DIABETISCHE KETOACIDOSE

Diabetische Keto-acidose (DKA) en Hyperosmolair Hyperglycemisch Non-Ketotisch syndroom (HNN) zijn complicaties die bij suikerziekte kunnen voorkomen, als er TE LANG GEEN of TE WEINIG INSULINE gegeven wordt. Alles bij elkaar over DKA en HNN.
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Jeanne
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DIABETISCHE KETOACIDOSE

Bericht door Jeanne »

Als de kat onvoldoende glucose als brandstof kan gebruiken, wordt de energie uit de verbranding van vetzuren in de lever gehaald. Bij deze omzetting komen ketonen, waaronder aceton vrij.
Ketonen onderdrukken de eetlust en kunnen de kat erg ziek maken.
Hopen zich erg veel ketonen op in het bloed, dan verandert de pH van het bloed en verzuurt het (acidose).
Als de toestand verergert, treedt er uitdroging, anorexie en braken op, gevolgd door stuipaanvallen en tenslotte de dood. De behandeling bestaat in het toedienen van vocht en elektrolyten naast snelwerkende insuline en een glucose-infuus.
Keto-acidose is een ernstige toestand die steeds door je dierenarts moet behandeld worden.

Afbeelding
Ketonen kan je in de urine opsporen door middel van sticks (Ketostix). Vind je sporen van ketonen, dan moet het dieet of de insulinetoediening (type, schema, dosering) of beide aangepast worden.
Ketostix zijn verkrijgbaar bij de apotheek, maar ook bij diverse online-medische leveranciers. Bij de Ketostix ben je afhankelijk of de kat wil plassen.


Afbeelding
Ook kan men via het bloed de ketonen meten met een glucosemeter die ook ketonen kan meten. Abott heeft hievoor de Precision Exceed ontwikkeld en is momenteel bij Abott gratis te bestellen http://www.abbottdiabetescare.nl/bestel ... ulier.html; echter hier moeten 2 soorten strips voor gebruikt worden 1 om de bloedsuikers te meten en 1 voor de bloedketonen. Deze laatste zijn wel duur maar wel nauwkeurig en handig omdat je eigenlijk op ieder moment kunt testen.

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Hieronder tref je zoveel mogelijk linken aan, in verschillende talen, over Diabetische Ketoacidosis en zo mogelijk ook (DKA) bij de kat.


* MSD Animal Health (vh Intervet/Schering Plough Animal Health nederlands
* World Small Animal Veterinary Association engelstalig met behandelplan
* Feline Diabetes engelstalig
* Pet Diabetes engelstalig
* FabCats engelstalig
* PubMed engelstalig
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Jeanne
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Re: DIABETISCHE KETOACIDOSE

Bericht door Jeanne »

Caninsulin®
Intervet -Schering-Plough Animal Health


9. Ketoacidose
Ketoacidose kent vergeleken met diabetes mellitus ernstiger verschijnselen: depressie, anorexie, braken, oligurie of anurie en hyperventilatie. Een kat met ketoacidose kan zelfs comateus worden aangeboden. Tevens kan aceton worden waargenomen in de uitademingslucht van de patiënt. De waarschijnlijkheidsdiagnose ketoacidose op basis van het klinisch beeld moet voor een definitieve diagnose worden bevestigd door aanvullend onderzoek. Hiertoe moeten hyperglycemie, acidose en ketonurie worden aangetoond.

Een kat met ketoacidose is een spoedeisende patiënt. Het is allereerst van belang dat de hydratietoestand en de verschuivingen in de pH en elektrolytenconcentraties van het bloed worden gecorrigeerd. Om dit te bereiken wordt intraveneus vloeistof toegediend. In verreweg de meeste gevallen (bloed pH > 7,10) is het niet nodig om de pH met bicarbonaatinfusen te normaliseren; door de correctie van de hydratietoestand zijn de longen en nieren over het algemeen zelf in staat de pH te normaliseren. Indien toch wordt gekozen voor correctie van de pH met bicarbonaatinfusen, dan moet voor overcorrectie worden opgepast. Overcorrectie gebeurt gemakkelijk omdat de pH-correctie door het herstel van de hydratietoestand moeilijk in te schatten is. Om de eventueel aanwezige hypokaliëmie te corrigeren, wordt berekend hoeveel kalium maximaal kan worden toegevoegd aan de infusievloeistoffen; hetzelfde geldt voor de correctie van een eventueel aanwezige hypofosfatemie. Hierbij moet worden opgepast dat het oplosbaarheidsproduct van calcium en fosfaat in het bloed niet wordt overschreden, aangezien dit kan resulteren in een hypocalcemie.

Terwijl de hydratietoestand en elektrolytenconcentraties in het bloed normaliseren, kan voorzichtig worden begonnen met het verlagen van de bloedglucoseconcentratie. Het geniet de voorkeur om hiervoor een kortwerkende insuline, zoals bijvoorbeeld Actrapid", intramusculair toe te dienen. Doel is te bereiken dat de bloedglucoseconcentratie met ongeveer 3 tot 4 mM per uur afneemt. Hierdoor kunnen de cellen, die zich hebben aangepast aan de hyperosmolaire situatie, zich weer geleidelijk aanpassen aan een isosmotische situatie. Als eenmaal de bloedglucoseconcentratie onder de 10 mM is gezakt en de elektrolytconcentraties in het bloed zijn genormaliseerd, kan geprobeerd worden de kat verder met Caninsulin® te reguleren. Het is verstandig met het begin van therapie met Caninsulin® te wachten tot minimaal 6 uur na de laatste injectie met Actrapid®, zodat de kortwerkende insuline is uitgewerkt.

