1167_1174_Ketoacidosis.

qxp_FAB 11/10/2017 09:31 Page 1167

Journal of Feline Medicine and Surgery (2017) 19, 1167–1174

CLINICAL Review

Diabetic ketoaciDosis
in the cat
Recognition and essential
treatment
Elke Rudloff

DKA – care plan essentials Practical relevance: Diabetic

Cats may live with diabetes mellitus (dM) without showing overt
signs of illness for a period of weeks to months. However, any increase
in metabolic rate and energy requirement due to concurrent illness
produces an increase in the release of glucose counter-regulatory hor-
mones, resulting in ketogenesis. Significant ketonemia overwhelms the
plasma buffering system, and produces a metabolic acidosis that can
alter normal cellular metabolism. The clinical
The clinical signs signs are related to ketoacidosis, hyperosmolar-
ity and concurrent illness.
are related to Feline diabetic ketoacidosis represents a
potentially fatal condition that is diagnosed
ketoacidosis, with a combination of findings including hyper-
glycemia, glucosuria, ketonemia or ketonuria,
hyperosmolarity
and a metabolic acidosis. The mainstay of ther-
and concurrent apy is immediate recognition and treatment
of life-threatening problems, careful volume
illness. replacement, and insulin administration for
glycemic control and elimination of ketonemia.
different insulin protocols exist for the acute
care of the cat with dKA. Electrolyte imbalances
are common sequelae, and need to be
recognized and corrected. Likewise, concurrent
conditions need to be recognized and treated. Prior to initiation of
intensive care, the client must be appraised of the long-term manage-
ment requirements for the cat with diabetes mellitus, including twice-
daily insulin injections and increased veterinary visits.
ketoacidosis (DKA) is a not uncommon
emergency in both newly diagnosed and
poorly regulated diabetic cats. When
there is a heightened metabolic rate and
energy requirement due to concurrent
illness, an increase in the release of glucose
counter-regulatory hormones causes insulin
receptor resistance, lipolysis, free fatty acid
release and ketogenesis. This necessitates not
only treatment to eliminate the ketosis and control
blood glucose, but also investigation of concurrent
illnesses.
Clinical challenges: A number of metabolic
derangements can occur with DKA, requiring a
comprehensive diagnostic evaluation, elimination
of ketones, careful correction of glucose, electrolyte
and acid base abnormalities, and close monitoring.
Audience: Any veterinarian that cares for cats in
urgent and emergency situations should understand
the pathophysiology of DKA in order to address
an individual’s clinical signs and metabolic
derangements.
Evidence base: This review draws evidence from
the peer-reviewed literature as well as the author’s
personal clinical experience.

Pathophysiology

Glucose is a necessary fuel that drives the production of energy, in the

form of adenosine triphosphate (ATP), by the mitochondria within the
cells. in all organs, other than the brain, insulin is needed to move
glucose from the blood into the cells where it is used to make ATP or is
converted and stored as glycogen (in the liver and muscles) or trigly-
ceride (in adipocytes). insulin also moves electrolytes such as potassi-
um from the plasma into the cells and limits the oxidation of fat.

Elke Rudloff
DVM, DACVECC
Lakeshore Veterinary Specialists,
2100 W Silver Spring Dr, Glendale,
WI 53024, USA
Emailr: erudloff@lakeshorevetspecialists.com

doi: 10.1177/1098612X17735762
© The Author(s) 2017 JFMS CLINICAL PRACTICE 1167
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R E V I E W / Essential treatment for feline diabetic ketoacidosis

When altered mentation exists, the cat must be carefully handled

to minimize stress and increases in intracranial pressure.

