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.
IF dehydration is significant in a patient with diabetic ketoacidosis how long should you wait until starting insulin therapy?
Insulin treatment is essential for the patient with a ketoacidotic crisis (once hypovolaemia has been addressed). If dehydration is significant this should also be managed, as discussed above, over 2-6hrs prior to starting insulin therapy
Describe what happens when insulin therapy starts in patients with diabetic ketoacidosis?
Insulin drives glucose into cells giving them an energy source – thus decreasing the need for further lipid metabolism. Additionally, insulin breaks down ketones and so directly helps to manage the cause of the acidosis. Insulin should be started once hypovolaemia and significant dehydration has been corrected. N.B. Insulin therapy should be continued until the ketosis has resolved- this may be beyond the point that
the blood glucose levels have normalised. This of course means that paradoxically glucose/ dextrose will have to be administered in the latter stages of insulin therapy to avoid hypoglycaemia. Soluble (neutral) insulin should be used to in the treatment
of ketoacidosis. Various protocols are described (Niessen, 2011) - examples are included below
How can soluble insulin be administered via intravenous fluid therapy?
Soluble insulin can be added to the intravenous fluids and administered as a constant rate infusion (CRI) of 2.2 IU/kg/day or it may be run ‘piggyback’ with the
IVFT.
What is the dose rate for soluble insulin as a CRI?
constant rate infusion (CRI) of 2.2 IU/kg/day
What is the protocol when administering insulin therapy intravenously for a patient with diabetic ketoacidosis?
Alternatively, in smaller patients, the insulin may be diluted and placed in a separate syringe driver from the rehydration fluids to ensure accurate dosage. Blood glucose levels are checked hourly and if the blood glucose level drops below 8 -15 mmol/l, 5% dextrose is administered as noted above. Once the animal starts to eat regularly, the blood glucose levels are less than 15 mmol/L and the ketone levels have decreased, IV insulin may be stopped and longer acting (intermediate) insulin started subcutaneously. This technique leads to a more rapid and controlled
stabilisation. Anecdotally, shorter hospitalisation times have been reported with this method as the absorption of insulin is not affected by dehydration or perfusion to the muscles. Additionally, this method is less likely to be stressful/ painful to the patient which is an important consideration due to the effect of ‘stress’ hormones on insulin activity. However, the patient will require 24-hour monitoring to ensure they do not become hypoglycaemic due to intravenous administration of rapid acting insulin
How should diluted IV soluble insulin be prepared prior to administration and why?
for IV/ CRI administration the first 50 mls of solution should be run through the fluid line for a few seconds before starting administration to the patient as insulin
binds to the plastic drip tubing and the syringe. After a few seconds this equilibrates and allows a steady rate of administration to be achieved. Insulin is also sensitive to UV light so infusions should be covered and replaced every 12-24hrs.
What is the protocol when administering insulin therapy intramuscularly for a patient with diabetic ketoacidosis?
An initial dose of 0.2 IU/kg of soluble insulin is administered by the intramuscular (IM) route. Hourly measurements of blood glucose levels are obtained and further IM injections of soluble insulin at 0.1 IU/kg IM are administered until blood glucose levels drop to within the normal range. If the blood glucose drops to (8 -15 mmol/l) then 5% dextrose should be added to the intravenous fluids. Soluble insulin therapy is continued until the patient is eating of its own accord, the glucose levels remain below 15mmol/L and the ketone levels have declined. At this point the patient may
be transferred on to longer acting (intermediate) insulin administered by the subcutaneous route.
Why is it important to monitor potassium levels when starting insulin therapy and how often should this be carried out?
Monitoring blood parameters
It is important to monitor potassium levels every 1-2 hours, during initial insulin therapy. As discussed previously, insulin causes movement of potassium into the cells and, hence, hypokalaemia will develop. Potassium can supplemented in accordance with the table below
Why is it important to monitor phosphate levels when starting insulin therapy?
In addition, phosphate levels should be monitored as this electrolyte will move intracellularly with glucose and be ‘washed out’ with intravenous fluids.
Hypophosphataemia will lead to intravascular haemolysis and phosphorus supplementation is required when plasma levels drop below 0.35mmol/L. Most formulations are presented as potassium phosphate and therefore the extra potassium needs to be factored into any calculations made for potassium
supplementation.
When is bicarbonate supplementation indicate in a patient with diabetic ketoacidosis and what is the dose?