Enerzijds door het herstel van de pH van het bloed en anderzijds doordat de door insuline geïnduceerde opname van glucose in cellen tevens gepaard gaat met opname van kalium en fosfaat, zullen de concentraties van deze elektrolyten in het bloed verder gaan dalen (zeker wanneer hiervoor niet wordt gecorrigeerd). Door hypofosfatemie kan een levensbedreigende hemolyse ontstaan. Daarentegen is het gebrek aan insuline bij adequate vloeistof therapie en correctie van verschuivingen van de elektrolytconcentraties in het bloed niet levensbedreigend. Als er sprake is van een ernstige hypokaliëmie of hypofosfatemie is het aan te raden eerst de concentraties van deze elektrolyten in het bloed te normaliseren, voordat wordt begonnen met de toediening van insuline.

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Intervet/Schering-Plough Animal Health
Postbus 50
5830 AB Boxmeer
Tel: 0485 587652
Fax: 0485 587653
http://www.intervet.nl" onclick="window.open(this.href);return false;

Caninsulin®. Samenstelling: 40 IE varkensinsuline per mI. Indicatie: diabetes mellitus bij hond en kat. Contra-indicaties: gebleken overgevoeligheid tegen eiwitten van porciene oorsprong. Bijwerkingen: in zeldzame gevallen kunnen systemische of lokale overgevoeligheidsreacties voorkomen.
Dosering en toedieningsweg: een- of tweemaal daags door s.c. injectie. Waarschuwingen: vermijd overdosering, controleer regelmatig
het bloedglucosegehalte. Registratie: REG Nl 08094 diergeneesmiddel UDA. Voor overige informatie zie bijsluiter.
Intervet/Schering-Plough Animal Health



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Jeanne
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Re: DIABETISCHE KETOACIDOSE

Bericht door Jeanne »

BRON: World Small Animal Veterinary Association http://www.vin.com/proceedings/Proceedi ... &O=Generic

Understanding Diabetic Ketoacidosis
Thomas Schermerhorn, VMD, DACVIM - Assistant Professor of Small Animal Medicine

Diabetic ketoacidosis (DKA) is a complication of unregulated diabetes mellitus (DM) that produces marked hyperglycemia, profound metabolic acidosis, and hyperketonemia in severely affected patients. DKA is often discussed as a condition that is separate from uncomplicated diabetes mellitus but, in fact, diabetes mellitus is a spectrum of disorders that ranges from non-ketotic hyperosmolar diabetes mellitus on one end to diabetic ketoacidosis on the other end. It is important to remember that most complicated diabetics have another medical problem. Thus, management of DKA must be performed in the context of any concurrent disorder.

DKA can be precipitated by factors such as inadequate insulin therapy, physiologic stress, drugs that affect insulin production or action, bacterial infection, and decreased fluid intake. Concurrent illness is common in animals with DKA. In one study, about half of cats with DKA had azotemia on admission; azotemia was moderate to severe in 20% of those cats. Other concurrent disorders found in that same group of cats included: inflammatory bowel disease, asthma, pancreatitis, hyperthyroidism, urinary tract infection, neoplasm, and corticosteroid therapy. In dogs, concurrent disorders include: urinary tract infection, neoplasia, pneumonia, pyometra, prostatitis, renal failure, hyperadrenocorticism, heart failure, and drug therapy (corticosteroids or progestins), among others.

Patient Factors

* Signalment: There is no characteristic or specific signalment for animals with DM or those likely to develop complicated DM.
* Gender. Middle-aged and older female dogs have an increased risk for the development of diabetes mellitus when compared to males. In addition, 80% of dogs with DKA were female in one study of DKA. It is generally accepted that male cats develop DM more frequently than females, although this is not supported by all studies.
* Age. Although dogs of any age can develop DKA, most dogs diagnosed with DKA are older than 7 yrs. of age. Most cats with DKA are 6 years or older.
*Breed predisposition. DKA is more likely to be diagnosed in those dog breeds that have a high incidence of DM, such as miniature and toy poodles, miniature schnauzers, beagles, and Cairn Terriers. Among cats, an Australian study reported an increase in the frequency of DM in the Burmese breed. There is no data to suggest that any breed is more likely than another to develop ketoacidosis.
*Presenting Complaint: DKA is associated with non-specific signs. Severely affected animals may present in shock or comatose without any supporting history. Careful questioning of the owner may elicit a history of signs more typical of diabetes mellitus.
- Polydipsia and polyuria are the most frequently reported complaints in dogs and cats with DKA.
- Other common complaints include:
* Lethargy and weakness
* Anorexia
* Vomiting
* Weight loss
* Signs of abdominal pain
* Neurologic impairment ranging from depressed mentation to coma.
* Other historical considerations/predisposition. Precipitating factors, such as the recent administration of glucocorticoid drugs or the presence of concurrent illness, are identified in over 70% of cases. Identification and correction of contributing factors is essential for a favorable clinical outcome.

Physical Examination Findings
* Dehydration (mild to severe).
* Abnormal body temperature (hyper- or hypothermia).
* Abdominal pain.
* Jaundice.
* Tachycardia diminished femoral pulses, prolonged capillary refill time, and cool extremities due to cardiovascular collapse and shock occur in severely hypovolemic patients.
* Neurological abnormalities range from mild (depressed mentation, quiet demeanor) to severe (stupor, coma).
* Other common findings are those also detected in animals with uncomplicated DM and include weight loss, muscle wasting, hepatomegaly, cataracts (dogs), and dermatological abnormalities.
* Abnormal physical exam findings caused by concurrent illness may also be detected.
* Acetone odor: The "fruity" odor of acetone is detected on the breath of some animals with DKA.

