U4 O2 - Endocrine emergencies Flashcards
What is Isosthenuria?
Production of urine that has the same specific gravity
as the plasma filtrate which passes through the
kidneys i.e. the kidneys are not concentrating or
diluting urine (1.008-1.015).
What is Hyposthenuria?
The production of urine of lower specific gravity than
plasma. Indicates decreased ability to concentrate
urine but normal ability to dilute urine i.e. some
kidney function is present (< 1.008).
What is ketoacidosis?
An uncontrolled break down of fat to produce large
numbers of ketones often leading to a metabolic
acidosis.
What is Paraneoplastic syndrome?
Alterations in physiology due to the production of
biologically active substances by neoplastic (tumour)
cells (tumour).
What is Calciuresis ?
Calcium excretion in urine
What is Pontine myelinolysis ?
Severe damage of the myelin sheath of nerve cells;
in the area of the brainstem known as the pons. This
is a rare condition that has been associated with
rapid correction of hyponatraemia in some patients
What is the most serious presentation of hypoadrenocorticism and why?
The most serious presentation of hypoadrenocorticism is ‘the Addisonian crisis’- this is the life-threatening result of insufficient glucocorticoids and mineralocorticoids. If not promptly recognised and treated the Addisonian crisis can be fatal.
What is primary hypoadrenocorticism usually caused by?
Primary hypoadrenocorticism is usually caused by generally associated with immune-mediated destruction of the adrenal cortex leading to, usually, both mineralocorticoid and corticosteroid deficiency. In some rare cases there may be only mineralocorticoid or glucocorticoid deficiency
What is atypical hypoadrenocorticism caused by?
Atypical hypoadrenocorticism is increasingly recognised- this is the caused by a glucocorticoid deficiency
How does diagnosis of atypical hypoadrenocorticism compare to typical hypoadrenocorticism?
The clinical signs are often like typical
hypoadrenocorticism but as this is a glucocorticoid only deficiency, there are minimal changes in electrolytes as would be caused by a lack of mineralocorticoid. This can make diagnosis more challenging as the hyperkalaemia and hyponatraemia that are usually present with typical hypoadrenocorticism are not likely to be present
What are the cause of secondary hypoadrenocorticism?
There are several causes of secondary hypoadrenocorticism. Hypoadrenocorticism can occur when prednisolone that is being administered to a
patient for medical reasons, is suddenly withdrawn. Iatrogenic hypoadrenocorticism may result secondary to treatment for hyperadrenocorticism with trilostane or mitotane.
What species/breeds is hypoadrenocorticism most common?
Hypoadrenocorticism is often encountered in larger breed, young to middle aged female dogs – although any dog can be affected. It is uncommon in cats.
Certain breeds are more prone to hypoadrenocorticism e.g. Border collies/Bearded
collies and Rough Collies, There may be a history of a recent ‘stressful’ event e.g. kennelling, grooming or recent illness
What is relative adrenal insufficiency (RAI) or critical illness-related corticosteroid insufficiency (CIRCI)?
More recently a condition known as relative adrenal insufficiency (RAI) or critical illness-related corticosteroid insufficiency (CIRCI) has been identified in critically ill patients e.g. with sepsis or pancreatitis (Burkitt Creedon, 2015). RAI/ CIRCI is
characterised by lack of an appropriate adrenal response to stress and is most commonly seen in septic animals
Why is hypoadrenocorticism often called the great pretender, what may there be a history of and what clinical signs may be seen?
Hypoadrenocorticism has been called the
‘great pretender’ as it can mimic many other conditions with non-specific clinical signs and waxing and waning illness (Klein and Peterson, 2010). There may be a history of polydipsia and polyuria, or a waxing and waning illness with intermittent GIT signs, weight loss and lethargy. Some patients presenting with acute abdominal pain may be suspected of having acute pancreatitis. Some of the clinical signs can be attributed to a lack of glucocorticoids (cortisol/cortisone) e.g. lethargy and GIT clinical signs; and others due to lack of mineralocorticoid (aldosterone) e.g. sodium loss, dehydration, altered neuromuscular and cardiac function (Mooney, 2015). This is most notable with the resultant hyperkalaemia that can induce bradycardia and other arrhythmias. Remember aldosterone is involved in potassium and hydrogen ion excretion- therefore a lack of aldosterone results in hyperkalaemia and hyponatraemia.