dM is a syndrome caused by insulin insuffi- Clinical signs and diagnosis

ciency, insulin receptor dysfunction, insulin
receptor downregulation, or some combina-
tion that results in lack of transport of glucose
into the cell, hyperglycemia and cellular star-
vation. Pancreatic islet cell destruction and
concurrent disorders that affect insulin recep-
tor sensitivity (eg, pancreatitis, chronic inflam-
matory diseases, obesity, endocrinopathies)
are conditions that are most commonly associ-
ated with feline dM.1,2 Hyperglycemia that
exceeds the renal threshold for glucose reab-
sorption results in glucosuria, increased urine
osmolality and urine production, as well as
increased plasma osmolarity and thirst.
Cellular starvation stimulates an increase in
appetite, mobilization of free fatty acids
(FFAs), an increase in plasma amino acids and
weight loss. oxidation of FFAs leads to hepatic
production of ketone bodies (acetoacetate,
beta-hydroxybutyrate and acetone), which are
used as an alternative energy source in the
peripheral tissues and liver.
Acquired dM can be tolerated for a period of
time. Since many cats free-feed, their waste
may not be cleaned daily, and/or they have
indoor–outdoor access, clients may fail to
immediately recognize the classic signs of dM
(increased food intake, drinking and urination).
As long as there is adequate, albeit reduced,
circulating insulin, hyperglycemia does not
lead to acute illness. However, when there is an
increased metabolic rate and energy require-
ment due to concurrent illness, the release
of glucose counter-regulatory hormones
(adrenaline [epinephrine], norepinephrine, cor-
tisol, glucagon and growth hormone) is stimu-
lated. These ‘stress’ hormones increase insulin
receptor resistance, lipolysis and FFA release,
and promote ketogenesis. Significant keto-
nemia related to dM overwhelms the plasma
buffering system, and results in a metabolic
acidosis (ie, dKA) that can alter normal cellular
metabolism. Similar to glucose molecules,
ketones are osmotically active. increased filtra-
tion of ketones by the kidney exacerbates
osmotic diuresis, electrolyte imbalances and
water loss, manifesting in hypovolemia and
interstitial dehydration. Untreated dKA causes
severe illness and death.
Cats suffering from dKA typically present
with problems of an urgent or emergency
nature. Client complaints are usually non-
specific and may include lethargy, anorexia
and vomiting. Weakness and gait abnormali-
ties may also be observed.3 A complete history
may uncover more classic signs of hyper-
Untreated DK glycemia including recent increased drinking,
urination and appetite, with weight loss.
causes severe Physical examination findings can include
illness clinical signs of poor perfusion, altered men-
tation, dehydration and poor body condition.
and death. in some cases, a sweet smell to the breath can
alert the examiner to the presence of exhaled
acetone.
Laboratory confirmation of dKA is based
on the presence of hyperglycemia, glucosuria,
ketonemia or ketonuria, and a metabolic aci-
dosis. Serum fructosamine can be evaluated in
cases with marginal glucose levels.
Client consultation
Client consultation and education is important prior to making a financial
commitment to hospital admission and initiation of intensive care. Clients must
be appraised of the fact that treatment of feline DM requires twice-daily insulin
injections and more frequent veterinary visits than needed for healthy cats. In
some cases, clients may not want, or be able, to administer injections in a
timely manner. Some clients may not want to restrict an indoor–outdoor cat to
a life indoors for consistent care. Rehoming and/or euthanasia should be
discussed in these situations.
Triage and fluid resuscitation
The primary survey performed during patient
triage will identify any immediate life-threat-
ening problems. The breathing effort is
characterized, and the lungs are carefully aus-
cultated for evidence of increased or absent
breath sounds. Perfusion is assessed, and
body temperature obtained. it is common for
poor perfusion in the cat to manifest as pale
mucous membranes, prolonged capillary refill
time, bradycardia, hypotension and hypother-
mia.4 When altered mentation exists, the cat
must be carefully handled to minimize stress

The mainstay of treatment for feline DKA is immediate recognition and

treatment of life-threatening problems, careful volume replacement, and insulin
administration for glycemic control and elimination of ketonemia.

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R E V I E W / Essential treatment for feline diabetic ketoacidosis

