Hi, so my name's Becky Robinson. I'm an anaesthetist working at Davies's Veterinary Specialists. And in today's webinar we're gonna be discussing anaesthesia for patients with diabetes mellitus.
We're gonna start by talking a little bit about normal physiology and the pathophysiology of diabetes mellitus, because this background information is really important in order for us to fully understand the principles behind the anaesthetic management of these patients. We'll then go on to cover some of the specifics, including potential perianesthetic problems and anaesthetic management of the diabetic animal. So as our companion animal species are living longer, we're seeing a growing number of patients presenting for anaesthesia with concurrent disease, including endocrinopathies like diabetes mellitus.
Very often, the reason for presentation is unrelated to the chronic endocrinopathy with which the animal is also living with. Regardless, such concurrent diseases will have an impact on the necessary anaesthetic management. The approach to such cases will depend upon what the presenting complaint is and the urgency of treatment weighed up against the stability of any underlying disease.
In an ideal situation, treatment for endocrinopathy such as diabetes should be initiated before surgery and anaesthesia to hopefully improve function and decrease the likelihood of morbidity. However, however, obviously in emergency situations, this may not be possible. There is often interaction between the endocrine and the autonomic nervous system, with many of the activities being coordinated in the hypothalamus.
This interaction is most notable with the hypothalamic pituitary, adrenal or HPA axis, which plays a vital role in the stress response. The stress response is the name given to the hormonal and metabolic changes which follow injury or trauma. And it can be triggered by many things, including tissue trauma itself, hypothermia, acidosis, hypoxia, hypertension, nociception, disease, or long-term restraint.
The stress response is characterised by increased secretion of pituitary hormones and activation of the sympathetic nervous system. Overall metabolic effects include metabolism with salt and water retention to maintain fluid volume and cardiovascular homeostasis. Activation of the sympathetic nervous system results in typical cardiovascular effects, including tachycardia and hypertension, along with modification of other organ functions, including liver, pancreas and kidney.
This stress response is essential in the perianesthetic period, as its function is to preserve or restore homeostasis. As cortisol plays a critical role in the stress response, any disease affecting its production can also affect the stress response and lead to increased morbidity. This is most typically seen in patients with hypoadrenal corticism or Addison's disease.
An inappropriate stress response can result in significantly increased patient morbidity in the post-anesthetic period. Despite this, while the stress response allows injured animals to survive by catabolizing their own stored body fuels, it has been argued that the response is unnecessary in current surgical practise. Efforts are therefore often made to modify and minimise the stress response during anaesthesia and surgery in order to improve postoperative outcome, reducing recovery times and improving overall patient experience.
This can be achieved in a variety of ways, including use of analgesic agents such as opioids and alphatagonists, and utilising techniques that include the use of local anaesthetics. Local anaesthetic techniques in particular, reduce thromboembolic events, improve pulmonary and gastrointestinal function, and also can reduce cardiovascular complications. Ensuring optimal perianesthetic technique, including measurement and monitoring of body temperature, blood pressure and oxygen saturation levels, combined with good surgical technique is also likely to minimise the negative aspects of the stress response and improve post-operative recoveries.
Modification of the stress response can be particularly relevant for patients with diabetes. As we've seen, the stress response is associated with secretion of catecholamines. Cortisol, growth hormones and sometimes glucagon.
All of these hormones have hyperglycemic effects. In effect, they are anti-insulin. While this may theoretically mean that insulin requirement is increased in the perioperative period, in reality, glucose and insulin requirements are often unpredictable, and so close monitoring is required.
Moving on now to think a little bit about normal insulin physiology and what can happen when things go wrong. We need to start with the pancreas. As we know, the pancreas is a combined exocrine and endocrine gland.
The exocrine portion of the pancreas is involved indigestion and won't be considered any further. The endocrine cells of the pancreas are concentrated in the islets of Langhans, scattered throughout the pancreas. Within the islets of Langerhans, there are two types of cells.
We have the alpha cells which produce glucagon and contribute to about 60 to 70% of the islet cells. And we have the beta cells which produce insulin and contribute to around 20 to 25% of the islet cells. Endocrinopathies involving the pancreas primarily involve insulin production or the lack of response in the body to insulin.
Insulin is the body's most important anabolic signal, while glucagon has a catabolic effect. The two hormones are antagonistic to each other and are responsible for maintaining. Containing normal blood glucose by feedback mechanisms that we can see in this diagram.