Bicarbonate supplementation is unnecessary in most ketoacidotic patients as the acidosis will generally resolve in most patients with insulin and fluid therapy alone.
However, if the patient is NOT responding to the insulin administration and plasma bicarbonate level is <8 mEq/l, bicarbonate supplementation could be considered as a final option. However, it must be is possible to measure blood pH as excessive administration could cause irreversible alkalosis. Bicarbonate should only be given by constant rate infusion and NOT by bolus injection. The bicarbonate dosage is calculated as per the equation belowBicarbonate dose (mEq/L) = body weight (kg) x 0.3 x base excess (BE).
One third of this calculated dose is administered and the response evaluated prior to any further administration.
What monitoring should be carried out after stabilisation of a patient with diabetic ketoacidosis?
Once relatively stable, acid-base and electrolyte levels should be rechecked every ~ 4-6 hours. The urine output should be monitored every 2 hours to ensure adequate hydration and perfusion status
It is important to remember that frequent blood sampling could cause anaemia, especially in small patients. Blood assaying and sampling techniques that require smaller volumes of blood should be used i.e. a veterinary approved glucometer.
The patient’s response to treatment needs to be regularly monitored, especially in the initial stages, as discussed above. Regular assessment of perfusion parameters,
TPR etc. should be performed. Regular assessment of the heart rate and rhythm should be performed to identify any arrhythmias. In the early stages, if the patient is collapsed, it should be managed as for any recumbent patient. As soon as the patient’s condition allows, appropriate enteral nutrition should be started.
The patient should be weighed at least twice daily to ensure IVFT is adequate but not excessive. PCV/TS and urinalysis should be performed regularly.
Blindness caused by cataracts, will also influence nursing care in some patients
What is hyperglycaemic hyperosmolar syndrome?
Hyperglycaemic Hyperosmolar Syndrome (HHS)
HHS is a rare form of diabetic crisis which can potentially occur in dogs and cats. It is characterised by extreme elevations in blood glucose, absent or low levels ketones and a high serum osmolality (because of the very high glucose levels).
As with DKA, HHS develops due to a complete lack or relative lack of insulin. It may occur in newly diagnosed or known diabetic patients. In a patient with concurrent
illness, stress hormones are present within the body at elevated levels- these hormones counteract the effect of insulin and lead to increasing levels of blood
glucose over days or weeks. Ketogenesis is uncommon in HHS and so ketone levels may be normal for these patients.
What are the clinical signs of hyperglycaemic hyperosmolar syndrome?
Clinical signs
These patients often present with similar clinical signs to those with diabetes mellitus or diabetic ketoacidosis as discussed previously. Affected patients will always
present with severe dehydration because of the increased serum osmolality and osmotic diuresis caused by the hyperglycaemia. In extreme cases they may present in a comatose state. The increased osmolality of the blood, due to increased levels
of glucose, can cause neurological abnormalities. Neurological abnormalities are more common in human diabetic patients. N.B. It is important to be aware that if the high osmolality is corrected too rapidly then cerebral oedema can develop.
Care must be taken to rule out underlying issues which could be responsible for decreased insulin activity or production such as inflammation and infection.
What treatment and nursing is required for hyperglycaemic hyperosmolar syndrome?
Treatment and Nursing care
Whilst the treatment is similar to a patient presenting with DKA, as discussed previously, it is essential to closely monitor the rate of glucose decline in response to treatment. If this is too rapid, there is a significant risk of cerebral oedema developing. Regular and frequent monitoring of mentation and as well as fluid
balance, electrolyte and acid base balance is essential. Nutritional support is also a very important part of the nursing care.
What are the many varied causes of hypoglycaemia?
There are many varied causes of hypoglycaemia (decreased serum glucose levels) in cats and dogs
- Beta cell neoplasia (insulinoma- insulin producing tumour of the pancreas)
- Hypoadrenocorticism
- Paraneoplastic syndrome - some tumours produce insulin-like factors
- Sepsis / SIRS
- Juvenile toy breed hypoglycaemia
- Hunting dog hypoglycaemia
- Neonatal hypoglycaemia
- Liver disease
- Iatrogenic (insulin overdose)
- Xylitol intoxication
- Other toxins – baclofen, metaldehyde, methylxanthines/caffeine
- Polycythaemia
N.B. in most cases prolonged fasting is not likely to be a cause of clinically significant
hypoglycaemia
What are the clinical signs of hypoglycaemia?