and increases in intracranial in the normothermic cat follow-

pressure. oxygen is supplied ing the infusion of 60 ml/kg
while immediate placement buffered isotonic crystalloid and
of a peripheral intravenous 20–40 ml/kg HES, causes of
(iV) catheter and collection non-responsive shock must be
of blood and urine samples investigated, and vasopressors
for analysis is performed. may be indicated.
intramuscular (iM) or iV Analysis of packed cell vol-
injection of 0.4–0.6 mg/kg ume, total protein, electrolytes,
butorphanol may reduce venous blood gas, glucose,
patient anxiety associated osmolality and lactate data is
with restraint. performed. Samples are saved
Resuscitation from hypo- for additional evaluation (com-
tension always involves the plete blood count, serum bio-
use of an isotonic crystalloid chemical profile, urine analysis
solution. Some clinicians pre- and culture, and thyroid profile)
fer to use 0.9% sodium chlo- after the cat is stabilized.
ride (308 mosm/l) to provide Figure 1 Critically ill cats with hypothermia must be carefully warmed Heparinized plasma can be test-
the least degree of transcellu- following initiation of fluid resuscitation. This patient is covered with a
blanket to prevent heat loss, and active warming is being provided by ed for ketones using urine
lar osmolar shift when severe placement of the fluid line through a warming device reagent strips (Figure 2).5
hyperglycemia is present, and Ketostix reagent strips use a col-
avoid the use of lactated orimetric method that measures
Ringer’s solution to reduce competition for a nitroprusside reaction for detecting acetoac-
hepatic conversion of lactate and ketones. etate in blood or urine; blood measurements
However, 0.9% sodium chloride is an acidic are more precise than urine measurements.6
fluid and may not correct an acidemia as effec- This method does not, however, measure
tively as a balanced buffered isotonic solution beta-hydroxybutyrate (which can be present
such as Plasma-Lyte A pH 7.4 (Baxter) or before detectable levels of acetoacetic acid),
Normosol-R pH 7.4 (Hospira) (~295 mosm/l), making it insensitive for monitoring the sever-
which contain acetate and gluconate buffers ity of ketoacidosis. Thus monitoring of beta-
that are metabolized by skeletal muscle. it is not hydroxybutyrate is preferred, and persistent
uncommon for hyponatremia to be present, and positive results are considered in conjunction
some clinicians might also choose to infuse with clinical signs when transitioning from
0.9% sodium chloride to correct this. Hypo- iCU to home care. Ketone testing using the
natremia, however, can be a spurious finding Precision Xtra or optium systems (Abbott)
when hypertriglyceridemia exists, and/or it will measure beta-hydroxybutyrate.
can be due to shift of water intravascularly in Figure 2 Reagent strips
response to increased plasma osmolality caused are used to test the urine
for glucose and ketones.
ICU management
by hyperglycemia (see box on page 1172). A serum blood sample can
Resuscitation of the hypovolemic cat differs also be tested for ketones once perfusion is restored, rehydration thera-
using the reagent strip.
from that of the dog.4 Large volume resuscita- Courtesy of Kate Hopper py is instituted (see box on page 1170). At the
tion, as typically used in the dog, may result point when the cat is
in volume overload in the cat. A more better hydrated, a multi-
measured approach using intermittent bolus lumen central venous
infusions of body temperature 10–15 ml/kg catheter can be placed in
isotonic crystalloid solution, with or the jugular or median
without 3–5 ml/kg hydroxyethyl starch saphenous vein to facili-
(HES), can be administered over 10–15 mins tate repeated blood
while monitoring the arterial blood pressure. collection and central
Repeated boluses are administered until the venous pressure monitor-
systolic arterial blood pressure is at least ing (Figure 3). Since fre-
40–60 mmHg. At this stage, active external quent blood collection in
rewarming is initiated by placing the cat in the cat can lead to ane-
a warming tent, on a circulating warm mia,8 some clinicians pre-
water/air blanket, and/or running the fluid fer to collect blood from
infusion line through a warm fluid bath or the marginal ear veins for
fluid warmer (Figure 1). Fluid administration periodic glucose checks
is continued at calculated maintenance and with a glucometer (Figure
rehydration rates until the rectal temperature 4). A portable glucometer
reaches 98ºF (36.7°C). if hypotension still Figure 3 Placement of a central venous catheter allows
repeated blood sampling for glucose monitoring without
(AlphaTRAK 2; Zoetis) is
exists after rewarming, crystalloid and HES having to restrain or repeatedly prick the patient with a specifically calibrated for
boluses are continued. if hypotension persists needle. The same catheter can be used for fluid and drug use in cats and dogs
administration. Courtesy of Elisa Mazzaferro

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R E V I E W / Essential treatment for feline diabetic ketoacidosis

Rehydration therapy
A balanced, buffered isotonic crystalloid is used for rehydration therapy. Rehydration rates are calculated
based on the estimated level of dehydration (Table 1).7

The calculation commonly used to estimate the volume of isotonic replacement

crystalloid needed to correct interstitial deficits is:
Deficit (ml) = body weight x % dehydration x 10

Rehydration typically takes longer than expected, because of osmotic diuresis. If the cat is conscious,
rehydration can be planned for a period over 6–8 h. If the cat has altered mentation, it may be more
desirable to mitigate rapid osmolar shifts across the blood–brain barrier and rehydrate over 12–24 h.

Maintenance requirement (ml) = 30 x body weight (kg) + 70 per day

The rehydration rate is added to the maintenance fluid rate (determined by the
above calculation) and to hourly replacement volumes of ongoing fluid losses
(eg, vomitus, gastric suction, diarrhea, body effusions, osmotic diuresis)

It may be difficult to regulate Table 1 Physical examination findings used to There is a

fluid balance in the critically estimate interstitial dehydration
ill cat with hyperglycemia.
misconception
Estimated %
Typically the patient will not dehydration Physical examination findings that insulin
< Tacky mucous membranes
drink, and underlying condi-
4–6 should not be
tions may cause nausea,
< Loose skin turgor
< Dry mucous membranes
gastrointestinal dysfunction 6–8
and ongoing fluid losses.
initiated until
< Loose skin turgor dehydration
< Dry mucous membranes
Osmotic diuresis from gluco- 8–10