Laboratory Findings

* Hyperglycemia (100% of patients): hyperglycemia may be severe (>500 mg/dl).
* Glucosuria (100% of patients): occurs when the blood glucose exceeds renal threshold for glucose (about 200 mg/dl in dogs and 220 mg/dl in cats).
* Ketonemia and ketonuria--are detected in essentially 100% of patients. Rarely, ketones are undetectable due to a laboratory error.
* Metabolic acidosis: Although the severity of acidosis varies, a decrease in blood pH and in bicarbonate concentration occurs in all patients with DKA due to ketoacid production.
* Increased anion gap: The anion gap increases in parallel to the production of ketoacid anions. The normal range for the anion gap is 12-24 mEq/L.
* Hyperosmolarity: The markedly elevated serum glucose increases the effective serum osmolarity (normal range (280-295 mOsm/L) in dogs and cats with DKA. Most animals with DKA also have an increase in total serum osmolarity.
* Azotemia: Pre-renal azotemia from dehydration is found in most animals with DKA. Patients with concurrent renal insufficiency may be severely azotemic from pre-renal and renal causes.
* Electrolyte abnormalities: Hyponatremia, hypochloremia, and hypokalemia are common in patients with DKA. Hypophosphatemia and hypomagnesemia may also be present, but usually develop after insulin therapy.
* Hyperlipidemia: Dogs and cats with DKA may have elevations in serum lipid and triglyceride concentrations.
* Pyuria, hematuria, proteinuria and bacteriuria are found when a urinary infection precipitates DKA.
* Mild anemia is common in dogs and cats with DKA.
* Leukocytosis (± a left shift) occurs when infection is present.

Treatment
The emergency management of DKA requires that life-threatening problems be identified and treated quickly. Typical problems associated with DKA are dehydration, hyperglycemia, electrolyte abnormalities, acid/base imbalance, and hyperosmolarity. These will be addressed in turn below.

DEHYDRATION
Dehydration results from:
1. Osmotic diuresis: sodium and glucose act as an osmolytes in urine.
2. Protracted vomiting and diarrhea.
3. Decreased fluid intake due to weakness, lethargy, and anorexia.

Treatment
Intravenous crystalloid fluids are preferred
The fluid of choice is physiologic saline (0.9% sodium chloride) solution. The initial rate of fluid administration depends on the patient's hydration status.
* Hypovolemic shock: The shock dose of fluid (90 ml/kg/hr for dogs; 50 ml/kg/hr for cats) is used for volume resuscitation of animals with hypovolemic shock. A recommended approach is to infuse a portion (e.g., 25-50%) of the total estimated shock volume as a bolus and re-evaluate the patient's need for additional fluid. Rapid administration of large fluid volumes is contraindicated when DKA precipitated by cardiac failure.
* Moderate to severe dehydration: Saline fluid should be administered at an hourly rate that provides maintenance fluid requirements (2-4 ml/kg/hr), replaces contemporary fluid losses, and will replace the estimated fluid deficit over 6-12 hrs.
Rehydration improves:
* Electrolyte disturbances: Rehydration with isotonic saline and potassium supplementation helps to replenish body stores of sodium and potassium. Without sufficient potassium supplementation, isotonic saline may lower serum potassium concentrations via a dilution effect. Serum magnesium and phosphate, other electrolytes of concern in diabetics, may also be decreases when isotonic saline is administered.
* Acid/base status: Most animals with complicated DM (especially those with DKA) have metabolic acidosis. Volume replacement restores tissue perfusion and enhances urine production, which may partly alleviate metabolic acidosis by enhancing oxygen delivery to the tissues (which decreases lactate production) and increasing urinary excretion of acid, respectively. Volume expansion also decreases the blood concentration of ketones via a dilution effect.
* Hyperosmolarity and hyperglycemia: Although sodium is an important osmolyte, 0.9% saline is hypotonic when administered to hyperosmolar diabetics. Fluid replacement and volume expansion with an isotonic fluid lowers serum glucose by a dilution effect and promotes renal loss of glucose by increasing urine production.

HYPERGLYCEMIA
* Insulin Therapy (Always use Regular Insulin): All complicated diabetics require insulin to lower blood glucose. Only regular insulin is appropriate for emergency management of DKA.
* Regular crystalline insulin[/u] is preferred for the initial treatment of DKA and is continued until the patient is stable and ketosis has resolved.
* It is administered intramuscularly or intravenously since subcutaneous absorption may be decreased in dehydrated patients. Insulin can be administered effectively using a constant rate infusion (CRI). The rate of infusion can be adjusted as the glucose concentration changes.
* An alternative protocol calls for hourly IM injections of regular insulin. Insulin is given IM at an initial dose of 0.2 to 0.25 U/kg and followed by 0.1 U/kg IM hourly.
* Therapy should be tailored to reach a target for blood glucose of 250-300 mg/dL in 12 hrs.
* The administration of insulin can be delayed until vascular volume is restored in some cases.
* Insulin enhances fluid and electrolyte movement into cells, which could precipitate vascular collapse.
* Volume expansion will lower serum glucose concentrations by a dilution effect and urinary excretion
* Increased urine production will enhance renal glucose loss and lower BG.

The goals of insulin treatment are to lower blood glucose and to halt ketone production. Insulin administration should continue until ketosis has resolved, even if this means that glucose supplementation must be given to maintain euglycemia.