Clinical signs
Any patient could be affected with hypoglycaemia - although there may be increased incidence in working dogs and young animals.
Depending on the underlying cause, the clinical signs vary and are often non-specific and waxing and waning. They may be associated with exercise or periods of fasting. Neurological signs may be present because of cerebral hypoglycaemia. However, signs will be acute onset in the case of toxicity. As ever obtaining a thorough history is of great importance.
A patient with an insulinoma could present as an emergency due to a massive insulin release causing seizures or coma.
Clinical Signs
The clinical signs of hypoglycaemia can include the following
1. abnormal behaviour
2. altered mentation
3. exercise intolerance
4. syncope
5. ataxia
6. muscle tremors/ twitching
7. collapse (usually after exercise/exertion)
8. lethargy
9. signs of collapse/lethargy that are responsive to feeding
10. polyphagia
11. impaired vision
12. seizures
13. coma
What blood glucose level are clinical signs generally seen with hypoglycaemia?
hypoglycaemia blood glucose is often very low <
3.3 mmol/l N.B. clinical signs are generally not present until blood glucose is < 2.8 mmol/l
Why are fluoride oxalate tubes used for measuring blood glucose when sending off to the lab?
blood is being submitted to an external laboratory for glucose measurement, it must be put into a fluoride-oxalate tube to prevent erythrocytes metabolising the glucose and giving an erroneously low blood glucose result.
How will a history help with the diagnosis of hypoglycaemia?
The history and clinical examination may be highly suggestive e.g. working Springer Spaniel/ Labrador retriever, ingestion of toxin or over administration of insulin. There may have been previous episodes suggestive of hypoglycaemia e.g. weakness on exercise. Patients with hypoadrenocorticism may have a history of a waxing and waning disease
What clinical signs may be alongside hypoglycaemia to help diagnose SIRs/Sepsis in a patient?
Patients with SIRS/sepsis are likely to be systemically very unwell on presentation with associated clinical signs e.g. decreased CRT, brick-red mucous
membranes, decreased blood pressure etc
What immediate treatment should be given to a patient that presents with hypoglycaemia?
Immediate treatment is necessary to prevent irreversible brain damage. Oral glucose gel (e.g. Hypostop) or glucose solution (10-50%) may be given as first aid onto the mucous membranes of the mouth (by the owners). If they do not have access to this,
which is likely to be the case unless the patient has diabetes mellitus and the owner is prepared for a possible hypoglycaemic episode, then liquid honey or syrup could be used at home in an emergency.
What dextrose concentration should be administered in a patient with hypoglycaemia?
If the patient has been admitted to a veterinary practice with neurological signs, an intravenous dextrose bolus (0.2-0.5g/kg of 10% dextrose solution) should be administered. However, this should be diluted to a 5% solution in saline before being administered via a peripheral intravenous catheter to prevent thrombophlebitis and haemolysis. The clinical response is often rapid. Once the patient is stabilised, dextrose may be added to IV fluids e.g. 0.9% saline to maintain glucose levels. N.B. If the dextrose concentration being administered is greater than 5% a central venous catheter should be used to prevent thrombus formation.
Why should a central venous catheter be used if a dextrose concentration greater than 5% is being administered?
If the dextrose concentration being administered is greater than 5% a central venous catheter should be used to prevent thrombus formation.
How often should a patient blood glucose be monitored after presenting with hypoglycaemia and receiving glucose?
Monitoring of
blood glucose level, every 30 minutes initially, is advised until it is above 3 mmol/l.
Following this, hourly measurements should be sufficient until the normal range has been reached. It should be noted that in some patients, the blood glucose will alter up and down rapidly so careful monitoring is needed on an ongoing basis. Ideally,
once stabilised, the glucose should be maintained in the normal range to minimise disruption of glucose/insulin homeostasis rather than ongoing, rapid fluctuations..
N.B. A potential complication of glucose administration to a patient with an insulinoma is a massive release of insulin which could cause seizures or a coma.
Therefore, these patients must be closely monitored. There could also be complications in a patient with an insulinoma when they start to be fed within the
practice.
What is a potential complication of receiving glucose if a patient has an insulinoma?
A potential complication of glucose administration to a patient with an insulinoma is a massive release of insulin which could cause seizures or a coma.
Therefore, these patients must be closely monitored. There could also be complications in a patient with an insulinoma when they start to be fed within the
practice.
What are the nutritional needs will working dogs, toy breeds or young animals that present with hypoglycaemia?
