20. Diabetes ketoacidosis(DKA) Flashcards
Diabetes ketoacidosis Pathophysiology?
Pathophysiology:
-Lack of Insulin {either absolute lack or relative due to increased resistance) leads to Increased lipolysis
releasing free fatty acids from adipose tissue. These are converted lo ketones. Excessive production·
of ketones results in a metabolic acidosis or ketoacldosis
-I’ Typically, this Is precipitated by an underlying disease that Increases the production of stress_
hormones which Increase Insulin resistance
Clinical signs of diabetes mellitus and diabetic ketoacidosis?
Clinical signs:
-Diabetes mellitus: Polyuria, polydipsia, polyphagia, weight loss, lethargy
-Diabetic ketoacidosis (OKA): Lethargy, vomiting, anorexia, severity depends on the degree of metabolic acidosis and nature of the concurrent disease
Diagnosis and Prognosis?
Diagnosis:
Must Investigate for precipitating factors
Diagnosis = hyperglycaemia, glucosuria, ketonuria, and metabolic acidosis
-Diabetes Mellitus: Blood glucose (persistent fasting >14mmol/l or >250mg/dl) and glucosuria
- Urinalysis and dipstick:
-Must perform urinalysis and culture and sensitivity to investigate concurrent disease
- Urine specific gravity - if low with azotaemia then concurrent intrinsic renal failure
- Ketonuria = diabetic ketosis:
Detects only acetoacetic acid, does not detect ~-hydroxybutyrate or acetone, BUT rarely does
OKA develop without production of acetoacetic acid
-Blood gas:
- Metabolic acidosis, pH <7, 1 is life-threatening
- Haematology:
Increased PCV due to dehydration
Stress or inflammatory leukogram
- Biochemistry:
, Hyperglycemia
;. Hyponatraemia and hypokalaemia - can be due to osmotic loss into the urine and osmotic haemodilution
+/- Azotaemia
Other changes depending on the underlying disease:
E.g. Liver disease, pancreatitis, hyperadrenocorticism
Ultrasound: Commonly see pancreatitis, cholangiohepatitis
-+/- Radiographs
Prognosis: The mortality rate of dogs and cats with DKA is 30 - 40%
Increased mortality rates with dogs with underlying disease
Treatment Goals?
Treatment:
Goals:
- Insulin to suppress breakdown of production of ketones
- Correct fluid and electrolyte Imbalances
- Correct melabolic acidosis
- Identify predisposing factors
- Slow correction of hyperglycaemia
Treatment protocol for healthy DKA?
Treatment protocol for healthy DKA:
- Bright alert and responsive, eating and drinking
- Correct underlying fluid deficits and electrolytes derangements
- Commence insulin therapy:
- Can start with either short acting regular crystalline Insulin (e.g. Actrapid ®) at 0.2 U/kg SC TID OR Intermediate-acting insulin at 0.5 U/kg SC BID
- Give food with insulin and free access 10 water
- Monitor blood glucose levels closely every 2 hours
- Monitor of any signs of illness
- Identification and treatment of underlying cause
- When ketoacidosis has resolved can start intermediate-acting insulin with less intensive monitoring
- Ketonuria may persist for several days despite treatment
Treatment protocol for sick OKA:
Depressed, anorexic and dehydrated with severe fluid and electrolyte derangements and marked_ acidosis
./ Fluld therapy:
;
;
;
;
> Correction of perfusion deficits and hypokalaemla:
* Selection of IV fluids should be based on sodium balance see “Fluld Therapy” for trealment
of hyponatraemia which is commonly seen with severe DKA’s
li> Begin correction of dehydration deficits whilst factoring In maintenance re”qulrements and ongoing
losses: ·
Restore half of fluid deficits over the followlng 6 hours, then the rest over 24-36 hours
> Potassium:
* Levels will decrease as therapy continues, hypokalaem!a Is common complication
* Insulin therapy move potassium back Into cells
* Hyperglycaemia and acidosis will mask hypokalaemla as potassium shifts from Intracellular
space to extracellular space. This Is then tosl into the urine, leads to a whole body potassium
deletion.
» Phosphate:
* Hypophosphataemla ::1 serum P04 <0.5mmolA..
* Haemolytic anaemia, weakness, ataxia, seizures
* Supplement with potassium phosphate at 0.01-0.03mmoVkg/hr in Ca+ free fluids recheck In 6
hours or give half K+ supplemenlallon as KCL and half as KP04 (potassium phosphate)
Insulin therapy: Use regular crystalline Insulin (e.g. Actrap!d ®)
» Alm for gradual reduction of blood glucose levels:
* Do not decrease blood glucose levels by >3-4mmol/L/hr or >70mg/dt/hr and serum OS11Jolallty
more than 0.5 to 1osmot/hr as can cause osmotic cerebral oedema
) lntennlttent low-dose Intramuscular injection:
* Loading dose of regular Insulin at 0.2 U/kg IM, followed by 0.1 U/kg IM every hour untll blood
glucose Is <15mmoVL
* When blood glucose is <14mmoVL or <25Dmg.tdl start a 2.5% * 5% dextrose drip and give
regular Insulin 0, 1 to 0.4 units/kg IM every 4 * 6 hours or SC every 6 * 8 hours until the patient
Is stable enough to begin intennittent acting insulin
> Continuous low-dose Intravenous Infusion:
* More gradual,,eductlon of blood glucose
Regular insulin at 0.05 U/kg/hr (cat) to 0.1 U/kg/hr (dog) continuously in a separat8 IV line. Use
an Infusion pump to insure accuracy .· . . ,.