Constant Rate Infusion (CRI) of regular insulin
1. Add a total dose of 2.2 U/kg of regular insulin to 250 ml of 0.9% NaCl fluid.
2. "Run out" and discard 50 ml of the insulin solution. This procedure allows insulin, which binds to plastic, to saturate the infusion tubing.
3. The insulin solution is infused at an initial rate of 10 ml/hr. (An infusion pump is recommended.)
4. The infusion should be continued until ketosis has resolved.
5. When the blood glucose falls to 250-300 mg/dl, the insulin infusion rate is decreased by 25-50% and a glucose-containing fluid (2.5-5% dextrose) is infused to prevent hypoglycemia. If the blood glucose is < 100 mg/dl, the insulin infusion is temporarily stopped.

Hourly IM administration of regular insulin
1. The initial dose is 0.2 to 0.25 U/kg IM.
2. Follow-up doses of 0.1 to 0.2 U/kg IM are given hourly.
3. Regular insulin administration is continued until the patient's ketosis is resolved.
4. When the blood glucose falls to 250-300 mg/dl the hourly dose is decreased by 25-50% and a glucose-containing fluid (2.5-5% dextrose) is infused to prevent hypoglycemia. If the blood glucose is < 100 mg/dl, the insulin administration is temporarily stopped.

Regardless of the protocol chosen, blood glucose measurements are performed q 1-2 hours in the initial stages of treatment. Glucose should remain around 250 mg/dL while the patient is being stabilized.

Intermediate- and long-acting insulin preparations
1. The administration of depot insulin preparations (e.g., NPH) is delayed until the patient is stable and eating, and ketone production is stopped.

Rationale for glucose supplementation
* Insulin treatment lowers blood glucose sooner than it reverses ketosis.
* An intravenous infusion of 2.5% or 5% glucose is used to prevent hypoglycemia (maintain blood glucose >250 mg/dl).
* The insulin dose is decreased by 25-50% as the glucose concentration falls.
* If hypoglycemia occurs, insulin is discontinued only long enough to allow the blood glucose to rise above 150-200 mg/dL.


ELECTROLYTE DISTURBANCES

Potassium
* The most common electrolyte disturbance associated with DKA is hypokalemia, which may be detected at the time of presentation or may develop during treatment. Body stores of potassium are depleted even if the blood concentration of potassium is normal. Insulin treatment can precipitate or worsen hypokalemia by driving potassium into cells. Fluid treatment can exacerbate hypokalemia via a dilution effect on serum potassium. Potassium supplementation should not exceed 0.5 mEq/kg/hr IV and is contraindicated in animals with hyperkalemia or acute renal failure.
* The amount of KCl added to fluids is adjusted relative to the serum potassium concentration.
* If serum [K+] is:
> 3.5--add 20 mEq KCl per liter
3.0-3.5--add 30 mEq KCl per liter
2.5-3.0--add 40 mEq KCl per liter
2.0-2.5--add 60 mEq KCl per liter
< 2.0--add 80 mEq KCl per liter

Sodium
Sodium deficits are addressed by the use of 0.9% NaCl for fluid and volume resuscitation. Generally, no additional sodium supplementation is required. Very severe hyponatremia (less than 120 mEq/L) may require hypertonic saline-containing fluids, but these will not be discussed here.

Phosphorous
* Routine phosphorous supplementation to prevent hypophosphatemia is controversial.
* Supplementation and is indicated when phosphorous is < 2.0 mg/dL. (normal range 2.7-6.8 mg/dL).
* Severe hypophosphatemia (1.0 mg/dL) may lead to hemolysis and neuromuscular signs.
* Phosphorous is given at a dose of 0.01-0.03 mmol/kg/hr IV for 6 hours.
* Phosphorous is commercially supplied as potassium phosphate (...K2PO4), which contains 3.0 mmol phosphate and 4.4 mEq potassium. per ml of solution.
* Serum phosphorous concentrations should be maintained > 2.0 mg/dL; Oversupplementation should be avoided. Phosphate supplementation can produce hypocalcemia in some circumstances.
* Phosphorous supplementation should not be attempted if serum concentrations cannot be monitored during treatment. Aggressive phosphate supplementation is contraindicated in patients with renal failure.
* Phosphate solutions are incompatible with many intravenous fluid solutions and drugs, but are reported to be compatible with 0.9% saline solution.

Magnesium
* Severe hypomagnesemia (total magnesium <1.2 mg/dL) is an indication for magnesium supplementation.
* Dose: 0.75-1.0 mEq Mg2+ /kg/day in D5W, given as an IV infusion.
* Magnesium chloride (9.25 mEq Mg2+/gm) and magnesium sulfate (8.13 mEq Mg2+/gm) are available commercially as 50% solutions. These solutions are diluted (maximum concentration 20%) in D5W for IV administration.
* Magnesium solutions are incompatible with many intravenous fluid solutions and drugs.

ACID/BASE IMBALANCE
The acid/base abnormality most frequently associated with DKA is marked metabolic acidosis, which develops by several mechanisms and usually causes an elevation in the anion gap. The most important cause is the generation of acidic ketones (beta hydroxybutyrate and acetoacetic acid). Ketones are the product of unregulated lipolysis occurring in adipose tissue. The non-esterified fatty acids that are released can be used as a fuel substitute by most tissues, including the liver. Without insulin (and with increased glucagon), FFA conversion to triglycerides in the liver is markedly impaired and the FFA are instead converted to fatty acyl-CoAs (acyl-CoA derivatives of the FFA), which are oxidized to acetyl-CoA and then converted to ketone bodies, rather than oxidized to CO2. Essentially the FFA metabolism of the liver is reset, both by the relative lack of insulin and the relative increase of glucagon and other counter-regulatory hormones, to favor ketone production over FA oxidation. Other mechanisms for acidosis is include lactic acid overproduction, impaired tissue perfusion from dehydration and shock, and reduced renal excretion of H+. Mixed disturbances are possible if neurologic compromise leads to depressed respiration (respiratory acidosis) or loss of gastric contents potentiates metabolic alkalosis.