Young animals and toy breeds with hypoglycaemia should be fed little and often complex carbohydrates will result in a gradual release of glucose. Working dogs should be fed before starting work and offered regular snacks
What drugs can be used in patients with hypoglycaemia that promote gluconeogenesis or anti-insulin drugs?
In addition, drugs that promote gluconeogenesis, such as prednisolone, could be used to combat hypoglycaemia; or anti-insulin drugs, such as diazoxide, can be used. Surgical or chemotherapeutic treatment of an of an insulinoma may be considered. As this is not emergency management, it is not considered further in
these notes. However, it is important to be aware that a potential complication of pancreatic surgery could be acute pancreatitis.
What are the several causes of hyperglycaemia?
There are several causes of hyperglycaemia and these include
- diabetes mellitus/insulin resistance e.g. acromegaly, hyperthyroidism
- stress associated especially in a cat
- head trauma
- hyperadrenocorticism
What can insulin resistance arise secondary to in cats?
Insulin resistance can arise secondary to hyperadrenocorticism (HAC) and acromegaly, especially in cats. This can lead to hyperglycaemia and clinical signs of diabetes mellitus. However, it is less likely to
cause diabetic ketoacidosis than insulin dependent diabetes mellitus.
What is acromegaly usually caused by?
Acromegaly (hypersomatrophinism) is usually caused by a growth hormone (somatotrophin) secreting pituitary tumour.
What can hyperadrenocorticism be caused by?
Hyperadrenocorticism can be caused by an ACTH releasing pituitary adenoma which leads to increased secretion of hormones from the adrenal cortex - mainly
cortisol in the dog. It can also be caused by a tumour of the adrenal cortex secreting cortisol.
What are the clinical signs of hyperadrenocorticism?
Clinical Signs
Clinical signs of HAC can include the following
1. polydipsia
2. polyuria
3. polyphagia
4. peripheral polyneuropathy
5. weight loss
6. pot-bellied appearance
7. muscle wastage/ weakness
8. skin/ hair changes e.g. alopecia, comedomes, increased skin fragility (in a dog), cats do not tend to have skin/hair changes with HAC
9. secondary infection due to immunosuppression
What are the clinical signs of acromegaly? What test can confirm diagnosis?
Clinical signs of acromegaly include the following
- polydipsia
- polyuria
- polyphagia
- organomegaly
- weight gain/increased size and prominence of feature e.g. paws, skull etc.
- +/- hypertrophic cardiomyopathy
- +/- chronic renal failure azotaemia
The history and development of ‘gigantism’ are suggestive of acromegaly in cats.
This condition can be diagnosed by measuring increased insulin-like growth factor 1 (IGF-1) concentrations
What test can confirm hyperglycaemia for the preceding 2-3 weeks?
A patient with DM will have a persistently raised blood glucose level – increased blood glucose for the preceding two to three weeks can be further confirmed by an elevated fructosamine result.
What will a cat with hyperadrenocorticism often present clinical signs of?
A cat with HAC will often present with clinical signs of
DM due to the increased cortisol levels antagonising insulin. Definitive diagnosis of hyperadrenocorticism is challenging but usually involves an ACTH stimulation tests and/or low and high dexamethasone suppression tests.
Where is calcium and phosphorus mainly stored in the body?
Along with phosphorus, most of the body’s calcium is within mineralised bone
Where are calcium ions in plasma found?
The calcium ions (Ca 2+) in plasma can be:
• free
• bound to other substances e.g. albumin or phosphate (PO4 3−).
What type of calcium is biologically active and what is tis often referred to as?
Only ‘free’ calcium is biologically active (involved in heart and muscle contraction)-
this is often referred to as ‘ionised’ calcium.
When testing ionised calcium, what forms can be measured?
Although both free calcium and albumin/protein bound calcium are ionised, when measuring ‘ionised’ calcium, it is the free, biologically active calcium which is actually being measured.
The calcium ions (Ca 2+) in plasma can be:
• free
• bound to other substances e.g. albumin or phosphate (PO4 3−).
What is total plasma calcium?
Total plasma calcium = calcium bound to phosphate + protein bound calcium + free/ ‘ionised’ calcium.
What is the total level of calcium affected by?
The total level of calcium is affected by pH, vitamin D level, albumin level and diet.
Where is calcium absorbed in the body and what particular diet can affect this?
The total level of calcium is affected by pH, vitamin D level, albumin level and diet.
