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Are You Poisoning your dog?
This tip is borrowed from the UK Vet – Vol 12 1 January 2007, it is the complete article except for 3 images, one being of a graph and a little amount of text relating to it. I would like to thank Sharon Bolt at www.good-dogs.co.uk for emailing me the original. The full version may be found by following this link http://www.ukvet.co.uk/ukvet/articles/toxicology%20-%20raisins.pdf
Grapes, Raisins & Sultanas, and other foods Toxic to Dogs
By Alexander Campbell BSc.
VPIS(London), Medical Toxicology Unit, Avonley Road, London, SE14 5ER
One of the more striking poisonings to have
emerged as a potential concern over the last few
years has been that of raisin poisoning in dogs. A
foodstuff thought unlikely to cause problems in the
past, it may well be that significant exposures had
been wrongly diagnosed for many years. Assuming
the incidence of ingestions has not changed much
over the years then there is certainly increased
awareness and reporting of such occurrences if the
call enquiry data to the Veterinary Poisons
Information Service (VPIS) are analysed.This article
intends to outline current knowledge based on both
the literature reports and the VPIS experience and to
offer some guidance as to an appropriate case
management strategy. In addition there will be a
brief reminder about other foodstuffs with the
potential to cause intoxication in dogs.
The VPIS reviewed all past cases, and
realising a potential problem alerted the veterinary
profession (Campbell and Bates, 2003). Although
some of the enquiries from 2003 onwards have been
prospective to ascertain the likely risks to dogs there
has been an increased reporting of actual incidences
too. All confirmed or suspected cases reported have
since been followed up by questionnaire and by the
end of 2005 the VPIS had 45 cases with good
follow-up information on its database. Of the 45
animals involved in these cases 22 (49%) showed no
clinical signs following ingestion. In a recently
published report on these cases (Sutton and
Campbell, 2006) it was notable that 80% of those
animals that showed no clinical signs throughout had
all received either emetics and/or absorbents in the
hours after the ingestion. However, there were eight
cases with a fatal outcome. Owing to severe
deterioration in their condition seven had been
euthanased, one after consuming a large amount of
fruitcake. The other case concerned a dog that had
died owing to renal failure. The ingested ‘doses’
involved in these fatal cases ranged from 10 to 57 g
of fruit per kg body weight. Interestingly, none of
these cases with fatal outcomes had received any
form of gastric decontamination, probably as they had
presented to surgery after developing clinical signs.
There are now several reports that confirm that
ingestion of these fruits can cause renal failure in
dogs.The toxic mechanism remains to be elucidated,
and the apparent lack of a reproducible dose
response relationship has led some authors to suggest
this may reflect either a component of the fruits that
is present in varying quantities, or the existence of an
extrinsic compound that may not always be present
(Eubig et al., 2005). Individual variations in response
may also occur. So the general consensus at present
is that potentially any dose should be considered a
problem. Certainly renal failure has occurred following
ingestion of raisins at estimated doses as low as 2.8
mg/kg (Eubig et al., 2005) and one dog was euthanased
after ingestion of 4.7 g/kg (Mazzaferro et al., 2004).
Where grapes are concerned 4-5 grapes caused renal
failure in an 8.2 kg dachshund (Mazzaferro et al.,
2004) doses as low as 19.6 g/kg caused similar effects
in another report (Eubig et al., 2005).
Clinical effects usually become apparent within 6 hours
of ingestion, and always within 24 hours. Early signs
are vomiting (in almost all cases), diarrhoea, anorexia,
abdominal tenderness and lethargy. Ingesta may be
present in the vomitus or faeces. Polydipsia may also
be apparent. Evidence of renal impairment,
characterised by elevated urea and creatinine, with
accompanying oliguria or anuria, is usually apparent
by 24 hours. Other laboratory findings in cases
reported to VPIS or detailed in the literature include
elevated phosphate, amylase, glucose, ALP and white
blood cell count. Urinalysis may reveal proteinuria,
glucosuria, microscopic haematuria and, rarely,
crystalluria (Eubig et al., 2005). It is generally agreed
that prognosis in dogs with oliguria or anuria is poor
(Gwaltney-Brant et al., 2001).
