Journal of Feline Medicine and Surgery

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Addisonian crisis and severe acidosis in a cat: a case of feline hypoadrenocorticism

Julia Sicken and Reto Neiger
Journal of Feline Medicine and Surgery 2013 15: 941 originally published online 12 March 2013
DOI: 10.1177/1098612X13480983

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480983
2013
JFM151010.1177/1098612X13480983Journal of Feline Medicine and SurgerySicken and Neiger

Case Report

Journal of Feline Medicine and Surgery

Addisonian crisis and severe 15(10) 941­–944

© ISFM and AAFP 2013
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DOI: 10.1177/1098612X13480983

hypoadrenocorticism jfms.com

Julia Sicken and Reto Neiger

Abstract
A 4-year-old female neutered British Shorthair cat was presented as an emergency owing to progressive apathy,
anorexia, adipsia, weight loss and weakness. Clinical findings showed severe weakness, collapse, weak
pulse, bradycardia, hypovolaemia and hypothermia. Blood examinations revealed marked metabolic acidosis,
hyponatraemia, hyperkalaemia, hyperphosphataemia, hypercalcaemia, hypochloraemia and azotaemia. The
diagnosis of feline hypoadrenocorticism was based on low cortisol and aldosterone plasma levels before and after
synthetic adrenocorticotropic hormone administration. Initial treatment consisted of intravenous fluid therapy. After
stabilisation a combination of fludrocortisone and prednisolone was given orally. One year after diagnosis the cat is
free of clinical signs and in good condition.

Accepted: 1 February 2013

A 4-year-old female neutered British Shorthair cat with a
body weight of 3.4 kg and a body condition score of 4/9
was referred to the Small Animals Clinic, University of
Giessen, as an emergency owing to lethargy, weakness,
anorexia, adipsia and weight loss. On the day of consul-
tation the cat’s health status declined drastically com-
pared with the previous days. Four weeks previously
the cat developed polyuria and polydipsia, and was
treated by the referring veterinarian with cefovecin
sodium (Convenia; Pfizer, dose unknown) without any
clinical improvement. The cat had not received exoge-
nous oral or topical glucocorticoids. The cat became pro-
gressively weak, lethargic and stopped eating and
drinking; the owners had been giving food and water
via a syringe for the previous 7 days. Furthermore, inter-
mittent vomiting was noticed by the owners. They also
described an uncoordinated gait/ataxia that had begun
a few weeks previously and had worsened progres-
sively. The cat lived exclusively indoors. It was
dewormed every 3 months, vaccinated annually and
was fed a commercial cat food.
On physical examination, the cat was initially atten-
tive and able to stand with support, but unable to walk.
With continued handling, the cat became progressively
weaker until she was unable to move and went into
sternal recumbency. Mucous membranes were mildly
pale and dry, capillary refill time was prolonged (>3 s)
and there was abnormal skin tenting; 10% dehydration
was estimated. The femoral pulse was not palpable
bilaterally. The cat was bradycardic with a heart rate of
120 beats per minute, but with a regular heart rhythm.
She showed a mild tachypnoea with a respiration rate of
44 breaths per minute. Body temperature was 32.7°C.
Neurological examination was unremarkable.
Blood gas analysis (Table 1) revealed a marked meta-
bolic acidosis with partial respiratory compensation and
marked hyponatraemia and hyperkalaemia. The
sodium:potassium ratio was 15. Haematology showed a
mild lymphocytosis {8.5 × 109/l, [reference interval (RI)
= 1.5–7.0 × 109/l]} and lack of a stress leukogram [neutro-
phils 4.5 × 109/l (RI 2.5–12.5 × 109/l); monocytes 0.11 ×
109/l (RI 0.04–0.85 × 109/l)], which was unexpected in a
chronically ill and stressed cat. Clinical biochemistry
revealed, in addition to the electrolyte abnormalities, a
severe azotaemia [urea 22.3 mmol/l (RI 7.1–10.7
mmol/l); creatinine 599 µmol/l (RI 0–168 µmol/l)] and
hyperphosphataemia [3.7 mmol/l (RI 0.8–1.9 mmol/l)].
Thoracic radiography (Figure 1) revealed a small cardiac
silhouette with a vertebral heart score of 6.2 (RI 6.7–8.1),
pulmonary hypoperfusion and a narrow caudal vena
cava. A blood pressure reading could not be detected in
any limb using the Doppler method. Unfortunately,
Small Animals Clinic, University of Giessen, Giessen, Germany
Corresponding author:
Julia Sicken, Small Animal Clinic – Internal Medicine, Frankfurter
Straße 126, Giessen, Germany
Email: julia-sicken@gmx.de