Calcium is absorbed via the gastrointestinal tract and so diet must have suitable levels; and absorption from the intestines must be appropriate. There may be issues with the relative levels of calcium and phosphorus in unbalanced, home-made ‘all meat’ and ‘raw’ diets.
What type of calcium testing is more useful and what can affect free/ionised calcium level when collecting a blood sample?
Measurement of the free/ ‘ionised’ calcium level is more useful than measuring total calcium, as it is not affected by albumin levels. Exposure to air
can affect the free/ ‘ionised’ calcium level- an important consideration when collecting a blood sample
What can blood calcium levels be affected by?
Blood calcium levels can be affected by nutrition, endocrine disease, renal disease and neoplasia amongst other conditions
Blood calcium levels can be affected by various factors including nutrition, endocrine
disease, renal disease and neoplasia.
What can hypercalcaemia lead to?
Hypercalcaemia can lead to cardiac
dysrhythmias and acute renal failure
What can be the causes of hypercalcaemia?
the most common cause is neoplasia (Rahilly,
2012). Hypercalcaemia can also be associated with renal failure, hyperparathyroidism, hypoadrenocorticism and vitamin D toxicity
How can the parathyroid affect calcium levels?
Hypocalcaemia can be caused by a low level of parathyroid hormone. This could be iatrogenic e.g. following inadvertent parathyroidectomy in a hyperthyroid cat who has undergone a thyroidectomy; or primary hypoparathyroidism caused by immune
mediated damage of the glands. The latter is rare in cats and dogs
What body systems are affected in a patient with hypocalcaemia?
The neuromuscular, cardiovascular, GIT, skeletal and respiratory systems can all be affected in a patient with hypocalcaemia
What signs do patients with hypoglycaemia usually have and why?
as calcium is involved in regulating nerve and muscle function, a patient with hypocalcaemia usually has
signs of increased neuromuscular excitability.
Hypocalcaemia can result in muscle tremors, tachycardia, seizures and tetany
What blood tube can cause artifactually low blood calcium?
It is possible to have an artefactually low blood calcium due to improper collection/ handling of the sample i.e. if the sample is put in a blood tube containing EDTA.
What are the causes of hypocalcaemia?
Causes of hypocalcaemia include 1. eclampsia 2. hypoparathyroidism- primary or iatrogenic (e.g. post-thyroidectomy) 3. acute pancreatitis 4. ethylene glycol toxicity 5. acute/chronic renal failure 6. diabetic ketoacidosis. 7. sepsis 8. iatrogenic- i.e. phosphate enema especially in small dogs and cats; citrate toxicity with blood transfusion diffuse intestinal disease leading to decreased calcium absorption e.g. alimentary lymphoma 9. hypomagnesia 10.hypovitaminosis D
Causes of hypocalcaemia include eclampsia, pancreatitis, ethylene glycol toxicity and diabetic ketoacidosis
What are the three most common reasons or hypocalcaemia?
Hypocalcaemia/ eclampsia is relatively common in a female dog (bitch) who has had puppies (whelped) recently. The signalment is often suggestive e.g. recent whelping (within the last three weeks) in a predisposed breed e.g. Yorkshire terrier with large litter recent second side/bilateral thyroidectomy or enema
administration
What are the main clinical signs of hypocalcaemia?
The main clinical signs associated with hypocalcaemia are 1. restlessness 2. hyperaesthesia (oversensitivity to stimuli) 3. muscle tremors 4. facial rubbing 5. tachycardia 6. seizures 7. tetanic spasms 8. hyperthermia 9. +/- anorexia 10.+/-PUPD 11.+/- panting 12. +/-stiffness/ataxia 13. +/-vomiting If not treated the patient with severe hypocalcaemia could go into respiratory arrest and die
These are mainly signs of increased neuromuscular excitability secondary to the low blood calcium.
What form of calcium should be measured?
It is important to be clear whether blood calcium results are for total or ionised calcium concentrations. As discussed above, ionised ‘active’ calcium should ideally be measured. Otherwise a calcium measurement is the total value for all of the extracellular calcium present in the circulation not just that which is active.
What will biochemistry reveal in a patient with hypoparathyroidism?
Biochemistry results reveal a hypocalcaemia (ionised and total). In a patient with hypoparathyroidism, blood calcium will be low whilst phosphate will be high.
Parathyroid hormone levels would also be low if assayed as part of a more comprehensive investigation.