In some of the cases with fatal outcomes reported to
VPIS (London) post mortem results were available,
and revealed proximal renal tubule necrosis and renal
calcification. Mineralisation or calcification of tissues
has also been reported, but these findings are not
always of a severity to fully account for the poor case
VPIS’ OUTLINE TREATMENT PROTOCOL
Ingestion of any quantity of grapes, raisins or
sultanas by a dog should be considered treatable.
Gut decontamination should be considered by
means of emesis or gastric lavage
Digestion of the fruits appears to be slow and
decontamination several hours post-ingestion
may be worthwhile as whole grapes and swollen
raisins have been recovered after remaining in
the stomach overnight (Eubig et al., 2005)
Activated charcoal may be of benefit, but care
should be taken to ensure bowel sounds are
regular before this is administered
If spontaneous vomiting is protracted consider
use of anti-emetics such as metoclopramide:
dosage 0.5-1 mg orally, SC or IM q 6-8h or
1-2 mg/kg per day by slow IV injection
Aggressive IV fluid therapy for at least 48 hours
for rehydration and support of renal function
Monitor renal function and electrolytes for at
least 72 hours post-ingestion
Monitor for signs of fluid overload and, if
possible, monitor central venous pressure
Where necessary use of furosemide or mannitol
may be considered to re-establish urine output
Dosage for furosemide 5 mg/kg IV initially
followed by IV infusion of 5 mg/kg/hour
Dosage for mannitol 0.25-0.5 g/kg IV over 5-
Note that the efficacy of these therapies
remains unproven and that there is evidence
that tubular necrosis and or renal tubule
obstruction may prevent urine flow
(Mazzaferro et al., 2004)
Dopamine may be used to enhance renal
perfusion – dosage 1-3 mcg/kg per minute as
constant IV infusion
It is worth noting that peritoneal dialysis has
reportedly been employed in several cases, over a few
days, with varying degrees of success.
OTHER DANGEROUS FOODSTUFFS
So what other dangerous foods lurk out there to
harm the unsuspecting pet? Well – some are relatively
well known and have been covered in many articles
before. Chocolate remains a big concern to the VPIS,
with cases occurring throughout the year but
particularly at Easter and at Christmas when there
may be more lying around the home in dog
accessible places. 475 enquiries concerning ingestion
of chocolate by dogs were handled in 2005 – the
second most common enquiry taken. In 2005 there
were three cases reported with fatal outcomes – so
death by chocolate is not a term to be used lightly.
The toxic component is the methylxanthine alkaloid
theobromine, which is present in variable
concentrations dependent on the quality of the
chocolate – the darker or richer in cocoa solids the
more dangerous the preparation.This topic has been
covered in an article in UK Vet (Campbell 2001,
UK Vet, 6 (6), pp40-42, 2001).
Several other foodstuffs spring to mind as regularly
common enquiries to VPIS. One such is onions, and
other members of the Allium species such as garlic,
shallots, leeks and even chives – although the onion
(Allium cepa) is the most commonly implicated of
this grouping in poisoning referrals. All parts of the
plant, whether raw or cooked, should be considered
toxic. Although the plants contain several toxic
substances it is widely agreed that n-propyl
disulphide is the principal toxin, and it appears that
this and the other toxins cause oxidative haemolysis,
sulphhaemoglobin formation and subsequent Heinz
body formation. These changes within the
erythrocytes alter their structure and render them
prone to damage. The toxic constituents appear to
have direct effects on erythrocyte membranes as
well. The net result is development of a broad
haemolytic anaemia, which may take 1-5 days to
reach full intensity. The clinical manifestations of
intoxication are initial gastrointestinal; effects such as
vomiting, diarrhoea, abdominal discomfort,
anorexia, depression and dehydration. Haematuria
and haemoglobinuria are common, and haematology
may reveal neutrophilia, lymphopenia, Heinz-body
anaemia and methaemoglobinaemia.
Treatment is advocated of ingestion of any quantity.
For recent ingestions gastric decontamination should
be considered, and use of adsorbents, but thereafter
management is largely supportive. It is important
that the animals remain hydrated; anti-emetics may
be given to control persistent vomiting. Nonenzymatic
reductants such as ascorbic acid may also be
useful (dog dose 30 mg/kg body weight IV q 6-8h).
In severely poisoned animals blood transfusions have
been successfully employed (Kay, 1983).