< Globes retracted within orbits

suria and ketonuria may be
profound. Frequent re-evalua- has been
<
<
tion and adjustment of the 10–12 Persistent skin tent due to complete loss of skin elasticity
corrected.
<
Dry mucous membranes
fluid rates may be necessary.
<
Retracted globes
Use of HES during fluid Dull corneas
<
maintenance therapy (eg, 6%
<
>12 Persistent skin tent
HES 130/0.4 at 2 ml/kg/h;
<
Dry mucous membranes

<
VetStarch [Abbott]) may Retracted globes

<
promote intravascular fluid Dull corneas
Signs of perfusion deficits (eg, pale mucous
retention when a systemic membranes, prolonged capillary refill time, poor pulse
inflammatory condition exists. quality, hypothermia, bradycardia)

(Figure 5). it requires only a 0.3 µl sample, and
blood from a marginal ear vein prick using a
25 G needle is sufficient.
Figure 4 Marginal ear vein sampling for glucose monitoring.
Courtesy of Zoetis
Figure 5 The AlphaTRAK 2
glucometer, specifically calibrated
for cats and dogs, requires only
0.3 µl of blood, and is suitable for
home monitoring. The monitor’s
reading range is 20–750 mg/dl.
A ‘HI’ reading indicates blood
glucose is >750 mg/dl; a ‘LOW’
reading indicates it is <20 mg/dl.
Courtesy of Mandy Nonnemacher
Insulin therapy and protocols
insulin infusion is started after perfusion has
been restored. There is a misconception that
insulin should not be initiated until dehydra-
tion has been corrected, to mitigate the impact
of dilution and increased glomerular filtra-
tion, which risk rapidly decreasing the effec-
tive osmolality and also potentially causing
cerebral edema.9 However, a retrospective
study in 60 dogs and cats with dKA or diabet-
ic ketosis showed that a delay to insulin ther-
apy of >6 h significantly delayed resolution of
ketonemia (by 19 h, on average), and no dif-
ference in complications was observed.10
There are several methods for insulin
administration in the cat with dKA.
Whatever method is prescribed, the ultimate
goal is to eliminate ketosis and correct acido-
sis without causing hypoglycemia.
< Intermittent administration of regular
insulin Administration of regular insulin

