Full text of DOI:10.1111/j.1751-0813.2001.tb12982.x

Clinical
Defaecation syncope and pulmonary thromboembolism
in a cat
ab
a
NT WHITLEY and RL STEPIEN
reductions in sodium (131 mmol/L, normal 148-157), chloride
(104 mmol/L, normal 114-126) and albumin (26 g/L, normal
28-39) and increases in urea (12.9 mmol/L normal 5-12),
glucose (16.8 mmol/L, normal 3.7-6.9), creatine kinase (666
U/L, normal 11-315) and alanine aminotransferase (318 U/L,
normal 17-138). Haematology showed anaemia (PCV 16 L/L),
thrombocytopaenia (41 x 109/L) with moderately enlarged
platelets, and neutrophilia (20.8x109/L) with band forms
present (0.9x109/L). Red cell morphology was characterised by
mild anisocytosis and polychromasia, moderate poikilocytosis,
and occasional schistocytes. Mean cell volume was normal and a
reticulocyte count not available. A voided urine sample had a
specific gravity of 1.045 and contained glucose (>111 mmol/L)
and blood (2+). A coagulation profile showed prolongation in
OSPT (19.7 sec), APTT (>110 sec) and TT (38.7 sec), and a
low fibrinogen (0.37 g/L) compared with control values
obtained from pooled plasma from healthy cats (12.3 sec, 11.4
sec, 21.1 sec and 0.99 g/L respectively). FDP concentration was
normal (<10 mg/mL). An additional study was performed, in
which equal volumes of plasma from the patient and a healthy
control cat were mixed. The same coagulation assays were run
on this mixed sample and results then compared with those
obtained from the pooled control sample from normal cats.
Failure of the APTT to correct completely with this
manipulation suggested that presence of an endogenous
coagulation inhibitor substance in the patient serum was more
likely than an absolute factor deficiency. (APTT for mixed
patient/healthy control sample 66.7 APTT for pooled control
sample:16.4 sec).
Thoracic radiographs taken upon admission demonstrated
obesity and caudal deviation of the gastric axis, but a normal
intrathoracic viscera. Abdominal ultrasound revealed hepatic
rounding, hyperechogenicity of the hepatic parenchyma, and a
large volume of echogenic peritoneal fluid. The
ultrasonographer found the intestinal tract difficult to evaluate
and reported that it was all clumped in the centre of the
abdomen. However, one bowel loop was isolated and measured
and was within normal limits. Initial emergency therapy
consisted of blood transfusion (50 mL of whole blood, matched
for blood type), intravenous lactated ringers solution (25 mL/h),
and administration of Vitamin K (18 mg SC q 12 h). Following
the blood transfusion, abdominocentesis was performed,
yielding a modified transudate with evidence of inflammation
(characterised by an increased protein content and an increased
number of mesothelial cells). A tentative diagnosis of chronic
pancreatitis, complicated by abdominal effusion, coagulopathy
and hepatopathy was made. Other differential diagnoses
considered included abdominal neoplasia, hypoadrenocorticism,
and partial gastrointestinal obstruction caused by neoplasia or a
foreign body.
A 7-year-old male neutered domestic shorthair cat was
referred for worsening gastrointestinal and haematologic
abnormalities. Physical status deteriorated further despite
intravenous crystalloids, blood transfusion and nutritional
support. Cardiorespiratory signs developed and the cat died
suddenly while straining to defaecate. Diffuse thrombosis,
pulmonary
thromboembolism,
metastatic
pancreatic
carcinoma and histologic evidence of cardiomyopathy were
present at necropsy. This is the first reported case of feline
pulmonary thromboembolism associated with defaecation
syncope. Predisposing factors for thrombotic disease in this
case and aspects of human defaecation syncope are
discussed. The risk of clot dislodgement by the Valsalva
manoeuvre in patients with a thrombotic tendency is
highlighted.
Aust Vet J 2001;79:403-405
Key words: Defaecation syncope, pulmonary thromboembolism, cat, DIC,
pancreatic carcinoma.