A patient with hypoadrenocorticism may have some or all what following clinical … ?
A patient with hypoadrenocorticism may have some or all the following clinical signs
1. vomiting
2. diarrhoea +/- melaena
3. abdominal pain
4. PUPD
5. inappetence/ anorexia
6. dull/ lethargic
7. weakness
8. collapse
9. hypovolaemia - poor pulse quality, pale mucous membranes, CRT>2 secs
bradycardia which is inappropriate to the presentation (i.e. evidence of hypovolemia)
On occasion an affected dog may present with signs of megaoesophagus.
N.B. some of the clinical signs can be attributed more to glucocorticoid deficiency e.g. lethargy/ dullness; PUPD and GI signs.
What will electrolytes usually demonstrate in a patient with hypoadrenocorticism?
Most cases of typical hypoadrenocorticism have a pronounced hyperkalemia, hyponatraemia and hypochloraemia due to a lack of aldosterone (mineralocorticoid).
The sodium: potassium ratio is typically below 27:1 (often < 23:1). N.B. this finding may not be present in a patient with atypical hypoadrenocorticism that is deficient in glucocorticoid only.
What will biochemistry usually demonstrate in a patient with hypoadrenocorticism?
In addition, there may be hypercalcaemia (~ 30% of cases), hypoglycaemia (~ 33% of cases), hypoalbuminaemia and azotaemia
Why are patients with hypoadrenocorticism usually azotaemic? Why will they have dilute urine?
Patients are often azotaemic due to fluid loss. However, rather than the classic findings of pre-renal azotaemia, these patients will often have dilute urine due to the lack of aldosterone. Consequently, it is important to try to differentiate a patient with kidney disease from a patient with hypoadrenocorticism. Noting bradycardia on a clinical examination of a sick canine patient is significant as this is far less likely to be present in a patient with kidney disease.
What will haematology usually demonstrate in a patient with hypoadrenocorticism?
Haematology
A mild-moderate, non-regenerative anaemia is possible as this is a chronic disease.
However, in a patient with intestinal haemorrhage there may be a more regenerative anaemia. Unusually and significantly for an animal with an acute illness, there will be usually not be a stress leukogram due to the lack of glucocorticoids. Cortisol causes an alteration in the pattern of circulating white blood cells - a stress leukogram is characterised by neutrophilia, lymphopaenia, eosinopaenia and potentially monocytosis. Conversely in a patient with hypoadrenocorticism, there may be neutropaenia, lymphocytosis and eosinophilia instead. Altered Na:K
alongside lymphocytosis could be significant in the investigation of this patient
What will urinalysis usually demonstrate in a patient with hypoadrenocorticism?
Urinalysis
Urine tends to be dilute/ isosthenuric (SG ~ 1.008-1.015) due to the lack of aldosterone (within the kidneys aldosterone normally retains sodium, chloride and water in exchange for potassium and hydrogen ions). This could cause confusion as this finding is also likely with chronic renal failure
What will electrocardiography usually demonstrate in a patient with hypoadrenocorticism?
Electrocardiography may show bradycardia and other changes consistent with hyperkalaemia e.g. spiked T-waves, shortened Q-T interval, prolonged QRS
complex, reduced/ absent P-waves and bradycardia Potassium levels of 7.5 - 8.0mmol/l can be associated with cardiac arrhythmias - higher levels can be fatal
What test is a definitive test for hypoadrenocorticism?
An adrenocorticotrophic hormone (ACTH) stimulation test is the definitive test for hypoadrenocorticism. Base line cortisol levels are measured N.B. the baseline cortisol may be suggestive of hypoadrenocorticism. Generally, when animals are stressed e.g. ill, their baseline cortisol levels will increase as a result of increased release from the adrenal cortex in a ‘stressful’ situation (review the function of cortisol). If the baseline cortisol is low in a sick dog, this can be a significant finding.
What level of baseline/ pre and the post ACTH cortisol would be indicative of hypoadrenocorticism?
Usually in dogs with hypoadrenocorticism both the baseline/ pre and the post ACTH cortisol are below normal (<20nmol/l). A dog with a resting cortisol above 50 nmol/l is unlikely to have hypoadrenocorticism (if cortisol production is affected i.e. the patient has typical hypoadrenocorticism).