Another unusual occurrence in dogs is ingestion of
macadamia nuts. These originate from the trees
Macadamia integrifolia and Macadamia tetraphylla. The
mechanism of toxicity is unknown; but may involve
a constituent of the nuts, processing contaminants or
mycotoxins (Hansen et al., 2002). Principal signs of
intoxication include weakness (more pronounced in
hind limbs), tremor, ataxia, vomiting, depression,
pyrexia, abdominal tenderness, lameness, stiffness and
recumbency. Ingestion of doses as low as 2.2 g/kg
have reportedly caused clinical effects. In an
experimental study doses of 20 g/kg given to dogs
caused clinical signs to develop within 2-3 hours.
These dogs deteriorated over the following 12 hours
but then recovered over the next 24-48 hours. It was
noted they developed mild elevations in serum
triglycerides and alkaline phosphatase (Hansen et al.,
2000). Management is generally supportive, with
decontamination appropriate for recent ingestions.
Use of mild laxatives may assist the passage of ingesta
through the gastrointestinal tract. Care should be
taken to ensure the animals remain hydrated.
In summary it is useful to remember these known
examples illustrate the potential hazards of feeding
animals foodstuffs that appear innocuous, and that
there may other toxic syndromes as yet unrecognised
that result from giving animals foods to which they
might not normally be exposed. The best advice
must surely be to give animals foodstuffs and or treats
specifically developed for their diets.
Grapes, raisins and sultanas
CAMPBELL A., BATES N. 2003 Raisin poisoning in dogs. Vet Rec 152
EUBIG P. A., BRADY M. S., GWALTNEY-BRANT S. M., KHAN S. A.,
MAZZAFERRO E. M., MORROW C. M. 2005 Acute renal failure in dogs
after the ingestion of grapes or raisins: a retrospective evaluation of 43
dogs (1992-2002). J Vet Intern Med 19(5):663-74.
GWALTNEY-BRANT S., HOLDING J. K., DONALDSON C. W., EUBIG
P. A., KHAN S. A. 2001 Renal failure associated with ingestion of grapes
or raisins in dogs. J Am Vet Med Assoc 218(10):1555-6.
MAZZAFERRO E. M., EUBIG P. A., HACKETT T. B., LEGARE M.,
MILLER C., WINGFIELD W. E., WISE L. 2004 Acute renal failure
associated with raisin or grape ingestion in 4 dogs. J Vet Emerg Crit Care
MEANS C. 2002 The wrath of grapes. Available on
http://www.aspca.org. Reprinted from ASPCA Animal Watch Summer
2002 22 (2).
PENNY D., HENDERSON S. M., BROWN P. J. 2003 Raisin poisoning in
a dog. Vet Rec 152 (10):308.
SUTTON N., CAMPBELL A. 2006 Grape poisoning in dogs – a case
series from the Veterinary Poisons Information Service, London Clin.
Tox. 44 (4): 526-527 (abstract).
COPE R. B. 2005 Allium species poisoning in dogs and cats Vet Med 100
KAY J. M. 1983 Onion toxicity in a dog. Modern Veterinary Practice 64:
KOBAYASHI K. 1987 The hemolytic effect of onions on canine
erythrocytes associated with inherited high Na, K-ATPase activity.
Japanese Journal of Veterinary Research 35: 137.
MIYATA D. 1990 Isolation of a new phenolic compound from the onion
(Allium cepa L.) and its oxidative effect on erythrocytes [abstract].
Japanese Journal of Veterinary Research 38: 65.
SMITH C. H., ELLISON R. S. 1986 Concurrent onion poisoning and
haematuria in a dog (letter). New Zealand Veterinary Journal 34: 77-78.
SOLTER P., SCOTT R. 1987 Onion ingestion and subsequent Heinz body
anemia in a dog: A case report. Journal of the American Animal Hospital
Association 23: 544-546.
YAMOTO O., MAEDE Y. 1992 Susceptibility to onion-induced hemolysis
in dogs with heredity high erythrocyte reduced glutathione and
potassium concentrations. Am. J. Vet. Res. 53: 134-137.
HANSEN S. R. 2002 Macadamia nut toxicosis in dogs. Vet Med 97(2).
HANSEN S. R., BUCK W. B., MEERDINK G., KHAN S. A. 2000
Weakness, tremors, and depression associated with macadamia nuts in
dogs. Vet Hum Toxicol 42(1):18-21.
UK Vet – Vol 12 No 1 January 2007 SMALL ANIMAL l TOXICOLOGY HH 3