Specific therapy for metabolic acidosis is rarely indicated in complicated DM unless the blood pH is < 7.1. Studies in human subjects with complicated DM have not demonstrated a beneficial effect of bicarbonate treatment on clinical outcome. Other studies have demonstrated that there is not a correlation between the blood pH and neurologic status or mortality in people with DKA. If therapy is warranted, bicarbonate therapy (as sodium bicarbonate) is the therapy of choice. In most patients treated with fluids and insulin, acidosis will usually improve without the need for bicarbonate. Fluid replacement increases blood volume, improves tissue perfusion and oxygenation, and restores oxidative metabolism and insulin therapy inhibits ketogenesis and promotes the replenishment of endogenous bicarbonate. Bicarbonate use is associated with potential detrimental effects. It can worsen

Hypokalemia and hypophosphatemia, contribute to the development of cerebral edema, promote tissue hypoxia (due to increased hemoglobin affinity for oxygen), precipitate hypernatremia and fluid overload, and produce paradoxical CSF acidosis.

Bicarbonate replacement
* Bicarbonate therapy is rarely needed to correct acidosis in DKA.
* Used only for life-threatening acidosis (pH < 7.0) and when blood pH can be monitored.
* Low Dose: 0.1 x base deficit x weight (kg) = amount (ml). Give IV slowly over 2 hours.
* Anion gap (AG) is the mathematical difference between the measured cations (sodium and potassium) and the measured anions (chloride and bicarbonate) and represents unmeasured anions (e.g., sulfates, phosphates, and serum proteins). The normal anion gap in is 12-24 mEq/L. The AG increases in DKA because the concentration of unmeasured anions in the blood is increased by the anions of ketoacids and also because the concentration of bicarbonate (a measured anion) is decreased by acidosis.

DKA AND HYPEROSMOLALITY
Plasma hyperosmolarity represents a free water deficit. Under normal physiologic conditions, sodium is the main determinant of serum osmolarity. In DM, glucose contributes substantially to hyperosmolarity, while sodium concentrations are usually normal or even decreased. Hyperosmolarity quickly approaches lethal levels (>400 mOsm/L) when marked hyperglycemia and hypernatremia are present.

A distinction must be drawn between measured and effective osmolarity. Measured osmolarity is of greater magnitude than effective osmolarity because it includes osmolytes (e.g., urea) that freely permeate all body compartments but do not influence fluid shifts. Effective osmolarity measures only osmolytes that draw fluid from one compartment, these include sodium, potassium, and glucose. Serum effective osmolarity is closely correlated with mental status and the degree of obtundation in human diabetics; coma ensues when the effective osmolarity exceeds 340 mOsm/L. Most dogs and cats with DKA have an increase in total serum osmolarity and an increase in the anion gap. Thus, the calculated serum osmolarity can differ greatly from the measured osmolarity in patients with DKA. The effective osmolarity is not readily measured but is estimated from the glucose and electrolyte concentrations.

Estimating osmolarity
*Total Osmolality: 2(Na + K) + (GLUCOSE/18) + BUN/2.8 = osmolarity (mOsm/L).
* Effective osmolarity: 2(Na) + GLUCOSE/20 = effective osmolarity (mOsm/L).

TREATMENT CONTRAINDICATIONS
* Steroidal drugs: Glucocorticoids and progestins are contraindicated in dogs and cats with DKA, unless there is a compelling reason for their use.
* Oral hypoglycemic drugs: Oral hypoglycemic drugs (for example, the sulfonylurea class of drugs) have no role in the treatment of DKA.
* Depot insulin preparations: Regular insulin is the preferred insulin for its better short-term control of glucose and its short duration of action. Insulin preparations with slow release and prolonged action (e.g., NPH or lente insulins) have no role in emergency treatment of DKA.

Thomas Schermerhorn, VMD, DACVIM (SAIM)
The Netherlands


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Jeanne
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Berichten: 19669
Lid geworden op: 18 sep 2005, 12:33
Locatie: Almelo - Mickey is over de Regenboogbrug maar kreeg ruim 8 jaar Caninsulin.
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Re: DIABETISCHE KETOACIDOSE

Bericht door Jeanne »

Bron: Feline Diabetes http://www.felinediabetes.com/ketones.htm

Ketones, Ketoacidosis and Diabetic Cats

Also see
Pet Diabetes Wiki: Ketoacidosis
A Ketone Primer by an FDMB user


What are Ketones?
Ketones or ketone bodies (acetone, acetoacetic acid, and beta-hydroxybutyric acid) are waste products of fatty acid breakdown in the body. This is the result of burning fat, rather than glucose, to fuel the body.

The body tries to dispose of excess ketones as quickly as possible when they are present in the blood. The kidneys filter out ketones and excrete them into the urine.

Should you care about ketones?
YES! If they build up, they can lead to very serious energy problems in the body, resulting in diabetic ketoacidosis, a true medical emergency. If the condition is not reversed and other systemic stresses are present, ketones may continue to rise and a condition known as diabetic ketoacidosis (DKA) may occur. This condition can progress very quickly and cause severe illness. It is potentially fatal even when treated. Recognition of DKA and rapid treatment by your veterinarian can save your cat's life.