What might radiography demonstrate in a patient with hypoadrenocorticism?
Signs consistent with hypovolaemia may be seen on thoracic radiographs e.g. microcardia, decreased liver size, decreased width of vena cava and decreased
pulmonary vasculature. There may be an oesophageal stripe associated with megaoesophagus.
What might ultrasound demonstrate in a patient with hypoadrenocorticism?
Ultrasound may demonstrate decreased size of the adrenal glands although the adrenal glands are challenging to image.
What should treatments be focused on when addressing the life-threatening conditions in an Addisonian crisis?
Stabilisation
As will all acutely ill patients the treatment should focus on addressing the immediately life-threatening conditions.
Treatments should be focused on-
• correcting hypovolaemia
• reducing potassium levels
• correcting hypoglycaemia (if hypoglycaemic)
• correcting any other electrolyte derangement
• correcting metabolic acidosis
Why should care be taken when trying to correct hyponatraemia?
Care, however, should be taken not to replace the sodium too rapidly, especially if the sodium is very low (< ~ 125mmol/L) at the outset, due to the dramatic movements of intracellular water that could occur. If sodium rises too rapidly, brain swelling could occur potentially resulting in severe irreversible
neurological changes - central pontine myelinolysis could arise. In addition, as 0.9% saline is acidifying it is less suited to a patient with metabolic acidosis
What fluids are indicated when fluid resuscitating a patient in Addisonian crisis?
Intravenous fluid therapy using isotonic crystalloids,
is required to rapidly address the severe hypovolaemia / hypovolaemic shock and t manage the fluid deficit. Traditionally, 0.9% NaCl has been recommended for
hypoadrenocorticism, over lower sodium containing fluids such as Lactated Ringer’s Solution (LRS), due to the hyponatraemia and hypochloraemia and likely
hyperkalaemia. Care, however, should be taken not to replace the sodium too rapidly, especially if the sodium is very low (< ~ 125mmol/L) at the outset, due to the
dramatic movements of intracellular water that could occur. If sodium rises too rapidly, brain swelling could occur potentially resulting in severe irreversible
neurological changes - central pontine myelinolysis could arise. In addition, as 0.9% saline is acidifying it is less suited to a patient with metabolic acidosis. Consequently, LRS is an appropriate fluid for volume resuscitation as it contains less sodium and
chloride and is alkalising. Even though it contains potassium the amount is insignificant and not likely to alter serum potassium levels. Correcting the
hypovolaemia with boluses of IVFT will often lead to an improvement in the electrolyte abnormalities, especially as diuresis is established. Many of these patients will have a significant fluid deficit alongside the hypovolemia dehydration should be addressed alongside the hypovolaemia. Careful monitoring of
fluid ins and outs, as well as bodyweight is indicated in these patients. Frequent changes to the fluid therapy plan are commonly needed based on the findings of
monitoring.
What steroid replacement therapy is required in a patient with Addisonian crisis?
Glucocorticoid and Mineralocorticoid Replacement
Both glucocorticoid and mineralocorticoid replacement therapy will be required in a patient with typical hypoadrenocorticism. There are various drugs available that can be administered according to the patient’s requirements.
Why should glucocorticoid treatment be delayed until an ACTH stimulation test is completed in a patient in an Addisonian crisis?
Unless dexamethasone is administered, glucocorticoid treatment should be delayed until the ACTH stimulation
test is completed since other glucocorticoids interfere with the cortisol assay. Dexamethasone may be required for a very unstable patient in the early stages of treatment although often there is a good initial response to IVFT.
Dexamethasone, however, has much less mineralocorticoid activity than glucocorticoid activity.
Why might Hydrocortisone sodium succinate potentially be administered as a constant rate infusion or as an intermittent IV bolus in the early management of
hypoadrenocorticism?
Hydrocortisone sodium succinate could potentially be administered as a constant rate infusion or as an intermittent IV bolus in the early management of
hypoadrenocorticism - this drug has both corticosteroid and mineralocorticoid activity. Using a product with both glucocorticoid and mineralocorticoid activity may,
in combination with IVFT, be sufficient to manage the hyperkalaemia without having to use specific treatment for this
What are the treatment options for correcting hyperkalemia in patients with hypoadrenocorticism?