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can be successfully employed at an initial
dosage of 0.1 U/kg iM followed by 0.05 U/kg
iM administered hourly until the blood glucose
level is <250 mg/dl.11
< Glargine insulin iM glargine (which has a
short half-life) administered with or without
subcutaneous (SC) glargine (which has a long
half-life) has also been shown to treat feline dKA
effectively, and may be considered in cases with
limited finances, when continuous insulin
infusion and in-hospital monitoring may not be
affordable. in a retrospective study reviewing
treatment of dKA in 15 cats,12 an initial dose of
1–2 U per cat was administered iM with 1–3 U
SC, followed by 1–2 U iM as needed (q2h or less
frequently) and 1–2 U SC q12h until regulated.
Based on the results of their study, the authors
recommend the use of 1–2 U SC glargine q12h,
with 0.5–1 U iM up to q4h, to achieve a blood
glucose concentration of 180–252 mg/dl.
inadequate perfusion and absorption from depot
sites may make this method of administration
less predictable, and it also requires more
frequent blood glucose checks (q1–2h) compared
with a continuous infusion method.
< Continuous infusion of regular insulin Use
of a constant rate infusion (CRi) of regular
insulin permits a more regulated decline in
serum glucose levels and plasma osmolarity
because adjustments in infusion rates can be
made. douglass Macintire first introduced the
concept of insulin continuous infusion for
veterinary patients in a hyperglycemic crisis in
1993,9 and it has become the standard of care in
many veterinary iCUs. Her recommendation
for a feline patient is to place 1.1 U/kg of regular
insulin in a 250 ml bag of 0.9% saline, drain out
50 ml of the solution to allow for insulin
adsorption by the plastic tubing, and administer
the mixture at a rate of 10 ml/h.
Example: 5 kg cat
1.1 U insulin x 5 kg per day = 5.5 U added to 250 ml bag of 0.9 % sodium
chloride
A higher dose of insulin infusion (up to 2.2
U/kg q24h) may be more effective at reducing
hyperglycemia in the cat and is associated with
a better outcome than a lower dose.13 There
does not appear to be a relationship between
osmolality at presentation, administered insulin
dose and mentation changes.14
A pilot study involving 29 cats with dKA
compared the concurrent use of regular
insulin iM (1 U up to q6h) and SC glargine
(0.25 U/kg q12h) with a continuous infusion
of regular insulin (1 U/kg q24h) in cats with
dKA.15 The latter regimen produced more
rapid resolution of ketosis, hyperglycemia
and acidemia, and an associated reduction in
the length of hospital stay. This author has
R E V I E W / Essential treatment for feline diabetic ketoacidosis
Table 2 Adjustment of regular insulin CRI based on blood
glucose levels
Blood glucose
(mg/dl) (mmol/l) Treatment changes
>400 >22 If glucose is not declining after two or three rechecks, ↑insulin
CRI by 25%
250–400 13.9–22 Continue as initially planned
200–250 11.1–13.9 ↓Insulin CRI by 25%
↓Insulin CRI by 25%
150–200 8.3–11.1
↓Insulin CRI by 25%
100–150 5.5–8.3
<100 <5.5 Stop insulin infusion, start 2.5% dextrose IV. If clinical signs
exist, slowly bolus 0.1–0.25 g/kg 50% dextrose (0.5–1 ml/kg)
and repeat blood glucose after 30 mins
CRI = constant rate infusion; IV = intravenously
Example
A 5 kg cat presented for vomiting and anorexia is diagnosed with DKA (initial
blood glucose 560 mg/dl, 31.1 mmol/l) and pancreatitis. A continuous rate IV
insulin infusion is initiated at 5.5 U regular insulin q24h at a rate of 10 ml/h and
1 IU insulin glargine SC q12h. After 4 h the blood glucose level is 450 mg/dl
(25 mmol/l) and at 10 h it is 210 mg/dl (11.7 mmol/). The regular insulin CRI is
reduced to 7 ml/h. After 16 h the blood glucose is 230 mg/dl (12.8 mmol/l), and
it remains between 200 and 250 mg/dl (11.1 and 13.9 mmol/l) over the following
36 h. The insulin CRI is discontinued when the cat is tolerating assisted feeding
and the 1 U glargine SC q12h is continued without incident.
used concurrent regular insulin continuous
infusion using the above rate of 1 U/kg q24h
and SC glargine (1 U q12h) in cats with success.
Patient monitoring and
additional treatment
Following the initiation of volume replacement
and insulin therapy, close monitoring is needed
to recognize alterations in fluid balance, main-
tain perfusion and hydration, prevent hypo-
glycemia, and identify and treat persisting or
developing acid–base and electrolyte abnor-
malities (see box on page 1172). Treatment can
become complicated when there is a need for
supplemental electrolytes and glucose. Placing
fluids with additives in a burette drip chamber
permits adjustment of additive concentrations
without sacrificing an entire bag of fluids.
Patient monitoring includes evaluating
blood glucose q2–4 h, and electrolytes, venous
The ideal blood blood gases, fluid ins and outs, and body
weight q12–24h (using the same scales at each
glucose level weigh-in to avoid discrepancies). The ideal
is between blood glucose level is between 150 mg/dl and
250 mg/dl. Regular insulin continuous
150 mg/dl and infusion therapy may be adjusted according to
glucose levels (Table 2). Traditionally, the