Signs of Diabetic Ketoacidosis (DKA)
Drinking excessive amounts of water OR no water
Excessive urination
Diminished activity
Not eating for over 12 hours
Vomiting
Lethargy and depression
Weakness
Breathing very fast
Dehydration
Ketone odor on breath (smells like nail-polish remover or fruit)

Causes of Diabetic Ketoacidosis (DKA)
Insulin dependent diabetes mellitus
Inadequate insulin dosing or production
Infection
Concurrent diseas that stresses the animal
Estrus
Medication noncompliance
Lethargy and depression
Stress
Surgery
Idiopathic (unknown causes)

Risk Factors for DKA
Any condition that causes an insulin deficiency
History of corticosteroid or beta-blocker administration

Diagnosis
Laboratory tests performed by your vet are necessary for diagnosis. Depending on how sick your cat is, the testing can be extensive (and expensive). Your veterinarian will determine what tests are necessary. At a minimum, testing is likely to include a number of blood tests and a urine test.

Treatment
If the cat is bright, alert, and well-hydrated, the cat will not require intensive care. Your cat will require insulin, food, constant access to water, and close monitoring for signs of illness such as vomiting, anorexia, and lethargy.

Treatment of cats who show signs illness require inpatient intensive care. The goal of treatment is to correct dehydration, electrolyte depletion, to reverse the high ketones in the blood and the metabolic acidosis that is present, and to increase the rate of glucose use by insulin-dependent tissues.

Veterinary care for DKA involves intravenous (IV) fluids, usually supplemented with potassium, monitoring by observation and urine and blood tests, and sometimes feeding by a tube. Treatment may involve a hospital stay of five days or more and often costs about US$2000. Without treatment, "sick" animals with DKA will die.

Testing for Ketones
Simple urine tests can detect ketones. This is done by collecting a urine sample and inserting a special dip stick into the urine. Some urine ketone strips detect only ketones while other types test for both glucose and ketone levels. Urine ketone strips will detect only some of the ketone bodies produced by the body, not all of them. Strip storage, handling, and testing procedures are similar to those used for glucose test strips. Strip test results are indicated by presence of color changes, indicating presence of ketones, either quantitatively (giving you a number for the ketone concentration) or by descriptive terms (for example, negative, trace, small, or large). False positives may occur if you are also using certain medications or vitamins, or if the strips have been handled or stored improperly. If you wish to test blood instead of urine for ketones, there is a meter that allows for home testing, the Abbott Precision Xtra meter. Outside of the US, the meter is known by the brand name Precision/Optimum/Xceed. The premise behind blood testing for ketones is the same as that for favoring glucose testing of blood over urine. The Precision Xtra meter is offered by Hock's online pharmacy for US$29.95 in October 2006. The ketone test strips are about US$30 for a box of 50. The Precision Xtra also does blood glucose testing with standard blood glucose test strips made for use with the meter.

When to call the vet
In a diabetic, any urinary ketones above trace or trace urinary ketones plus some of the signs listed above, are cause to call a veterinarian immediately. If your vet doesn't offer after-hour emergency care, be sure to have the number and location of a 24 hour emergency veterinarian.


Last updated 10/10/06

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Jeanne
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Re: DIABETISCHE KETOACIDOSE

Bericht door Jeanne »

Bron: Pet Diabetes Wikia http://petdiabetes.wikia.com/wiki/Ketoacidosis

Ketoacidosis

Ketones in the urine, as detected by urine testing stix or a blood ketone testing meter[1], may indicate the beginning of diabetic ketoacidosis (DKA), a dangerous and often quickly fatal condition caused by low insulin levels combined with certain other systemic stresses. DKA can be fixed if caught quickly.

* 1 Emergency Info
* 2 False Testing Results-Urine Ketones
* 3 When to come to the vet
* 4 How it happens
* 5 How likely is it?
* 6 Testing for ketones
* 7 Further Reading
* 8 References

Emergency Info

Diabetics of all species therefore need to be checked for ketones with urine testing stix, available at any pharmacy, whenever insulin level may be too low, and any of the following signs or triggers are present:

Ketone Monitoring Needed:
* Little or no insulin in last 12 hours
* High blood sugar over 16 mmol/L or 300 mg/dL (though with low insulin, lower as well...)
* Dehydration (skin doesn't jump back after pulling a bit gums are tacky or dry)
* Not eating for over 12 hours due to Inappetance or Fasting
* Vomiting
* Lethargy
* Infection or illness
* High stress levels
* Breath smells like acetone (nail-polish remover) or fruit.

Note that the triggers and signs are somewhat interchangeable because ketoacidosis is, once begun, a set of vicious circles which will make itself worse. So dehydration, hyperglycemia, fasting, and presence of ketones are not only signs, they're also sometimes triggers.

In a diabetic, any urinary ketones above trace, or any increase in urinary ketone level, or trace urinary ketones plus some of the symptoms above, are cause to call an emergency vet immediately, at any hour of the day.
Ketodiastix--measures urine glucose and ketones.
Ketostix--measures urine ketones.

False Testing Results-Urine Ketones
Possible False Urine Ketone Test Results Drugs and Supplements
* Valproic Acid (brand names) Depakene, Depakote, Divalproex Sodium - Positive. Common use: Treatment of epilepsy.
* Cefixime/Suprax - Positive with nitroprusside-based urine testing. Common use: Antibiotic.
* Levadopa Metabolites - Positive with high concentrations.
* Tricyclic Ring Compounds - Positive. Common use: Treatment of depression.
* Captopril other drugs with free sulfhydryl groups - Positive. Captopril Common use: Hypertension (high blood pressure), various heart conditions, preserving kidney function in diabetic nephropathy.
* Phenazopyridine Pyridium, Geridium, Pyridiate, or Urogesic. Positive. Common use: Urinary tract infections.
* Glucocorticoids/Steroids - Positive. Common use: Allergies, replacement therapy, others.
Vitamin C Supplements - Negative.