APTT
DIC
Activated partial thromboplastin time
Disseminated intravascular coagulation
Fibrin degradation products
One stage prothrombin time
Packed cell volume
Pulmonary thromboembolism
Every 12 hours
Subcutaneously
FDP
OSPT
PCV
PTE
q 12 h
SC
TT
Thrombin time
Case report
A 7-year-old male neutered domestic shorthair cat (6.3 kg)
was referred for evaluation of multiple problems. Profound
weight loss, constipation, intermittent vomiting and lethargy
had occurred over the previous 3 months. Radiographs
following oral barium administration were reported to show
delayed gastric emptying. Therapy with lactulose, multiple
enemas (containing sodium citrate, sodium lauryl sulfoacetate
and sorbitol), cisapride and glucocorticoids had been employed.
At the time of referral, lactulose and cisapride had not been
given for 2 weeks, and glucocorticoids had not been given for 2
days. During the days prior to referral, the vomiting had
worsened, and abdominal pain, declining haematocrit and
ecchymotic haemorrhages were reported. Feline leukaemia and
feline immunodeficiency virus tests (whole blood ELISA tests,
Idexx Laboratories Inc.) were negative.
On emergency referral, abnormal physical examination
findings included extreme lethargy, tacky mucous membranes,
with multiple ecchymotic haemorrhages, bruising at previous
venipuncture sites, weak pulses, dehydration and apparent
abdominal pain on palpation. Serum biochemistry revealed
a
Department of Medical Sciences, Veterinary Medical Teaching Hospital,
University of Wisconsin-Madison, 2015 Linden Drive West, Madison, WI 53706,
USA
On day 2 of hospitalisation, PCV was 26 L/L and body weight
6.5 kg. Mild hypercholesterolaemia (5.5 mmol/L, normal 1.7-
5.0) and hyperglycaemia (8.4 mmol/L, normal 3.7-6.9) were
b
Current address: Department of Veterinary Clinical Sciences, Evelyn Williams
Building (B10), The University of Sydney, New South Wales 2006
Aust Vet J Vol 79, No 6, June 2001
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Clinical
present. A voided urine sample still contained blood but was
negative for glucose. A cardiac gallop rhythm was detected on
auscultation. The cat ate small amounts of food, after intravenous
diazepam administration (0.5 mg/kg).
pathological process responsible for altered coagulation in this
patient. Several mechanisms have been suggested for
inappropriate coagulation in cancer patients, including
production of procoagulant proteins by tumour cells and
monocytes, and elaboration of platelet proaggregatory
substances by tumour cells.3
On day 3 PCV was 18 L/L and body weight 7 kg. The
abdominal effusion was more pronounced and jugular distension
was now present. Heart rate was 180/minute and femoral pulse
strength was poor. Syringe feeding was commenced and the cat
passed firm faecal pellets following administration of a
chlorhexidine solution enema. A limited echocardiographic
examination was performed. Abnormal echocardiographic
findings included marked right atrial and right ventricular
dilation, mild tricuspid regurgitation, thickening of the tricuspid
valve and apparent hypercontractility (left ventricular shortening
fraction 54%). These findings were interpreted as compatible
with acute onset of right-sided congestive heart failure. The
intravenous fluid rate was reduced to 12 mL/h and frusemide
therapy was instituted at 1 mg/kg SC q 12 h.
On day 4 of hospitalisation, the cat’s heart rate was 200/min.
Therapeutic abdominocentesis removed 200 mL of fluid. Rectal
temperature was 39.4oC. Nasal congestion and sneezing had
developed but the cat ate very small amounts of food. Thoracic
radiographs revealed mild generalised cardiomegaly, a small
pleural effusion and enlarged pulmonary arteries and veins.
By the fifth day of hospitalisation the cardiac gallop rhythm
was still present intermittently. Thoracic radiographs revealed
worsening pleural effusion. Hypothermia developed (37oC). A
nasogastric feeding tube was placed and feeding instituted. PCV
was 21 L/L. Thrombocytopenia, hypofibrinogenaemia (0.70 g/L,
control 1.04) and elevated FDP concentrations (>10 and < 40
mg/mL) suggested DIC; 25 mL of fresh frozen plasma was
administered intravenously. Several hours later, the cat was
observed to be straining to defaecate in its litter tray, then
vocalised, became ataxic, cyanotic, collapsed and subsequently
experienced cardiac arrest. Resuscitation attempts were not made.