Correcting Hyperkalaemia
Depending on the response to fluid therapy +/- steroid therapy, the potentially life-threatening effects of hyperkalaemia may still need to be treated. Treatment options include-
• Calcium gluconate (protects the cardiac myocytes from the effects of hyperkalaemia although does not actually decrease potassium levels)
• Insulin/dextrose (insulin drives potassium into cells; dextrose prevents hypoglycaemia and stimulates further insulin release). However, care must be
taken to stabilise blood glucose levels appropriately before this treatment in a patient that is hypoglycaemic on presentation
• Whilst bicarbonate theoretically could be used to reduce potassium levels, this treatment option is least likely to be used and should not be used if it is not
possible to monitor blood pH). In the majority of cases bicarbonate is not indicated and should only be considered once the perfusion and fluid deficits
have been addressed.
What monitoring is usually required for a patient with hypoadrenocorticism?
The patient will require regular monitoring of demeanour, perfusion parameters, TPR
etc. and auscultation for arrhythmias. Additionally, arterial blood pressure should be monitored.
An ECG should be used to monitor the patient’s heart rate and to check for arrhythmias. Electrolytes should be monitored ~ every 4 hours until stable -
monitoring can then be decreased to once every 12 hours.
The urine output should be measured every 1-2 hours, along with assessment of perfusion and hydration status, to determine whether fluid therapy is being
successful.
What nursing considerations are required for a patient with hypoadrenocorticism?
Patients with hypoadrenocorticism often respond well and dramatically to emergency management. If they do not start to eat voluntarily, nutritional support may be required. Appropriate dietary management of a dog which has had episodes of vomiting and diarrhoea will be required and may include the use of anti-emetics if
nausea persists or probiotics. A palatable diet offered little and often is indicated for these patients. Dogs with hypoadrenocorticism are often very depressed on
admission and showing signs of abdominal pain. Their demeanour should improve as they respond to treatment. In addition to pain assessment and management, it is important to provide them with appropriate attention and environmental enrichment.
Due to the nature of the presenting signs, in some patients (haemorrhagic gastroenteritis), the patient may be placed in isolation facilities with barrier nursing. If
these patients remain in the hospital for longer periods of time (over 24hrs) then careful discussion of the normal routine, feeding and walking with the owners can help reduce stress induced hormone release and therefore reduce the risks of relapse. Stressful events for these patients, such as struggling for blood sample for example, can lead to worsening of their condition. The nursing team need to protect the patient as much as possible from this occurring.
What is the long term treatment for patients with hypoadrenocorticism?
Long term management
Until recently (2016) oral fludrocortisone which has mainly mineralocorticoid activity and a small amount of glucocorticoid activity, has been the mainstay of treatment.
The mineralocorticoid activity helps to counteract the sodium, chloride and water loss and potassium retention – thus managing the isosthenuria and hyperkalaemia.
Traditionally, dogs with hypoadrenocorticism have been maintained on long-term fludrocortisone supplemented with glucocorticoids e.g. prednisolone as required.
Desoxycortone pivalate (DOCP) has been licenced for use in dogs in the UK for treatment of hypoadrenocorticism since 2016 (Ramsey et al., 2016). This is used for maintenance therapy but as it has no glucocorticoid activity, dogs must be
maintained on long term glucocorticoids (prednisolone) as well.
What is primary hyperaldosteronism otheriwse known as? What species does it affect and what are the clinical signs?
Primary hyperaldosteronism, Conn’s syndrome, is a rare but increasingly recognised condition that affects cats. Clinical signs relate to excess aldosterone activity- retention of sodium, chloride and water which can cause hypertension related signs e.g. retinal haemorrhage, renal failure and hypokalaemia due to excessive excretion of potassium. Hypokalaemia can cause various clinical signs including weakness, cervical ventroflexion, plantigrade stance.
What does diabetic ketoacidosis occur secondary to?
DKA occurs secondary to uncontrolled diabetes mellitus (DM). This is either because the condition has not been previously recognised and treated (quite common) i.e. a patient has recently developed diabetes mellitus and has not yet been diagnosed; or because, despite being managed for diabetes mellitus with insulin, diet and controlled exercise, concurrent illness (e.g. infection, pancreatitis) destabilises the condition (very common); or there are management issues and the DM is not controlled properly e.g. incorrect storage, administration of insulin. Cats that present with DKA are generally not yet diagnosed or recently diagnosed but not yet or poorly controlled.