Diabetes mellitus is not a single disease, but it is a syndrome which is characterised by a hypoglycemia, which results from either defects in insulin secretion, which is known as type 1, or insulin sensitivity in target tissue known as type 2, or a combination of the two. Diabetes mellitus is relatively common in veterinary medicine, with an estimated annual prevalence of between 0.26% and 0.36% in dogs, and about 0.58% in.
Cats. It is often considered that type 1 diabetes is more common in dogs and type 2 more common in cats, although this broad classification is now thought to be a little bit too simplistic. Regardless of the underlying classification in diabetes, the patient loses the ability to regulate their blood glucose concentration adequately because of a functional lack of insulin.
Insulin is an anabolic hormone with a short elimination half-life of about 5 minutes. While insulin has multiple physiological functions that we can see on this slide, clinical signs of diabetes occur due to the inability of the cells to utilise carbohydrates and the resulting hyperglycemia. And the clinical signs can therefore include polyuria and polydipsia.
Weight loss with an increased appetite and lethargy. When the blood glucose is above the renal threshold for reabsorption of glucose, which happens around 12 to 14 millimo per litre, glucose is lost in the urine, which results in a cricosuria. This causes an osmotic diuresis and is responsible for the polyuria.
Polydipsia occurs to try and maintain fluid balance, but patient dehydration and hyper osmolarity often still occur. Potassium and sodium are also lost as a result of the diuresis and to compensate for hyper osmolarity, respectively. This can therefore result in hypokalemia and hyponatremia.
Weight loss occurs due to a lack of intracellular glucose uptake and muscle wastage, while the intracellular hypoglycemia causes the increased appetite. Other signs which may occur include cataract formation in dogs and peripheral neuropathies which can cause a plan degrade posture in cats. Typical laboratory findings in a patient with diabetes mellitus include hyperglycemia, which may be extreme, especially if dehydration is present.
Elevated liver enzyme activity, increased cholesterol levels, increased triglycerides, and increased urea and creatinine concentrations, which is often pre-renal due to con concurrent dehydration. Ultimately, the chronic hyperglycemia can lead to damage and dysfunction of multiple organs, including the kidney, eye, autonomic nervous system, heart and vasculature, if it's left untreated. Where the diabetes has been left untreated for a prolonged period, or the hyperglycemia is particularly severe, diabetic ketoacidosis, also known as DKA, or hyper osmola syndrome can occur.
Such animals often present in a more critical condition with clinical signs including vomiting, anorexia, severe dehydration with or without hypovolemia. Depression or coma, a metabolic acidosis with hyperglycemia and electrolyte disturbances. Patients presenting in such a manner often require hospitalisation and critical care, including fluid therapy, intensive insulin management, possibly with infusions of neutral insulin, and extensive monitoring of glucose, electrolytes and acid-based status.
The management of such patients is beyond the scope of this talk. However, what I will say is that animals with DKA are not considered good candidates for anaesthesia and will require aggressive stabilisation before consideration of any procedure which may require sedation or anaesthesia. When we start thinking about an anaesthetic approach to these patients, as with any anaesthetic, if a logical, systematic approach is taken to every case requiring anaesthesia, problems are more likely to be identified, prepared for, and hopefully averted.
One example of such an approach is to firstly identify a patient's signalment and their pertinent history with presenting complaint. Perform a thorough clinical examination and if appropriate clinical investigations. Identify any potential problems.
Perform pre-anesthetic stabilisation if it's required, and then go on to consider our anaesthetic plan, taking all of this information into account. When presented with a compromised patient, most people are primarily focused on what is either the best or the safest drug protocol to use. However, while it is important to have an understanding of potential suitable.
Or protocols for particular scenarios such as the diabetic patient, there is never a single correct recipe that can be used. Rather drug choice is actually a relatively small aspect of what it results in a positive outcome. Selection of an anaesthetic technique should be based on understanding of the physiology and consequences of the individual patient's disease or injury, which is why we've covered some of the, the basic physiology and path.
With physiology in the previous slides. Knowledge of the specific drug pharmacology and effects, and also a personal familiarity with the technique. When dealing with a diabetic patient, clinicians must not forget the potential problems or risks associated with the individual procedure they're about to undergo.
However, in addition to these, there are a number of immediate specific periopererative problems which the diabetic patient faces. This can include the surgical induction of the stress response with catabolic hormone secretion. As we've already said, surgery will evoke the stress response.