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942 Journal of Feline Medicine and Surgery 15(10)

Table 1  Blood gas analyses (bold entries indicate values outside the reference interval)

Parameter Initial 3h 6h 12 h 16 h 34 h 48 h 72 h 96 h Reference interval (units)

pH 7.14 7.14 7.23 7.32 7.36 7.36 739 7.41 7.42 7.31–7.39
pCO2 31 35.9 30.3 37.1 39.3 36.2 30.3 30 28.2 33.5–50.7 (mmHg)
HCO3– 10.4 12 13.7 19.0 21.4 20.1 18.1 18.7 19.9 15.5–23.9 (mmol/l)
Base excess –19 –18 –15 –7.9 –4.6 –5.7 –6.6 –4.9 –5.3 –10.2 to 1.2
Lactate 1.6 1 1 1.6 1.3 1 1.1 1.2 1.8 0.4–2.2 (mmol/l)
Sodium 121 121 122 129 130 136 133 142 146 141–150 (mmol/l)
Potassium 8.0 8.42 6.64 3.7 3.8 4.33 5.28 4.43 4.47 3.6–4.8 (mmol/l)
Chloride 90.8 92 94.2 94.6 94.3 102.2 100.5 109.5 112.9 110–125 (mmol/l)
Ionised calcium 1.45 1.49 1.3 1.54 1.66 1.41 1.43 1.29 1.32 1.12–1.32 (mmol/l)
Urea 23.6 23.6 21.8 15.4 12.3 4.5 4.4 4.1 5 7.1–10.7 (mmol/l)
Glucose 4.0 3.9 10.6 11.5 10.6 6.8 6.1 5.7 5.6 3.8–6.1 (mmol/l)
Haematocrit 0.47 0.40 0.33 0.32 0.31 0.24 0.24 0.17 0.18 0.24–0.45 l/l

pCO2 = carbon dioxide partial pressure; HCO3– = bicarbonate ion

spiked with 40% glucose was continued at 6 ml/kg/h.

Figure 1  Thoracic radiograph after initial stabilisation
cystocentesis and urinalysis were not possible because,
ultrasonographically, the urinary bladder was empty. An
adrenocorticotropic (ACTH) stimulation test was per-
formed by injecting 125 µg synthetic ACTH (Synacthen;
SIGMA-TAU) intravenously. Serum cortisol and serum
aldosterone levels were measured at baseline and
60 mins after stimulation by a commercial laboratory
(Biocontrol, Ingelheim, Germany) by chemilumines-
cence immunoassay method for quantitative measure-
ment of cortisol and with a radioimmunoassay for
quantitative determination of aldosterone.
Initial treatment consisted of intravenous (IV) fluid
therapy and of rewarming the cat. A bolus injection of 20
ml/kg 0.9% saline and 6 ml/kg hydroxyethyl starch,
given over 1 h, was instigated. Sodium bicarbonate at a
dose of 1 mmol/kg to correct the metabolic acidosis and
1 ml 10% calcium–gluconate as a cardioprotective agent
were administered IV. After rehydration, 0.9% saline
Body temperature increased slowly to 37.8°C over a
period of 12 h. The cat was monitored closely (blood gas
analyses every 3 h; continuous electrocardiography
monitoring), and, over the next 12 h, several blood gas
parameters normalised, but a marked hyponatraemia
persisted (Table 1). Clinically, the cat became more alert,
was able to move into sternal recumbency and drink
with assistance. The cat’s heart rate increased to 180
beats per minute and systolic blood pressure was meas-
ured repeatedly to be >100 mmHg. The next day treat-
ment for hypoadrenocorticism was started with 0.025
mg fludrocortisone/cat twice daily PO (Astonin H 0.1
mg; Merck) and 0.3 mg/kg prednisolone once daily PO
(Prednisolone 5 mg; CP-Pharma). Fluid therapy was
continued as before with electrolyte replacement accord-
ing to blood gas analyses findings. ACTH stimulation
test results confirmed the diagnosis of hypoadrenocorti-
cism, with both cortisol and aldosterone levels below the
detection limit of the assay at baseline and after stimula-
tion (Table 2). Ultrasonographic investigation identified
the left adrenal gland with a diameter of 0.3 cm, while
the right adrenal gland could not be visualised. Over the
next few days the cat stabilised and all clinical signs
resolved. In the course of the cat’s hospitalisation hae-
matology showed a moderate, non-regenerative anae-
mia [haematocrit 0.17 l/l (RI 0.24–0.45 l/l); haemoglobin
3.6 mmol/l (RI 4.9–9.3 mmol/l]; reticulocytes 24.3 ×
109/l]. The cat was discharged with the same dosages of
fludrocortisone and prednisolone as given during
hospitalisation.
Re-examination after 6 days revealed normal behav-
iour and no abnormality was detected during physical
examination. Blood testing showed only mild electro-
lyte abnormalities. Anaemia was now regenerative
[haematocrit 0.21 l/l (RI 0.24–0.45 l/l), haemoglobin 4.0
mmol/l (RI 4.9–9.3 mmol/l), reticulocytes 123.2 × 109/l].