What should be the priority alongside treatment of diabetic ketoacidosis in a previously diabetic patient?
In a previously diagnosed diabetic patient that has been on insulin and has
previously been stable, identifying the reason for destabilisation, such as presence of
infection (UTI) or inflammation (pancreatitis), should be a priority alongside treatment
of DKA.
What is the cause of acidosis in a patient that had diabetic ketoacidosis?
The lack of insulin/ insulin activity and increase in counter-regulatory ‘stress’ hormones (mainly glucagon but also cortisol, growth hormone and the
catecholamines (adrenaline and nor-adrenaline) leads to altered/ ‘stressed’ hepatic fat metabolism (McGrotty, 2010) (Skelly, 2018). Glucagon causes glycogenolysis. In the absence of insulin, free fatty acids are metabolised to acidic ketone bodies (ketones) rather than triglycerides. As the ketones are acidic, this leads to a drop in the pH of the blood creating a metabolic acidosis which is called (diabetic) ketoacidosis (DKA). As the patient becomes more unwell because of DKA, the acidosis will be further compounded if hypovolaemia develops. Decreased perfusion
will result in anaerobic respiration and lactic acid production as outlined in previous units (McGrotty, 2010). The ketones that are produced are beta-hydroxybutyrate, acetoacetate and acetone. If ketones are produced at a greater rate than they can be metabolised, ketoacidosis and ketonuria will develop. The rate of ketone production increases significantly in the presence of stress e.g. infection.
What signs can be associated with diabetic ketoacidosis?
The following clinical signs can be associated with ketoacidosis
1. vomiting +/- diarrhoea
2. anorexia
3. dullness and collapse
4. hypoperfusion (review these signs)
5. dehydration (review these signs)
6. anuria/ oliguria
7. poor body condition with muscle wasting
8. tachypnoea (due to metabolic acidosis) +/- Kussmaul respiration
9. ketotic halitosis
10.clinical signs associated with an underlying concurrent illness that has
destabilised the diabetic patient (e.g. pancreatitis).
11.cats, especially, may present with jaundice/icterus
12.cats may also have a plantigrade stance
13.dogs may have cataracts
Unit 4 Outcome 2: September 2020
How will a patient with diabetic ketoacidosis present in an emergency setting? What will be the clinical signs?
- The patient will be very unwell- in the most serious cases, the patient will present in a collapsed state with hypovolaemia and dehydration, secondary to
vomiting, diarrhoea and osmotic diuresis. Signs of hypovolaemia may be present e.g. tachycardia, rapid pulse, weak/ absent peripheral pulses, pale
mucous membranes and prolonged CRT (> 2 seconds). Patients will commonly be tachypnoeic due to metabolic acidosis but can also develop a breathing pattern called “KussMaul respiration”. This is the body’s response to severe acidosis and is characterised by deep, rapid, laboured breathing. The history may be suggestive e.g. recent PUPD, nocturia and polyphagia etc.
However, by the time DKA has developed the patient is unwell so unlikely to be eating/ drinking. It is also likely to be oliguric/ anuric due to hypovolaemia/
dehydration.
What will diagnostic testing usually reveal in a patient with diabetic ketoacidosis?
Hyperglycaemia, ketonaemia, glycosuria and ketonuria are highly suggestive of DKA. It is important to remember that a stressed/ ill cat can have hyperglycaemia and glucosuria. However, the hyperglycaemia is not likely to be > 15 mmol/l. Cats
with DM and DKA will often have a blood glucose > 20 mmol/L. Also, it is unlikely that significant ketonaemia or ketonuria will be present in a stressed cat unless caused by an underlying disease process e.g. hepatic lipidosis.
What will biochemistry usually demonstrate in a patient with diabetic ketoacidosis?
Hyperglycaemia will be present due to the lack of insulin activity and there is likely to be a pre-renal azotaemia (increased creatinine and urea). It is likely that there will be increased liver enzymes in both dogs and cats although this is a non-specific finding.