Necropsy examination showed an adherent thrombus on the
tricuspid valve apparatus. Another large thrombus occupied the
lumen of one of the main pulmonary arteries. In addition,
histopathological examination showed subacute, severe
thrombosis of the portal vein, smaller pulmonary arteries and
multiple small vessels in the myocardium and adrenal glands.
Pathological cardiac findings included myofibres that were
fragmented or contained vacuolated cytoplasm, and were
separated by a clear space, sometimes containing loose fibrous
connective tissue. These findings suggested cardiomyopathy.
Multifocal, necrotising pancreatitis and pancreatic carcinoma
were present, with extension of the neoplasm into the
duodenum. Carcinoma metastases were present in the liver,
lymph nodes and lung, and abdominal carcinomatosis was
present.
This cat’s sudden death may have been caused by a cardiac
arrhythmia triggered by the structural cardiac disease
documented at necropsy, but the temporal association between
attempted defaecation and cardiac arrest is compatible with
defaecation-associated syncope. In people, defaecation syncope
is classified as a situational syncope in the broader grouping of
reflex-mediated vasomotor instability syndromes. Other
examples of situational syncope identified in people include
micturition-, cough- and swallowing-related syncope. Neural
impulses from gut wall tension receptors are thought to be
transmitted via vagal afferents to the CNS, resulting in
hypotension and bradycardia.4 The history of constipation in
this cat and the straining observed prior to collapse may have
caused significant activation of gut wall tension receptors,
resulting in sudden hypotension and bradycardia.
Defaecation syncope associated with pulmonary embolism
has also been documented in humans.5-7 Increases in
intrathoracic and intra-abdominal pressure during defaecation
tend to reduce venous return and hence reduce cardiac output
and peripheral blood flow (the Valsalva manoeuvre). Release of
the Valsalva manoeuvre on completion of defecation and the
attendant sudden increase in cardiac output and the ‘vacuum
effect’ caused by the sudden reduction in intra-abdominal
pressure may cause dislodgement of intravascular or intracardiac
clots and subsequent pulmonary embolisation.6 Pulmonary
thrombi may have embolised from the portal vein, adrenal
vessels or the tricuspid valve in this cat. Due to the high
suspicion for DIC in this cat, it is also possible that some of the
smaller pulmonary thrombi formed in situ. The clinical
sequence of defaecation-induced syncope followed by acute
PTE apparently resulted in this animal’s sudden death.
Tricuspid insufficiency in this cat is likely to have developed
secondary to pulmonary hypertension caused by smaller emboli
(suggested by the enlarged pulmonary vasculature on
radiographs and by the echocardiographic findings) and to have
been worsened by the thrombus adherent to the valve
apparatus. Thrombolytic therapy was contemplated, but
postponed until the cat’s haemorrhagic tendencies could be
controlled. Despite anaemia, a plasma transfusion was chosen
over fresh whole blood in treatment of suspected DIC to avoid
adding even more volume to the circulation of a patient in
right-sided heart failure. In retrospect, heparin therapy may
have been beneficial. Structural myocardial disease may have
been present before onset of other clinical signs and contributed
to right-sided heart failure. The contribution of apparent
multiple myocardial infarctions, identified at necropsy, to any
clinical myocardial dysfunction in this cat is unknown. Based
on limited antemortem echocardiography and on necropsy
findings the cardiomyopathy was not typical of dilated,
hypertrophic or restrictive disease and should therefore be
placed in the category of feline unclassified cardiomyopathy.
Gallop rhythms in cats are a cardinal sign of myocardial
dysfunction, although could also have been present in this case
due to severe anaemia or relative volume overload.
Discussion
A recent retrospective study on feline PTE suggested possible
predisposing conditions in all cases.1 These authors also
described clinical features and radiographic markers of PTE. A
comprehensive list of the principle causes of PTE has been
published by other authors.2 In the case reported here, several
factors may have been implicated in the genesis of the PTE.