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Sicken and Neiger 943
Table 2  Adrenocorticotropic hormone stimulation test
Baseline Stimulated (60 mins)
Cortisol (µg/dl) <0.3 <0.3
(RI <4.0)
Aldosterone (ng/dl) <2.0 <2.0
(RI 5.4–15.5)
RI = reference interval
Fludro­cortisone was continued at the initial adminis-
tered dose, while prednisolone was discontinued.
When, 2 weeks later, polyuria and polydipsia resumed,
prednisolone was reinstituted and clinical signs
resolved. The dosage of prednisolone was decreased
slowly (to 0.2 mg/kg once daily) over the following
months, during which time the cat gained weight (cur-
rent body weight 4.7 kg vs 3.4 kg at initial presentation).
The cat is doing well 1 year after initial presentation.
Hypoadrenocorticism or Addison’s disease is a rare
disease in cats, with approximately 40 cases reported in
literature.1–12 In contrast to Addison’s disease in dogs,
there is no evidence for sex, age or breed predisposition
in cats.3,10 Age at presentation ranges between 1.5 and
14.0 years (median 4.0 years). The majority of patients
are domestic shorthair and longhair cats.
The diagnosis is usually confirmed by measuring
cortisol at baseline and following exogenous ACTH
stimulation. While aldosterone in response to ACTH
administration has been measured in healthy cats,13,14 to
our knowledge this is the first hypoadrenocorticoid cat
in which aldosterone has also been measured. Not sur-
prisingly, both values were below the detection limit of
the assay, confirming that hypoaldosteronism was
responsible for the marked electrolyte abnormities seen
in this cat. Other causes of electrolyte abnormalities,
such as effusion, other endocrine diseases or urinary
problems could therefore be excluded.15,16
In contrast to dogs, where the majority of cases are
thought to be caused by primary immune-mediated
adrenal destruction, the cause of adrenal insufficiency
in cats is largely unknown.3,4,6,8,10–12 There are few case
reports that found some causes, such as bilateral
destruction of the adrenal glands by an infiltrating
lymphoma in two cats2 and two cases as a result of
trauma.5,6 Unfortunately, only one adrenal gland could
be visualised with ultrasonography in the present case,
which was considered small, so the cause remains
unclear.13
This cat’s history and physical examination findings
were typical for cats suffering from hypoadrenocortici-
sim.1–12 In decreasing order, anorexia (100%), lethargy
(93%), weight loss (86%), vomiting (36%), waxing–
waning course of illness (29%), previous response
to symptomatic therapy (21%), polyuria/polydipsia
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(21%), dehydration (92%), weakness (85%), hypother-
mia (77%), slow capillary refill time (38%), weak pulse
(38%), collapse/inability to rise (23%), a painful abdo-
men (23%) and bradycardia (15%) have been reported10
and were almost all seen in the present case. This
cat also had typical clinicopathological abnormalities,
including hyperkalaemia (90%), hyponatraemia (100%),
a markedly decreased sodium:potassium ratio,
hypochloraemia (90%), azotaemia (100%), hyperphos-
phataemia (100%), hypercalcaemia (10%), lymphocyto-
sis (20%), lack of a stress leukogram and anaemia
(30%).3,4 It was thought that anaemia was masked ini-
tially by haemoconcentration based on high-grade
dehydration.
Besides the mentioned clinicopathological abnor-
malities, this cat had a marked metabolic acidosis. The
presence of (generally mild) metabolic acidosis is well
known in hypoadrenocorticoid dogs,3 but has, to our
knowledge, never been described in cats. About 50% of
dogs with hypoadrenocorticism have a mild metabolic
acidosis; severe metabolic acidosis (serum bicarbonate
between 9 and 12 mmol/l) is an infrequent finding in
dogs (<10%).3 This cat had a severe metabolic acidosis