As previously stated, cats will commonly be icteric with evidence of hyperbilirubinaemia. Therefore, it is important to realise that a jaundiced cat presenting as an emergency could have DKA rather than liver disease.
What will blood gas analysis usually demonstrate in a patient with diabetic ketoacidosis?
Blood gas analysis will reveal a metabolic acidosis which may be severe- there will be an increased anion gap with decreased bicarbonate and a
compensatory hypocapnia
What will haematology usually demonstrate in a patient with diabetic ketoacidosis?
Haematology may demonstrate neutrophilia due to infection and/or a stress leukogram. A stress leukogram is characterised by neutrophilia, lymphopaenia, eosinopaenia and potentially monocytosis. The PCV and TS will usually be elevated
if the patient is dehydrated although the patient may have non-regenerative anaemia (of chronic disease). It is important to consider this when measuring the PCV of a clinically dehydrated patient.
What will the PCV/TP usually demonstrate in a patient with diabetic ketoacidosis?
The PCV and TS will usually be elevated
if the patient is dehydrated although the patient may have non-regenerative anaemia (of chronic disease). It is important to consider this when measuring the PCV of a clinically dehydrated patient.
What will blood electrolytes usually demonstrate in a patient with diabetic ketoacidosis?
Blood electrolytes should be measured as there is often a potassium deficit- this may not, however, become apparent until after insulin is administered. Normally, insulin causes cellular uptake of potassium i.e. it makes potassium move into cells. In the
absence of insulin, relatively more potassium will be present in plasma due to failure of the ATP Na:K pumps and decreased renal excretion. Whilst there may appear to be hyperkalaemia initially, the patient will likely have an absolute potassium deficiency. This will become apparent once IVFT is started as the potassium will be diluted and diuresis is re-established; additionally, once insulin is administered potassium will move into cells. Hypokalaemia leads to muscular weakness and cardiac arrhythmias. This is often why cats have a plantigrade stance/ ventroflexion
of the neck.
What can serum ketones be measured with?
Serum ketones can be measured using commercially
available dipsticks, urine dipsticks or handheld blood monitors. N.B. Note the urine dipstick pads can detect acetate and acetoacetate but not beta hydroxybutyrate.
What type of ketones can urine dipstick pads detect?
urine dipstick pads can detect acetate and acetoacetate but not beta hydroxybutyrate.
Why will a patient with diabetic ketoacidosis usually have hyperkalaemia initially, how will insulin therapy help with this?
Blood electrolytes should be measured as there is often a potassium deficit- this may not, however, become apparent until after insulin is administered. Normally, insulin causes cellular uptake of potassium i.e. it makes potassium move into cells. In the absence of insulin, relatively more potassium will be present in plasma due to failure of the ATP Na:K pumps and decreased renal excretion. Whilst there may appear to be hyperkalaemia initially, the patient will likely have an absolute potassium deficiency. This will become apparent once IVFT is started as the potassium will be diluted and diuresis is re-established; additionally, once insulin is administered potassium will move into cells. Hypokalaemia leads to muscular weakness and
cardiac arrhythmias. This is often why cats have a plantigrade stance/ ventroflexion of the neck. It is most likely that potassium supplementation will be required for a patient with DKA. The amount of potassium required to replace deficits is outlined in the table below. N.B. if potassium is supplemented into the main bag of IV fluids, it is important to be aware of the risk of causing hyperkalaemia if the fluid rate is
increased. The maximum rate of intravenous potassium administration is 0.5 mmol/kg/hr. The actual rate being delivered should be calculated for the patient and
reviewed if the fluid rate is altered
What is the maximum rate of intravenous potassium administration?
The maximum rate of intravenous potassium administration is 0.5 mmol/kg/hr. The actual rate being delivered should be calculated for the patient and
reviewed if the fluid rate is altered
What can hypophosphataemia lead to and why is this likely to arise in a patient with diabetic ketoacidosis?
Plasma phosphate levels may be also be decreased which can lead to red blood cell
lysis (haemolysis). This is most likely to arise once insulin treatment commences as like potassium, insulin drive phosphate into cells. During the first few days of treatment, phosphate levels should be monitored regularly.
Why may magnesium be low in a patient with diabetic ketoacidosis?