What three different forms of calcium is present in the body?
Calcium is present in three different forms – ionised, complexed and protein bound
What is ionised calcium and what percentage of total calcium value does it make up?
• Ionised calcium is the active form of calcium and is usually ~ 55% of the total calcium value
What is complexed calcium and what percentage of total calcium value does it make up?
Complexed calcium is bound to anions such as bicarbonate and is usually ~ 10% of the total calcium value
What is protein bound calcium and what percentage of total calcium value does it make up?
Protein bound calcium is bound to proteins such as albumin and is usually ~ 35% of the total calcium of the total calcium value
How could hypoalbuminaemia affect calcium levels?
As circulating calcium is partly bound to albumin, if blood albumin is low
(hypoalbuminaemia) then the total calcium level may be low. However, the
physiologically active ionised calcium could still be within normal limits.
What ECG changes may be seen with hypocalcaemia?
ECG changes associated with hypocalcaemia can include • Tachycardia or bradycardia • Prolonged S-T segment • Prolonged Q-T segment • Wide T waves
Why is subcutaneous administration of calcium not advised?
Subcutaneous administration of a calcium solution is not advised as it is very irritant.
What emergency care and treatment is involved in a patient with hypocalcaemia?
Emergency care involves administering intravenous calcium (boro) gluconate (0.5- 1.5ml/kg of 10% solution) slowly over 10-20 minutes. Alternatively, an intravenous constant rate infusion of 10mg/kg/hr can be administered. ECG monitoring is advised to detect cardiac arrhythmias - if bradycardia and Q-T shortening develops the calcium infusion should be stopped and restarted at a slower rate once the arrhythmia has resolved. Pulse quality and heart rate should be monitored closely especially if ECG is not available.
Subcutaneous administration of a calcium solution is not advised as it is very irritant.
What is the dose range for calcium gluconate and time frame should it be administered over?
calcium (boro) gluconate (0.5- 1.5ml/kg of 10% solution) slowly over 10-20 minutes. Alternatively, an intravenous constant rate infusion of 10mg/kg/hr
How often should blood calcium be measured in a patient that presents with hypoglycaemia?
Blood calcium levels should be checked every 4-6 hours. Depending on the underlying cause, there is a risk of recurrence especially during the first 24 hours This is a particular risk in a bitch with eclampsia due to reduced calcium availability and depletion of calcium stores. In a bitch with eclampsia, the puppies should be weaned if possible; the nutritional status of the bitch should be reviewed and supplemental oral calcium and vitamin D should be provided.
What should be the nursing considerations in a patient with hyperaesthesia from hypocalcaemia?
As patients with hypocalcaemia are hyperaesthetic, it is important to nurse them in an environment with dimmed lighting where sudden, loud noises or other stimuli are avoided. During monitoring it is important to be aware of equipment such as ECG machines, blood pressure monitors and infusion pumps – the volume should be turned down on these items
What are the nursing considerations for a patient with hypocalcaemia?
If hypocalcaemia is secondary to other causes e.g. pancreatitis, treatment and nursing should be directed towards the primary cause. Patients with acute kidney
injury e.g. secondary to ethylene glycol toxicity will require IVFT. In oliguric/anuric patients, it is very important to monitor urine production and for signs of over infusion of fluids. Intensive nursing care and monitoring will be required in such patients e.g.
arterial blood gas analysis, blood pressure, central venous pressure etc.
A patient may develop hyperthermia secondary to panting, restlessness and seizures. The patient should be monitored closely to detect hyperthermia with
appropriate treatment and nursing care instigated if required.
It is important to encourage the patient to eat as soon as is feasible to ensure intestinal absorption of calcium.
Why is hypercalcaemia a serious condition?
Hypercalcaemia is a serious condition as it can cause acute kidney injury (AKI), previously called acute renal failure, and cardiac dysrhythmias. The most common
cause is neoplasia - hypercalcaemia of malignancy. Lymphoma, anal sac adenocarcinoma and multiple myeloma are the commonest causes of
paraneoplastic hypercalcaemia. Hypercalcaemia can also be associated with chronic renal failure, hyperparathyroidism, hypoadrenocorticism and vitamin D toxicity amongst other things. N.B. hypercalcaemia can be idiopathic in cats.
What is the most common causes of neoplastic hypercalcaemia?
The most common cause is neoplasia - hypercalcaemia of malignancy. Lymphoma, anal sac adenocarcinoma and multiple myeloma are the commonest causes of paraneoplastic hypercalcaemia
What are the main causes of hypercalcaemia?