250 mg/dl. recommendation has been to supplement dex-
trose when the blood sugar is <250 mg/dl,9,11
but this can become costly when frequent
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R E V I E W / Essential treatment for feline diabetic ketoacidosis
Correction of electrolyte imbalances
When a significant metabolic acidosis exists, bicarbonate
administration should be withheld until the patient is reperfused
and better hydrated. If the serum bicarbonate (HCO3) level
remains <10.0 mmol/l and pCO2 is normal or low, then a
slow sodium bicarbonate infusion should be considered (see
box on the right); one-quarter to one-half of the calculated
dose is administered over 30–60 mins, followed by repeat
venous blood gas analysis to determine if additional infusion is
needed. The goal is not to restore serum bicarbonate levels to
normal, but rather to increase them to a more acceptable level
(>12 mmol/l).
Plasma sodium disorders are not uncommon in the cat with
DKA. In many cases a reduction in measured sodium is a result
of increased plasma glucose holding water in the vascular space
and diluting the plasma sodium concentration.
The corrected sodium can be calculated by:
adding the measured sodium to
1.6 x (glucose [mg/dl] – 100)/100
Example
A cat with plasma glucose of 675 mg/dl has a plasma
sodium level of 159 mmol/l. The corrected sodium =
159 + 1.6(675 – 100)/100 = 168.2 mmol/l
Hyponatremia generally corrects with fluid replacement and
the establishment of normoglycemia.
Hypernatremia can be a consequence of solute-free water
loss in the urine or through the respiratory tract. In such cases,
once the cat is reperfused and rehydrated, a half strength isoton-
ic sodium chloride solution or amino acid solution can be used
at maintenance rates to replace solute-free water needs, while
concurrently administering isotonic solutions for ongoing water
losses.
As insulin therapy is instituted and the acidemia resolves,
potassium will move into the cells, which can lead to a drop in
the serum potassium concentration. Potassium supplementation
is calculated according to the serum level and, in general, the
rate should not exceed 0.5 mEq/h.16 Suggested supplementation
changes in supplementation (including elec-
trolytes) necessitate additional fluid bags, iV
administration sets and burette drip chamber
sets. it also may increase the time it takes to
determine when the patient may be ready to
transition from a CRi to twice-daily insulin
injections. This author’s experience is that,
with adequate monitoring, adjustments can be
made to the insulin infusion, and the addition
of dextrose may not be necessary until the
blood glucose drops below 100 mg/dl.
Based on the patient’s cardiovascular and
volume status, additional monitoring may
include periodic evaluation of arterial blood
pressure, body temperature, hydration level
and body weight.
1172 JFMS CLINICAL PRACTICE
Hypokalemia:
Table 3 Supplementation rates for
hypokalemia
Suggested
Patient’s serum potassium supplementation Suggested fluid
concentration (mEq/l) dose (mEq KCl/l) rate (ml/kg/h)
3.1–3.5 28 18
2.5–3.0 40 12
<2.5 60 8
<2.0 80 6
Hypophosphatemia:
KPO4: 0.01–0.09 mmol phosphate/kg/h, up to 0.2 mmol/kg/h
if serum PO4 <1.5 mg/dl (0.484 mmol/l)
Low HCO3:
NaHCO3 (mEq) =
(desired HCO3 – patient HCO3) x 0.3 x body weight (kg)
rates are given in the box above. The use of potassium phos-
phate for correction of hypokalemia is not recommended.
However, should potassium phosphate be used for correction of
hypophosphatemia, adjustments in potassium chloride infusion
rates may be necessary. When potassium levels are difficult to
normalize, supplemental magnesium at 0.75–1 mEq/kg/day may
be necessary.17
Serum phosphorus is an additional electrolyte that should be
closely monitored after initiation of insulin treatment and volume
replacement in the cat with DKA. With the correction of acidemia
and institution of insulin therapy there will be a relocation of
serum phosphorus into the cells, coupled with use of
phosphorus in the production of ATP. There is a serious risk for
hemolysis and anemia should the serum phosphate level fall
below 1.5 mg/dl (0.484 mmol/l). Patients with serum phosphorus
levels <2.0 mg/dl (0.646 mmol/l) will likely benefit from phospho-
rus replacement (see box above).18–20 Most potassium
phosphate solutions contain 3 mmol/ml (93 mg/ml) of phospho-
rus and 4.4 mEq/ml (4.4 mmol/l) of potassium.
Broad spectrum intravenous antibiotic ther-
apy (eg, ampicillin-sulbactam 20 mg/kg iV
q8h) may be indicated when a left shift is
identified, a fever is present, severe gastro-
intestinal signs exist, or there are overt signs
of a bacterial infection. Thoracic radiographs,
abdominal ultrasound and urine culture are
used as screening tools for identifying pul-
monary, intra-abdominal or genitourinary
infections, respectively.
Nasogastric tube feeding, with or without
partial parenteral nutrition, is necessary to
preserve enterocyte function, reverse protein
catabolism and promote hepatic function until
the patient is eating voluntarily. Assisted feed-
ing also limits the development of food aver-
1167_1174_Ketoacidosis.qxp_FAB 11/10/2017 09:32 Page 1173