These include obesity, recumbency, glucocorticoid therapy,
transient diabetes mellitus, the indwelling intravenous catheter,
cardiac disease, pancreatitis, pancreatic carcinoma and DIC. It is
probable that metastatic pancreatic carcinoma was the dominant
This report describes a case of neoplasia- and DIC- related
pulmonary embolism in a cat, with sudden death apparently
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Clinical
3. Fox LE. The paraneoplastic disorders. In:Bonagura J, editor. Kirk’s current
veterinary therapy XII. Saunders, Philadelphia, 1995:530-542.
4. Kapoor WN. Syncope and hypotension. In:Braunwald E, editor. Heart
associated with defaecation-induced syncope and subsequent
PTE. Straining to defaecate may be a risk factor for sudden
death in animals with underlying diseases associated with
thromboembolism.
disease:
a textbook of cardiovascular medicine. 5th edn. Saunders,
Philadelphia, 1997:863-876.
5. Kollef MH, Schachter DT. Defecation syncope caused by pulmonary
embolism. Ann Intern Med, 1990;113:86.
References
6. Kollef MH, Schachter DT. Acute pulmonary embolism triggered by the act of
defecation. Chest, 1991; 99:373-376.
7. Kollef MH, Neelon-Kollef RA. Pulmonary embolism associated with the act of
defecation. Heart Lung, 1991;20:451-454.
1. Norris CR, Griffey SM, Samii VF. Pulmonary thromboembolism in cats: 29
cases (1987-1997). J Am Vet Med Assoc, 1999;215:1650-1654.
2. Pouchelon J-L, Chetboul V, Devauchelle P et al. Diagnosis of pulmonary
thromboembolism in a cat using echocardiography and pulmonary scintigraphy.
J Small Anim Pract, 1997;38:306-310.
(Accepted for publication 24 January 2001)
BOOK REVIEW
Rabbits: Health, Husbandry and Diseases. Richardson VCG, Blackwell Science, Melbourne, 2000, 178
pages. Price $70.40. ISBN 0 632 05221 X.
n enduring image of my time in private practice was the miserable demeanour so often exhibited by pet
rabbits, most of whom spent their lives confined to a cramped hutch in some distant corner of the garden.
A
It is therefore encouraging to read a book dedicated to the better care of pet rabbits. In this monograph, the
emphasis is on practical issues and common sense. There are useful tips on handling, feeding, clinical
examination, surgical procedures and administration of drugs. There is also a possibly unique chapter on
behavioural problems. Unfortunately, given the book’s quick reference format, there are some unexpected
deficiencies: there is relatively little discussion of differential diagnoses, the amount of space devoted to some
diseases is out of proportion to their practical importance, and it would have been useful to highlight certain
anatomical peculiarities such as the thick-walled appendix and the round sac of lymphoid tissue at the ileo-
caecal junction, both of which have the potential to be misinterpreted as gross lesions.
It is important to stress that this text should not be viewed as a source of ‘scientific’ information on rabbits.
Discussion of disease diagnosis is based largely on clinical signs with sporadic mention of rather non-specific
gross necropsy findings. The comments on clinical biochemistry are brief and generic in nature, and the
modest amount of attention paid to laboratory confirmation of disease is not always helpful – in particular, the
suggestion that myxomatosis and calicivirus disease can be confirmed by virus isolation is impractical and
distracts from the value of far more accessible tests such as histopathology. There is also frequent reference
to remedies based on vitamins, probiotics and various plants, the precise rationale for which is not clear.
Having said that, the next time I see a rabbit with hair loss, I might be tempted to try some of the author’s
suggestions such as feeding groundsel, codliver oil or vitamin B1. If it works in rabbits…
Richardson’s unsubstantiated claim that rabbits are now the third most popular pet is one I suspect has
been made for other, admittedly less fecund, species. Nevertheless, rabbits don’t bark, don’t maul children
and have bodily emanations that are far less offensive than those of their carnivorous counterparts.
Practitioners with a city-based clientele will undoubtedly be seeing more of these creatures and as long as the
limitations of this rough and ready guide are clearly recognised, it is not a bad starting place for those seeking
a working knowledge of this species.
Malcolm France
Dr France is Director of Laboratory Animal Services at the University of Sydney
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