The causes include:
1. dogs – primary hyperparathyroidism (especially Keeshonds)
2. primary hyperparathyroidism (rare in cats)
3. paraneoplastic syndrome
4. hypoadrenocorticism
5. hypervitaminosis D secondary to ingestion of cholecalciferol rodenticides or
skin creams containing vitamin d e.g. psoriasis treatment
6. excessive calcium supplementation
What body systems can hypercalcaemia affect?
Hypercalcaemia mainly affects the renal, GIT, neuromuscular and cardiovascular systems
What us the most serious problem associated hypercalcaemia?
The most serious problem caused by hypercalcaemia is acute kidney injury. Whilst cardiac dysrhythmias may be apparent on an ECG tracing,
actual cardiovascular signs are not common
What signs are associated with hypercalcaemia?
The clinical signs can be vague and non-specific. Patients are often inappetent or
anorexic and lethargic with PUPD (Boag, 2018).
Clinical signs may include1. polydipsia and polyuria
2. muscle tremors/twitching
3. vomiting
4. constipation
5. cardiac dysrhythmias
6. depression
7. lethargy
8. dental and bone pain
9. other signs may be possible if the cause is paraneoplastic syndrome e.g.
enlarged lymph nodes
10.clinical signs associated with hypoadrenocorticism e.g. waxing/waning illness; collapse etc.
What may biochemistry reveal on a patient with hypercalcaemia?
Biochemistry will show elevated serum calcium (both total calcium and ionised
calcium). If the hypercalcaemia is a result of primary hyperparathyroidism, there will
also be high circulating levels of parathyroid hormone although this could not be
measured as part of an emergency panel
What may electrolytes reveal on a patient with hypercalcaemia?
If the cause is typical hypoadrenocorticism, there will be low cortisol, hyponatraemia,
hypochloraemia and hyperkalaemia as previously discussed. The history may suggest access to rodenticide poison or ingestion of the owner’s psoriasis
medication
What may ultrasound reveal on a patient with hypercalcaemia?
Hyperparathyroid nodules may be imaged as hypoechoic areas using ultrasound.
As increased calcium levels affect the functioning of ADH, the patient may have azotaemia and decreased S.G.
What may radiography reveal on a patient with hypercalcaemia?
Radiography may demonstrate soft-tissue mineralisation including renal mineralisation. Deposition of calcium in the kidneys can cause acute kidney injury.
What treatment and nurse care should a patient with hypercalcaemia receive?
Treatment and nursing care
Persistent high circulating calcium levels will lead to acute kidney injury damage amongst other problems.
To provide the most effective treatment, the underlying cause should be identified as quickly as possible e.g. diagnose lymphoma, or hypoadrenocorticism although this can prove challenging. IVFT is the mainstay of treatment for volume expansion and to promote calciuresis.
Fluid therapy should be instituted using 0.9% sodium chloride solution – the high renal sodium levels promotes calcium diuresis. Additionally, isotonic IVFT helps to address hypovolaemia and correct of fluid deficits associated with e.g. vomiting. 0.9% NaCl is the fluid of choice as this promotes the greatest degree of calciuresis, as well as being a calcium free solution. An appropriate fluid plan should be created that allows for maintenance and replacement of any deficit. IVFT alone may be sufficient to revert to normocalcaemia. If not, however, once the dehydration and hypovolaemia is corrected, the loop diuretic furosemide may be administered IV alongside intravenous fluids to further promote calciuresis.
Careful monitoring of the patient’s fluid status must be performed to ensure it is neither under nor over infused. The patient should be weighed twice daily. Fluid balance calculations should be recorded every 6-12hrs to ensure ongoing balance is maintained.
Alongside other supportive/ decontamination treatments, a patient with vitamin D toxicity should be prevented from exposure to UV light to prevent further production of vitamin D.
Glucocorticoids will cause calciuresis but they should not be used unless a full diagnostic work-up has already been performed (or there is no plan to perform one) as conditions such as lymphoma may be missed.
Haemodialysis or peritoneal dialysis may be required in very serious cases of acute kidney injury secondary to hypercalcaemia
What fluid type and therapy is most likely indicated in a patient with hypercalcaemia and why?