* OR add 25U to 500mls of 0.9% sailne and run at 1 mVkg/hr (cat) or 2mVkg/hr (dog), must run* ‘ .
through 50mls of solution to coat Infusion set to all6w correct administration ·
When blood glucose Is <14mmol/L or <250mg/dl change IV fluids to 0.9% NaCl+ 5% dextrci~e
(remove 100ml out of 1L of saline and add 100ml Of 50% glucose) and add K+ if required
Dextrose drl~e: · · ·
> Provision of carbohydrates to prevent hypoglycaemla
> Do not stop insulin therapy (unless hypoglycaemic), Increase and decrease concentration of·
dextrose Infusion to prevent hyperglycaemia and hypoglycaemla
Transition to Intermediate acting Insulin therapy:
> When blood glucose is 6-12mmolll.. or 110·21Dmg.tdl, anlmal Is drinking and eating,_ remaining
hydrated with mlnlma1 ketones (In urine and serum), begin treating as an uncomplfcated case
Bicarbonate therapy:
J.- Controversial
> lndlcattons: patient has pH < 7 .2 or total CO2 (HC03) Is < 12mmoVL
> Restore deflcits slowly (over 36 - 48 hours)
* Amount: mEq of HC03 = BWl(kg) x 0.3 x (base dellcit OR !he amount of HC03 you want to
correct), give 1/3 IV and the rest into IV fluids and give slowly over 12 hours OR
1mmol/kg or 1mVkg of 8.4% solutlon slowly over 20mins
Monitor Ionised calcium levels (may drop with correction of ac!dosfs)
> Adverse effects of acidosis: Vasodilalion, hypotension, CNS and respiratory depression,
arrhythmias
> Why therapy ls controversial: Both lluid and Insulin therapy will help to resolve acidosis. One mmol
of HC03 Is generated from each mmor of ketoacid metabolized
> Adverse effects of HC03: May worsen hypokalaemla, cause paradoxlcal cerebral acidosis (with
associated CNS dysfunctio~) and delay decrease In blood lactate and ketone levels
Monitoring:
./ Insulin therapy will usually resolve hyperglycaemia over 6 * 8 hours and ketosis over 1 O * 48 hours
(although ketone synthesis is immediately inhibited)
./ Kelouria may get worse before it gets better as 13-hydroxybutyrate is initially converted to acetoacetate
./ Evaluate blood glucose levels every hour and electrolyte/acid-base status every 4 * 6 hours. Adjust
therapy accordingly
Complications of therapy:
./ Hypoglycaemia:
> Treatment:
* Give SmVkg dextrose 5% IV or 0.5-1ml/kg dextrose 50% IV diluted with saline
* Continue with glucose supplementation in IV fluid as indicated above
./ Hypokalaemla:
> Due to JnsuUn and resolullon of acidosis driving potassium into cells
:,. Treatment:
* See “Fluld Therapy” and add 20mmoVL of potassium into IV fluids as a maintenance adjusl
accordingly
./ Hypophosphataemla:
, Due to insulin and resolution of acidosis driving phosphorus into cells
, Treatment:
See “Fluid Therapy”
./ Renal failure:
> Due to a combination of pre-renal and primary renal disease:
Pre-renal disease due to hypovo!emia and hypotenslon
, Monitor urine output by placing a urinary catheter:
Alm for >1 * 2 ml/kg/hr after correction of perfusion and hydration deficits and after obtaining
normotenslon
> Treatment:
* Correct underlying flufd delfclts, if normotens!ve but no urine output then treat as per acute
kidney injury. See “Renal Disease”
./ Cerebral oedema:
> Fast reductions In blood glucose can cause cerebral oedema …… brain makes sorbitol when the
serum is hyperglycaemic to maintain osmolality and retain water-+ when hyperglycaemia Is
resolved-+ water moves Into the brain cells due to the osmotic draw of the sorbitol - swertrng and
cerebral oedema
> Prevent by slow reduction in BG <3·4mmoVL/hr or <70mg/dl/hr and slow reduction serum
osmolality <0.5 to 1 osmol/hr:
Serum Osmolality?
Serum osmolallty (mOsm/kg) = 2 x (Na mmol/L) + (glucose (mg/di)/ 1 B) + (BUN {mg/di) / 2.8)
» Clln!cal signs:
Neurological signs, altered mentation, seizures
> Treatment:
* Mannitol 0.5· 1 gm/kg stow IV CID
Slow down rate of BG reduction