sion, and the cephalic and gastric phases of
digestion that can promote vomiting in cats
with nausea. Nasogastric tube placement per-
mits evaluation of gastric emptying function
with periodic aspiration, as well as immediate
administration of liquid nutrition. CliniCare
(Zoetis) can be infused as a continuous infu-
sion starting with a 50% solution at 0.5
ml/kg/h. over a 48 h period, this is increased
to a 100% solution at ~2 ml/kg/h, provided
that gastric residual volumes are minimal.
Emeraid intensive Care (Emeraid) can also be
bolused at 2–6 h intervals. Prokinetic medica-
tion such as metoclopramide and/or cisa-
pride can promote gastric emptying.
FreAmine (B Braun) is an intravenous 3%
amino acid solution that can be used as a daily
maintenance fluid and provides partial parenter-
al nutrition when administered at a mainte-
nance fluid rate once the patient has started
insulin therapy. ProcalAmine (B Braun) is
another intravenous amino acid (3–4%) solu-
tion that contains glycerin as a carbohydrate
source. Both solutions contain potassium and
can be administered via a peripheral catheter.
Since they are given as a continuous infusion,
additives such as antiemetics and vitamin B
can be administered with these fluids.
Additional evaluation
Ketoacidosis, by itself, has not been associated
with a poor outcome in the diabetic cat;21 how-
ever, coexisting conditions (see box below) may
affect the prognosis and outcome, and should
be identified and addressed. Serum biochem-
istry, thyroid function testing, a complete blood
count, and urine analysis and culture are indi-
cated. Although not predictive of mortality, ele-
vations in serum creatinine, blood urea nitro-
gen, magnesium and total bilirubin are associ-
ated with a worse outcome in the cat with
dKA.13 Thoracic and abdominal radiographs as
well as abdominal ultrasound are necessary for
uncovering evidence supporting liver disease,
pancreatitis, kidney abnormalities, infection
and neoplasia. When liver enzymes are elevat-
ed and/or biliary changes exist, liver aspi-
rate/biopsy collection for cytopathological and
Concurrent diseases
< Pancreatitis
< Neoplasia
< Renal failure
< Cholangiohepatitis
< Infection
< Cardiac disease
<
Inflammatory bowel disease
< Hepatic lipidosis
<
Endocrinopathy
R E V I E W / Essential treatment for feline diabetic ketoacidosis
Coexisting
conditions may
affect the
prognosis and
outcome, and
should be
identified and
addressed.
Figure 6 Reagent strips
specific for measuring
urine glucose and ketone
can be used by owners for
home monitoring. Courtesy
of Steve Epstein
Figure 7 A single
glucometer reading showing
an elevated blood glucose
level. ‘Spot check’ glucose
tests are only useful if
hypoglycemia is suspected
(see text). Courtesy of Megan
Tremelling
culture analysis may be indicated. A common
concurrent disease finding in cats is hepatic
lipidosis, which may require additional thera-
peutic measures.22 When chronic gastro-
intestinal (Gi) signs occur, endoscopic biopsy of
Gi mucosa may uncover infiltrative diseases.
Preparing for hospital discharge
once the cat is hydrated and voluntarily eat-
ing or tolerating tube feeding, and the ketosis
is cleared, long-term insulin therapy can be
initiated.21 The insulin CRi is discontinued at
least 4 h prior to starting long-acting insulin
injections, unless the cat is already receiving
insulin glargine. The blood glucose is evaluat-
ed at the time insulin injections are to be
given, as determined by the owner’s sched-
ule. if the serum glucose is <150 mg/dl,
insulin is not administered. At the next sched-
uled time for insulin therapy, the glucose level
is checked. on the basis it is >250 mg/dl, 0.5–1
U glargine or protamine zinc insulin q12h SC
is administered. This dose is recommended in
the previously diagnosed diabet-
ic, as well as newly diagnosed
cases, since insulin requirements
may have altered.
A glucose curve is evaluated
over the following 12 h and adjust-
ments are made to insulin injec-
tions as necessary. The goal is to
have a glucose nadir no lower than
150 mg/dl in the hospital, rather
than try to determine the ideal
dose for long-term management.
When prescribing insulin at the
time of discharge, consideration
should be given to the fact that the
environmental conditions at home
will be less stressful than in the
hospital, and therefore a lower
dose of insulin may be required
than was given in hospital.
The patient is discharged with
instructions for feeding and for
home urine glucose monitoring
(Figure 6), with a glucose curve
evaluation scheduled for 1 week
later.23 The client is instructed to
call a veterinarian if the urine glu-
cose is repeatedly negative or
>2000 mg/dl. A glucose curve
and/or serum fructosamine esti-
mation are needed to determine
any future adjustments in insulin
therapy. ‘Spot check’ glucose tests
are only useful if hypoglycemia is
suspected (Figure 7), since a single glucose
value that is normal or increased cannot differ-
entiate adequate therapy from too much or too
little insulin. For example, a cat receiving too
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R E V I E W / Essential treatment for feline diabetic ketoacidosis