Magnesium is also involved in the Na: K ATPase pump. It may also be decreased in a patient with DKA which can lead to arrhythmias, muscle weakness, tremors and
tetany (Odunaya, a, 2014). For this reason, a patient with hypokalaemia that is not responding to treatment might require additional magnesium supplementation
What will urinalysis usually demonstrate in a patient with diabetic ketoacidosis?
There will be ketonuria and glucosuria- additionally there may be proteinuria, haematuria +/- pyuria if the patient has a urinary tract infection. The urine specific
gravity may be high > 1.030 in dogs (due to the presence of glucose in the urine).
Urine dipstick testing (e.g. Ketodiastix® may give negative results for ketones. This could be because the predominant ketone present is beta-hydroxybutyrate which is not detected by urine stick tests -they only detect acetone and acetoacetate. Adding hydrogen peroxide to urine converts beta-hydroxybutyrate to acetoacetate which is detectable using urine dipsticks. One-part hydrogen peroxide to nine-parts urine is
usually sufficient. Cytology of urine sediment may demonstrate neutrophils, erythrocytes and bacteria if the patient has a urinary tract infection. Urine culture and sensitivity should ideally be performed even if there is no pyuria, since patients with DM are predisposed to developing urinary tract infections- this is often the reason for destabilisation of the patient
Why might a patient with diabetic ketoacidosis test negative for ketones on a urine dipstick?
Urine dipstick testing (e.g. Ketodiastix® may give negative results for ketones. This could be because the predominant ketone present is beta-hydroxybutyrate which is not detected by urine stick tests -they only detect acetone and acetoacetate.
How can you convert beta-hydroxybutyrate on a urine dipstick?
Urine dipstick testing (e.g. Ketodiastix® may give negative results for ketones. This could be because the predominant ketone present is beta-hydroxybutyrate which is not detected by urine stick tests -they only detect acetone and acetoacetate. Adding hydrogen peroxide to urine converts beta-hydroxybutyrate to acetoacetate which is detectable using urine dipsticks. One-part hydrogen peroxide to nine-parts urine is
usually sufficient
What are the goals of treating a patient with diabetic ketoacidosis?
Treatment and Nursing Care The goals of treating a patient with DKA are- • Correct hypovolaemia • Correct metabolic acidosis (reduce ketone levels and lactate levels) • Correct electrolyte derangements • Correct dehydration • Treat underlying cause • Manage hyperglycaemia
why should careful consideration should be given to the optimal site for catheter placement in a patient with diabetic ketoacidosis?
Prior to starting fluid therapy, careful consideration should be given to the optimal site for catheter placement as they may need multiple infusions and blood sampling over the course of the hospitalisation. A central line (jugular catheter) can be usedwith practice it is relatively simple to place. If using a triple lumen catheter, multiple lines can be used. Blood samples can be taken from the distal port. If this is not an option, then adaptions can be made to peripheral catheters e.g. using a triple lumen octopus catheter for example. Blood sampling can also be carried out from a peripheral catheter using the push-pull technique reducing the need for repeated venepuncture
What should be managed prior to start insulin therapy in a patient with diabetic ketoacidosis?
Intravenous Fluid therapy
This is the priority and hypovolaemia should be managed prior to starting treatment with insulin
What is the primary aim of fluid therapy in a patient with diabetic ketoacidosis?
The primary aim of fluid therapy is to correct hypovolaemia and secondarily to correct the dehydration. Hypovolaemia should be treated as previously described with initial bolus therapy and assessment of response to treatment. The fluid
requirement for maintenance and replacement of losses should be calculated- 50% of the fluid deficit should ideally be replaced in the first 4-6 hours and the remainder over the following 18-20 hours (McGrotty, 2010). It should be noted that due to the
DM induced polyuria in these patients, ongoing fluid losses from the urinary tract can be significant and as such ongoing monitoring of urine output is a vital to ensure correct fluid balance – monitor the ins and outs.
Managing the hypovolaemia and dehydration, with IVFT, and initiating insulin treatment is often sufficient to manage the acidosis without additional treatment
being required.
What type of fluid should ideally be used in a patient with diabetic ketoacidosis?
Whilst any isotonic crystalloid solution (e.g. 0.9% NaCL) can be used, a buffered/alkalising solution such as LRS is preferred for treating the metabolic acidosis.