Possible False Urine Ketone Test Results-Other Reasons
* Pigmented Urine - Positive-Any other color except yellow or clear. May be the result of other disease processes.
* Dehydration - Positive-lack of fluids can concentrate ketones
* Old Urine Sample - Negative-ketones can evaporate rapidly.

When to come to the vet?
Trace urinary ketones may or may not be an emergency, depending on the case. If a vet is unavailable, look for some of the other signs or triggers, and try to remedy any you can. Give extra water and food, by syringe if necessary. If it's nearly time for an insulin shot, give one. Continue testing and call a vet when possible.

DKA cannot be treated at home. Veterinary care for DKA involves intravenous (IV) fluids to flush the animal's system of the ketones and when necessary, to replace depleted electrolytes, such as bicarbonate; intravenous or intramuscular fast-acting insulin to bring the blood glucose levels down; measured amounts of glucose or force feeding, sometimes by feeding tube, to force the metabolism back from fat-burning to glucose-burning.

Dehydration becomes involved with ketoacidosis, which can mean that subcutaneous insulin injections are not properly absorbed; when this occurs, intravenous treatment with soluble, short-acting insulin is needed, along with rehydrating intravenous fluids.

Veterinary care for DKA may involve a hospital stay of five days or more and cost, in the U.S., $2,000 or more. Some animals are DKA prone, and may have multiple episodes of the condition.

Veterinarians have sometimes been known to send pets home from a DKA episode while still displaying ketones in the urine due to owner financial constraints -- this can turn into a fatal mistake. Your chances of fixing the problem yourself are slim. If your cat or dog comes back from the hospital and still has ketones showing on urine testing stix, it's usually best to find the financial means to go right back to the vet's as your pet may need to stay in hospital longer.

How it happens?
When there's not enough insulin to allow conversion of glucose to energy, the body begins to break down fat cells, which produce fatty acids. These fatty acids are converted to ketones which can fuel the brain in emergencies.
Our bodies normally are "fueled" by burning glucose; they are able to do this provided they have enough insulin (normally or by injection). When there's not enough insulin to allow the body to burn glucose for energy, it begins metabolizing fat to fuel its cells. In particular, the brain cannot go without energy even for a second, so it demands fat conversion to ketones when glucose energy is unavailable. Continuing this process using fat and ketones instead of glucose without sufficient insulin intervention is the path to ketoacidosis.

Adapted from the Wikipedia:
Energy Production-Untreated/Inadequately Treated Diabetes-without enough insulin to regulate fat & carbohydrate metabolism, the process intensifies. The liver, despite high blood glucose levels, produces still more in gluconeogenesis. It also speeds up the transformation of fatty acids resulting in ketones.
Normally, ketone bodies are produced in minuscule quantities, feeding only part of the energy needs of the heart and brain. When insulin is inadequate, fat must be turned into ketones for energy instead, and they rapidly become a major component of the brain's fuel. As a result, the bloodstream is filled with an increasing amount of glucose that it cannot use (as the body continues adding glucose to the blood with gluconeogenesis and perhaps also glycogenolysis). This extra glucose significantly increases its osmolality.

At the same time, massive amounts of ketone bodies are produced, which in addition to increasing the osmolal load of the blood, are acidic. As a result, the pH of the blood begins to change. The trace element balance of the system is altered by falling bicarbonate blood levels and rising serum potassium levels. The potassium level of the body as a whole is reduced by the polyuria of ketoacidosis. There can be changes in breathing (deep, sighing breaths) because the ketones themselves are acids. Any type of acidosis can affect the respiratory system.

Glucose begins to spill into the urine as the proteins responsible for reclaiming it from urine reach maximum capacity. As it does so, it takes a great deal of body water with it, resulting in dehydration. Dehydration worsens the increased osmolality of the blood, and forces water out of cells and into the bloodstream in order to keep vital organs perfused. The vicious cycle is now set, and if untreated will lead to coma and death.

How likely is it?
Since diabetic dogs are considered insulin-dependent--unable to naturally provide any of their own insulin needs once diagnosed with diabetes--they are prone to ketoacidosis. About 40% of newly-diagnosed canine diabetics have some amount of ketones when they are brought to the vet.

Undiagnosed diabetic cats are also likely to be ketoacidotic by the time they're brought to a vet, but not all cats are prone to ketoacidosis. It is suggested that cats who are prone to ketoacidosis may benefit from a slightly lowered protein diet, but note that this is lowered from an ideal mouse diet, not from an average domestic cat-food diet! Note also that some ketone-prone cats are ketone-prone due to pancreatitis, which requires just the opposite, a lowered-fat diet. Best to stick with an ideal cat diet unless you know for certain otherwise.

Ketones occur quickly in younger animals.

Testing for ketones
The usual method of testing for ketones is with urine testing stix, available at any pharmacy. When testing urine for ketones, the sample needs to be as fresh as possible. Ketones evaporate quickly, so there's a chance of getting a false negative test result if you're testing older urine.

At low levels, ketones can be detected in the urine (ketonuria) before they are found in the blood (ketonemia/ketonaemia).

At present there is only one device for consumers who wish to test blood instead of urine for ketones--Abbott's Precision Xtra glucometer. The meter is known by the brand name Precision/Optimum/Xceed outside of the US.

The premise behind blood testing for ketones is the same as that for favoring glucose testing of blood over urine. The urine ketone measurement, like urine glucose measurement, can be hours old; testing blood for both gives current values as of testing time.

Children with Diabetes advises every family with a child with diabetes should have this type of meter because of its blood ketone testing ability. The ketone test strips are about $30 for 10 individually-wrapped strips. The Precision Xtra also does blood glucose testing with standard blood glucose test strips made for use with the meter.