with partial respiratory compensation. The main mech-
anisms for these findings are thought to be the decreased
renal excretion of hydrogen ions due to hypoaldoster-
onism fortified by hypotension, and poor perfusion of
tissues and a decreased glomerular filtration rate.3 We
decided to administer sodium bicarbonate to correct
severe metabolic acidosis and to lower serum potas-
sium concentration more quickly. The bicarbonate defi-
cit was estimated by the following formula: 0.3 × body
weight (kg) × (24 × patient bicarbonate). One fourth of
the calculated dose was given slowly IV. Potential com-
plications resulting from sodium bicarbonate adminis-
tration include metabolic alkalosis, hypokalaemia,
hypocalcaemia, hypercapnia and paradoxical intracel-
lular or central nervous system acidosis, which can
cause respiratory arrest. On this account sodium bicar-
bonate therapy should be reserved exclusively for life-
threatening cases.
A retrospective study by Bell et al. described 49 cats
with sodium to potassium ratio <27.16 Interestingly, none
of the cats suffered from hypoadrenocorticism. Hypoad­
renocorticism was excluded with either a negative
ACTH stimulation test, a lack of clinical signs compati-
ble with hypoadrenocorticism or resolution of decreased
sodium:potassium ratio after therapy other than gluco-
corticoids or mineralocorticoids. At least two of these
three criteria had to be met. Systems affected were, in
decreasing order, gastrointestinal, urinary, cardiorespi-
ratory and endocrine systems; rarely, other organ sys-
tems, such as the eye or skin were reported.16 Only
recently a cat with hypoadrenocorticism and marked
hypoglycaemia has been reported.8 We assumed that
944 Journal of Feline Medicine and Surgery 15(10)
hypoglycaemia resulted from a combination of lack of
cortisol (reduction of glucose mobilisation) and ano-
rexia. The present case had low normal glucose at initial
presentation and mild hyperglycaemia during hospitali-
sation (Table 1), likely due to stress.
Microcardia as a sign of dehydration, hypovolaemia
and hypotension has been reported in 87% of cats when
thoracic radiographs were available. This was equally
seen in the present case. This is not surprising as most
cats were markedly hypovolaemic, as manifested by the
physical examination.4,6,7
All things considered, the clinical and clinicopatho-
logic findings (lateral recumbency, decompensated
hypovolemic shock, hypotension, electrolyte shifts and
metabolic acidosis) were indicative for an Addisonian
crisis. This seems to be a rare condition in cats, as, to our
knowledge, it has never been described before, but is
well known in dogs suffering from hypoadrenocorti-
cism. The term describes a life-threatening condition
that is characterised by hypotension, dehydration,
hyperkalaemia, hyponatraemia and acidosis.3 All of
these findings were recognised in the present case.
Initially, blood pressure was not detectable in any leg by
Doppler method, so it had to be assumed that this cat
was markedly hypotensive. After stabilisation, systolic
blood pressure increased to >100 mmHg at every subse-
quent measurement.
Conclusions
With appropriate treatment, prognosis for long-term
survival, once the Addisonian crisis has been managed,
seems favourable.3,4,6,7,12 Still, it has to be mentioned that
most case reports (including this one) have been reported
during the life time of the described cats so that, to our
knowledge, there are no long-term survival times pub-
lished yet.
Funding  The authors received no specific grant from any
funding agency in the public, commercial or not-for-profit sec-
tors for the preparation of this case report.
Conflict of interest  The authors do not have any potential
conflicts of interest to declare.
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