KEY points
< Essential treatment for the cat with DKA includes judicious fluid replacement, insulin administration and correction
of electrolyte imbalances. Ketonemia will not resolve without insulin administration.
< Insulin therapy for patient stabilization can be customized as long as blood glucose is closely monitored.
< Treatment of DKA in itself is relatively straightforward. What must be included in the care plan for the cat with DKA
is investigation and treatment of concurrent illnesses that cause increased counter-regulatory hormone release.
< Clients must be prepared to treat their diabetic cat with twice-daily insulin and additional veterinary
visits prior to committing to treatment of the cat with DKA.

much insulin can become hypoglycemic, then rebound, the resulting hyperglycemia can be
experience a rebound hyperglycemia related to misinterpreted as inadequate insulin adminis-
stress hormone release (ie, Somogyi effect); if tration. increasing insulin in such cases can
the blood glucose is measured during this cause life-threatening hypoglycemia.

Conflict of interest
The author declared no potential conflicts of interest with respect
to the research, authorship and/or publication of this article.
Funding
The author received no financial support for the research, author-
ship and/or publication of this article.
References
1 Feldman EC and Nelson RW. Feline diabetes mellitus. in: Feldman
EC and Nelson RW (eds). Canine and feline endocrinology and repro-
duction. 3rd ed. Philadelphia: Elsevier Science, 2004, pp 539–579.
2 Rand JS. Pathogenesis of feline diabetes. Vet Clin North Am
Small Anim Pract 2013; 43: 221–231.
3 Kerl ME. Diabetic ketoacidosis: treatment recommendations.
Compend Contin Educ Pract Vet 2001; 23: 330–339.
4 Rudloff E and Kirby R. Feline circulatory shock. in: Little S (ed).
August’s consultations in feline internal medicine. Vol 7. St Louis,
Mo: Elsevier, 2016, pp 843–858.
5 Brady MA, dennis JS and Wagner-Mann C. Evaluating the use
of plasma hematocrit samples to detect ketones utilizing
urine dipstick colorimetric methodology in diabetic dogs
and cats. J Vet Emerg Crit Care 2003; 13: 1–6.
6 Zeugswetter F and Pagitz M. Ketone measurements using dip-
stick methodology in cats with diabetes mellitus. J Small
Anim Pract 2009; 50: 4–8.
7 Rudloff E. Assessment of hydration. in: Silverstein d and
Hopper K (eds). Textbook of small animal critical care.
Philadelphia: WB Saunders, 2014, pp 307–331.
8 Lynch AM, Respess M, Boll AE, et al. Hospital-acquired anemia
in critically ill dogs and cats: a multi-institutional study.
J Vet Intern Med 2016; 30: 141–146.
9 Macintire dK. Treatment of diabetic ketoacidosis in dogs by
continuous low-dose intravenous infusion of insulin. J Am
Vet Med Assoc 1993; 202: 1266–1272.
10 diFazio J and Fletcher dJ. Retrospective comparison of early-
versus late-insulin therapy regarding effect on resolution of
diabetic ketosis and ketoacidosis in dogs and cats: 60 cases
(2003–2013). J Vet Emerg Crit Care 2016; 26: 108–115.
11 Feldman EC and Nelson RW. Diabetic ketoacidosis. in: Feldman
EC and Nelson RW (eds). Canine and feline endocrinology and repro-
duction. 3rd ed. Philadelphia: Elsevier Science, 2004, pp 580–615.
12 Marshall Rd, Rand JS, Gunew MN, et al. Intramuscular
glargine with or without concurrent subcutaneous adminis-
tration for treatment of feline diabetic ketoacidosis. J Vet
Emerg Crit Care 2013; 23: 286–290.
13 Cooper RL, drobatz KJ, Lennon EM, et al. Retrospective
evaluation of risk factors and outcome predictors in cats
with diabetic ketoacidosis (1997–2007): 93 cases. J Vet Emerg
Crit Care 2015; 25: 263–272.
14 Claus MA, Silverstein dC, Shofer FS, et al. Comparison of
regular insulin infusion doses in critically ill diabetic cats:
29 cases (1999–2007). J Vet Emerg Crit Care 2010; 20: 509–517.
15 Gallagher BR, Mahony oM and Rozanski EA. A pilot study
comparing a protocol using intermittent administration of
glargine and regular insulin to a continuous rate infusion of
regular insulin in cats with naturally occurring diabetic
ketoacidosis. J Vet Emerg Crit Care 2014; 25: 1–6.
16 Riordan LL and Schaer M. Potassium disorders. in: Silverstein
dC and Hopper K (eds). Small animal critical care medicine. 2nd
ed. St Louis, Mo: Elsevier, 2015, pp 269–273.
17 Bateman S. Disorders of magnesium: magnesium deficit and
excess. in: diBartola SP (ed). Fluid therapy in small animal prac-
tice. 3rd ed. Philadelphia: WB Saunders, 2006, pp 210–226.
18 Barton L and Kirby R. Electrolytes. in: Kirby R and Linklater A
(eds). Monitoring and intervention for the critically ill small ani-
mal: the rule of 20. Ames: John Wiley & Sons, 2017, pp 73–94.
19 Barton L. Magnesium and phosphate disorders. in: Silverstein
dC and Hopper K (eds). Small animal critical care medicine. 2nd
ed. St Louis, Mo: Elsevier, 2015, pp 281–288.
20 Statz G. Feline diabetic ketoacidosis. in: Little S (ed). August’s
consultations in feline internal medicine. Vol 7. St Louis, Mo:
Elsevier, 2016, pp 836–842.
21 Callegari C, Mercuriali E, Hafner M, et al. Survival time and
prognostic factors in cats with newly diagnosed diabetes mel-
litus: 114 cases (2000–2009). J Am Vet Med Assoc 2013; 243: 91–95.
22 Armstrong PJ and Blanchard G. Hepatic lipidosis in cats.
Vet Clin North Am Small Anim Pract 2009; 39: 599–616.
23 Sparkes AH, Cannon M, Church M, et al. ISFM consensus
guidelines on the practical management of diabetes melli-
tus in cats. J Feline Med Surg 2015; 17; 235–250.

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