dogs with hemangiosarcoma had much higher concentrations of cTnI (2.77 ng/dL; range: 0.09 to 47.18 ng/dL) than did dogs with idiopathic pericardial effusion (0.05 ng/dL; range: 0.03 to 0.09 ng/dL) (P < 0.001) (14). Our data were similar to the values obtained with idiopathic pericardial effusion. Gastrointestinal bleeding could be a possible cause of elevated serum urea nitrogen, CRSC, ALP, and NH3. Increased serum AST, LDH, and CK might be caused by tissue damage in this case.

In veterinary medicine, if a pericardial effusion is suspected as a result of rodenticide intoxication, it is important for veterinarians to confirm the presence of the pericardial effusion by using echocardiography, and then perform a routine pericardiocentesis for a better therapeutic prognosis.