Page 632 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Anticoagulant Chapter | 46 597

VetBooks.ir (2 of 104) at 24 h after exposure. The recommended times nature, but sudden death may occur as the result of acute
Many cases of anticoagulant poisoning are subacute in
to check for prothrombin in children is 24 and 48 h after
internal hemorrhage. Evidence of external hemorrhage,
exposure (Smolinske et al., 1989). Routine measurement
of the INR is unnecessary in young children because the such as melena, epistaxis, hematemesis, hematuria, gingi-
amount of rodenticide ingested is invariably small (Watt val bleeding, or excessive bleeding from an open wound,
et al., 2005). may or may not be seen. However, internal hemorrhage
Although some bias in pediatric brodifacoum exposure involving the lungs, pleural and/or peritoneal cavities, and
data (Osterhoudt and Henretig, 2003) is suspected, pro- facial planes are commonly reported (Murphy and
spective studies of acute, unintentional, pediatric super- Gerken, 1989; DuVall et al., 1989). Massive tracheal
warfarin ingestions managed without (Ingels et al., 2002) and esophageal hemorrhage 2 days after bait ingestion
or with (Smolinske et al., 1989) decontamination have was reported in a dog (Stowe et al., 1983). In New
been conducted. Some argue against the need for a PT in Zealand, where brodifacoum was used in control of wild
unintentional pediatric superwarfarin exposures (Mullins rabbits, 43 rabbit carcasses were found with massive hem-
et al., 2000). See also cases of acute pediatric brodifa- orrhage in the abdominal cavity (52%) and thoracic cavity
coum ingestions (Shepherd et al., 2002). Although less (17%), and the remaining 31% of cases were found with
treatment is often better (Kanabar and Volans, 2002) for hemorrhage of muscles, cecum, stomach, kidney, mesen-
accidental pediatric brodifacoum exposures, rare pediatric tery, and placenta of pregnant does (Rammell et al.,
cases have coagulopathies despite early treatment 1984). Postmortem findings in warfarin poisoning have
(Montanio et al., 1993). been described similarly by Dakin (1968).
In all other cases, the INR should be measured
36 48 h postexposure. If the INR is normal at this time, Response to Vitamin K 1 Treatment
even in the case of long-acting formulations, no further
Remission of the coagulopathy 24 h after vitamin K 1
action is required (Watt et al., 2005).
treatment supports a clinical diagnosis of a vitamin K 1
The most significant elevation of PT, PTT and PIVKA
responsive coagulopathy (Tvedten, 1989). A clinical diag-
was observed 72 hours after a single dose of diphacinone
nosis is not sufficient in all cases. Some cases require that
of 2 mg/kg in ground squirrels (Spermophilus beecheyi),
an etiological diagnosis be made. Analytical chemistry
although elevations were seen at 24 h (Whisson and
testing is required in such cases.
Salmon, 2002). The increase in ACT, APTT, and OSPT
are often used to support a clinical diagnosis of anticoagu-
lant rodenticide poisoning in dogs (Dorman, 1990). Treatment
Coagulation factor synthesis may be inhibited for up to
General, supportive, and specific treatments are available
30 days in diphacinone-exposed dogs (Mount and
for anticoagulant rodenticide toxicosis. Prospective study
Feldman, 1983).
of the outcome of patients with excessive warfarin expo-
PT should be checked 48 h after stopping vitamin K 1
sure is described by Hylek et al. (2000).
therapy to detect any recurrence of coagulopathy
(Chataigner et al., 1989). PT times in sheep were stable in General
samples stored at 0, 20, and 30 degrees for 24 h.
Emetic, adsorbent, and cathartic therapies are indicated
Vitamin K-dependent factor activity has been sug-
if the ingestion of the anticoagulant rodenticide has
gested for rapid identification of surreptitious brodifa-
occurred within the last few hours (e.g., peak serum
coum poisoning (Miller et al., 2006).
brodifacoum concentrations occur 2 h after oral dosing
of dogs).
Clinical coagulopathy normally occurs 2 5 days after
Necropsy/Autopsy oral exposure, so emetics and cathartic at the time of pre-
Pleural, pericardial, mediastinal, and subarachnoid hemor- sentation is not normally indicated if clinical signs are
rhages have been reported in humans with brodifacoum present. Oral-activated charcoal therapy, however, may be
exposure (Kruse and Carlson, 1992; Tahir et al., 2008). useful for those chemicals that undergo enterohepatic
Hemoperitoneum, hemothorax, and pulmonary hemor- circulation.
rhage are the most common necropsy findings in dogs
and cats with anticoagulant rodenticide residues in liver Supportive
(DuVall et al., 1989; Rickman and Gurfield, 2009). Recommendations for humans with anticoagulant rodenti-
Pulmonary edema, pleural effusion, pericardial effusion cide toxicosis have recently been reported by Watt et al.
(Schulman et al., 1986), and intratracheal hemorrhage are (2005). If active bleeding occurs, prothrombin complex
reported as well (McGuire et al., 1999). concentrate (which contains factors II, VII, IX and X) 50