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Jeanne
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Re: DIABETISCHE KETOACIDOSE

Bericht door Jeanne »

Bron: FabCats http://www.fabcats.org/owners/diabetes/info.html

Ketoacidosis
Ketoacidosis is an uncommon complication of poorly controlled diabetes. It can be rapidly fatal if not treated so requires immediate action where suspected. The clinical signs most frequently seen with ketoacidosis are:

• Loss of appetite
• Lethargy/weakness
• Vomiting/diarrhoea
• Dehydration/collapse

The breath may have a fruity odour (pear drops). Owners of diabetic cats should be provided with urine glucose and ketone sticks by their veterinary surgeon to allow periodic monitoring of the urine. This should be done as part of the normal routine (once or twice a week initially) or if there is any suspicion of ketoacidosis, for example if any of the above clinical signs are seen in a previously well diabetic cat. Ketoacidosis can also be confirmed by demonstrating the presence of ketones in the saliva, tears or blood using reagent strips.

If a positive ketone result is seen, immediate veterinary advice should be sought. This rule applies even if the cat seems quite well in itself. Ketotic cats require immediate intensive treatment with insulin given intravenously or intramuscularly for a rapid effect to regain control of the diabetes. In addition to this other treatments including intravenous fluid therapy, antibiotics and bicarbonate may be required. Treatment for ketoacidosis usually requires hospitalisation.

Additional causes for concern
Large variations in any of the things being monitored (food and water intake, demeanour, urinalysis results, etc) are generally a cause for concern and should be investigated. These may indicate poor control of the diabetes (eg, inadequate dose of insulin), mild ketoacidosis or presence of other diseases which complicate the control of the diabetes. If any of these are seen, a veterinary surgeon should be consulted for advice.

Updated November 2008

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Re: DIABETISCHE KETOACIDOSE

Bericht door Jeanne »

Bron: PubMed

J Small Anim Pract. 2009 Jan;50(1):4-8. doi: 10.1111/j.1748-5827.2008.00657.x. Epub 2008 Nov 13.
Ketone measurements using dipstick methodology in cats with diabetes mellitus.
Zeugswetter F, Pagitz M.
Source
Clinical Department of Small Animals and Horses, University of Veterinary Medicine, Veterinärplatz 1, A-1210 Vienna.
Abstract
OBJECTIVES:
To compare the results of urine and plasma ketone dip test in a group of diabetic cats with possible ketosis or ketoacidosis, using laboratory plasma beta-hydroxybutyrate measurements as the gold standard.
METHODS:
According to clinical examinations, plasma beta-hydroxybutyrate measurements and venous blood gas analysis, 54 cats with diabetes mellitus were classified as non-ketotic (n=3), ketotic (n=40) or ketoacidotic (n=11). Plasma and urine acetoacetate concentrations were determined using urine reagent strips.
RESULTS:
Although there was a significant positive correlation between blood and urine ketone measurements (r=0.695, P<0.001), the results differed significantly (Z=-3.494, P<0.001). Using the differential positive rates, the best cut-off value to detect cats with ketoacidosis was 1.5 mmol/l for urine and 4 mmol/l for plasma. The sensitivity/specificity was 82/95 per cent for urine and 100/88 per cent for plasma, respectively.
CLINICAL SIGNIFICANCE:
The urine and plasma ketone dip tests have a different diagnostic accuracy, and results have to be interpreted differently. Because of its high sensitivity, the plasma ketone dip test performs better than the urine ketone dip test to identify cats with impending or established ketoacidosis.
PMID: 19037889 [PubMed - indexed for MEDLINE]


Google vertaling:
. J Kleine Anim Pract 2009 Jan; 50 (1) :4-8. doi: 10.1111/j.1748-5827.2008.00657.x. Epub 2008 13 november
Keton metingen met peilstok methodiek bij katten met diabetes mellitus.
Zeugswetter F , Pagitz M .
Bron
Klinische Afdeling Kleine Dieren en Paarden, Universiteit van Diergeneeskunde, Veterinärplatz 1, A-1210 Wenen.
Abstract
DOELSTELLINGEN:
Om de resultaten van urine en plasma keton dip test bij een groep van diabetische katten met mogelijk ketose of ketoacidose, met behulp van laboratorium plasma beta-hydroxyboterzuur metingen als de gouden standaard te vergelijken.
METHODEN:
Volgens klinische onderzoeken, plasma beta-hydroxybutyraat metingen en veneuze bloedgasanalyse werden 54 katten met diabetes mellitus geclassificeerd als niet-ketotische (n = 3), ketotic (n = 40) of ketoacidotic (n = 11). Plasma en urine acetoacetaat concentraties werden bepaald met behulp van urine reagens strips.
RESULTATEN:
Hoewel er een significante positieve correlatie tussen bloed en urine keton metingen (r = 0,695, p <0,001), de resultaten significant verschilden (Z = -3,494, P <0.001). Met behulp van de differentiële positieve tarieven, de beste afkappunt voor katten detecteren met ketoacidose was 1,5 mmol / l voor urine en 4 mmol / l voor plasma. De sensitiviteit / specificiteit was 82/95 procent voor urine en 100/88 procent voor plasma, respectievelijk.
KLINISCHE BETEKENIS:
De urine en plasma ketonen dip testen hebben een andere diagnostische nauwkeurigheid, en de resultaten moeten anders worden geïnterpreteerd. Door zijn hoge gevoeligheid, de plasma keton dip-test beter presteert dan de urine keton dip test om katten te identificeren met dreigende of bestaande ketoacidose.
PMID: 19037889 [PubMed - indexed for MEDLINE]


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