Fluid therapy should be instituted using 0.9% sodium chloride solution – the high renal sodium levels promotes calcium diuresis. Additionally, isotonic IVFT helps to address hypovolaemia and correct of fluid deficits associated with e.g. vomiting. 0.9% NaCl is the fluid of choice as this promotes the greatest degree of calciuresis, as well as being a calcium free solution. An appropriate fluid plan should be created that allows for maintenance and replacement of any deficit. IVFT alone may be sufficient to revert to normocalcaemia. If not, however, once the dehydration and hypovolaemia is corrected, the loop diuretic furosemide may be administered IV alongside intravenous fluids to further promote calciuresis.
When might a dog with severe hypothyroidism present in an emergency setting?
On very rare occasions a dog with severe hypothyroidism may present with stupor or
coma – this is called myxoedema coma.
Why might a cat with hyperthyroidism present as an emergency?
A cat with hyperthyroidism may present as an emergency because of congestive,
cardiac failure, pleural effusion, hypertension related problems e.g. retinal
haemorrhage or aortic thromboembolism
State 10 main clinical signs shown by a dog presenting with an Addisonian crisis
Anorexia Lethargy Depression Vomiting Weakness Diarrhoea Trembling Collapse Polyuria Polydypsia Cold extremities Poor pulses Pale mucous membranes Increased CRT Decreased heart rate Decreased body temperature
State 6 clinical signs that could be present in a cat which has developed hypocalcaemia, following surgery to remove a thyroid mass
Muscle twitching Hyperaesthesia Stiffness Ataxia Seizures Hyperthermia Decreased blood pressure Arrhythmia Prolapse of the 3rd eyelid
Outline 6 nursing and monitoring considerations for a cat which has developed hypocalcaemia following surgery to remove a thyroid mass
Monitor closely
Quiet environment
Dimmed light
Minimal handling
Encourage eating
Monitor wound site
TPR, perfusion parameters, hydration status
Auscultate and check ECG for arrhythmias
Take samples to measure blood calcium & other electrolytes on direction N.B. review what type of sample is best **
Record activity and clinical signs
Slow IV calcium ( if directed) whilst monitoring ECG
Administer medication on vet direction e.g. oral vitamin D
List 8 main points of nursing and monitoring a dog presenting in an Addisonian crisis
Administer IVFT and medications on veterinary direction e.g. Provision of IV fluids (0.9% saline) Dexamethasone Dextrose (if required) Mineralocorticoid therapy Monitor pulse rate and strength Monitor heart rate & rhythm (ECG) Mucous membrane colour Blood pressure Blood glucose Electrolytes Urine output Avoid stress Encourage eating
List 10 clinical signs that may be present in a dog presenting with ketoacidosis
Vomiting Weakness Collapse Dullness Tachypnoea (some cases can have decreased RR) Dehydration Slow CRT Sweet smelling breath Polyuria/oliguria Polydipsia (previously but may not be drinking now) Polyphagia (previously but now anorexia) Weight loss
Urine analysis of an animal presenting with ketoacidosis may not detect ketones. Explain why this occurs.
Commercial stick tests detect acetoacetate whereas the predominant ketone may be beta hydroxybutyrate. Adding hydrogen peroxide will convert beta hydroxybutyrate to acetoacetate which will make it detectable.
Name 3 causes of hypoglycaemia in dogs or cats
Beta cell neoplasia (insulinoma) Hypoadrenocorticism Paraneoplastic syndrome Sepsis / SIRS Iatrogenic (insulin overdose)
State 2 causes of hyperglycaemia in dogs or cats
Insulin resistance / Diabetes mellitus
Stress associated
Hyperadrenocorticism
Acromegaly ( cats)
Isothenuria is the production of
Select one:
a. Small amounts of urine
b. Concentrated urine
c. Urine which is more dilute than plasma
d. Urine with the same specific gravity as that of the renal filtrate
The correct answer is: Urine with the same specific gravity as that of the renal filtrate
Insulin can be used to lower blood potassium levels because it will
Select one:
a. Drive potassium into cells
b. Prevent potassium being absorbed across the gastrointestinal tract
c. Increase the amount of potassium excreted in faeces
d. Increase the amount of potassium excreted in urine
The correct answer is: Drive potassium into cells
An animal presenting with hypokalaemia could show which of the following signs?
Select one:
a. Bradycardia & normal muscle tone
b. Normal heart rate & normal muscle tone
c. Arrhythmias & muscle weakness
d. Tachycardia & increased muscle tone
The correct answer is: Arrhythmias & muscle weakness