This is associated with the secretion of catecholamines, cortisol, growth hormones, and as we said, sometimes glucagon. We know that these hormones all have hypoglycemic effects, and as we said, they can be in effect anti-insulin. The result is that gluconeogenesis is stimulated and peripheral glucose uptake decreased.
So this can impact on the patient's insulin requirement and blood glucose levels throughout the perianesthetic period. There will be inevitably an interruption in the patient's food intake because patients do tend to be fasted for an anaesthetic, which can lead to a period of hypoglycemia. This is especially true if the patient receives all or part of their insulin dose prior to the anaesthetic or if patients are receiving longer acting insulin.
The altered consciousness associated with sedation and anaesthesia can mask the symptoms of hyperglycemia and it therefore results in the need for frequent blood glucose measurements in our diabetic patients. There can be circulatory disturbances associated with anaesthesia and surgery, for example, hypertension and haemorrhage, which may alter the absorption of any administered subcutaneous insulin. And then post-operative wound healing infections can also be influenced by the adequacy of perioperative glycemic control.
Rather than maintaining a perfect glucose balance in the perioperative period, which is almost impossible even in the well control patient, it is probably more important to try and avoid extremes of glucose values, whether that be hypo or hyperglycemia. Unstable diabetic patients should have every effort made to stabilise their disease prior to any elective procedures. Patients with unregulated diabetes can have marked fluctuations of blood glucose concentrations and insulin administration prior to anaesthesia, which can result in unpredictable perioperative blood glucose concentrations.
Should also be noted that glucose control can be influenced by underlying concurrent pathology. Bacterial infections, including notably of the urinary tract and skin, or inflammation, for example, with concurrent dental disease or pancreatitis can induce a degree of insulin resistance and influence glucose homeostasis in a previously well-controlled patient. Such conditions may need to be addressed before adequate control can be gained.
An evaluation of how stable the animal's disease is can be made using a variety of different tools, including taking a full clinical history. For example, the presence of PUPD, polyphagia and weight loss can indicate poor control. Performing, performing a full clinical examination, including assessment of the patient's hydration.
Status. Evaluation of blood fructosamine concentration, measurement of detectable ketonuria or ketonemia. And if ketonuria and ketonemia are present, potentially assessment of an acid-based status.
It is generally recommended that routine haematology, biochemistry and neuroanalysis is performed prior to anaesthesia of the diabetic patient, if there are no recent assessments. Alternatively, a minimum database, including PCV total protein, blood glucose, urea and creatinine with electrolytes is suggested as an absolute minimum. Urinalysis should be performed to determine for the presence of glycosuria or ketonuria.
If it is not possible to obtain a urine sample, handheld monitors to determine blood ketone levels are available. With uncontrolled diabetes, skeletal and cardiac muscle cells are deprived of glucose as an energy source. To provide an alternative energy source, the liver starts to produce ketones from free fatty acids.
While this can be life saving, ketone bodies are acidic, which is what in part can lead to the clinical signs associated with DKA. A patient may not show clinical signs associated with DKA but still have low level production of ketone bodies. This indicates less than adequate control of the diabetes, and it is recommended to test for their presence prior to anaesthesia.
These ketone bodies can either be detected on commercially available urinalysis sticks or handheld blood machines. Unfortunately, the commercially available urinalysis sticks are not sensitive to beta hydroxybutyrate, only acetoaccetate and acetone. Beta hydroxybuyrate is the main ketone produced in cats, and it is also the ketone associated with the severity of ketoacidosis.
Therefore, this simple test is only effective for dogs. It should also be remembered that ketonuria can be seen as a result of prolonged starvation, not simply uncontrolled diabetes. If ketonuria or ketonemia is present, it is recommended that the patient receives intravenous fluid therapy prior to anaesthesia.
If possible, it is also suggested to perform a venous blood gas analysis to determine the acid base status of the patient. While it is often acceptable to anaesthetize a patient who is ketotic, providing adequate preoperative sterilisation has been performed. If a patient is ketoacidotic, that is their pH is less than 7.35, it is recommended to delay anaesthesia until this has been corrected.
Fructosamine is a glycosylated protein, which is formed by non. Somatic, irreversible binding of glucose to serum proteins, mainly albumin. The rate of formation is proportional to the average blood glucose level.
Therefore, the higher the mean blood glucose level is over time, the greater the fructosamine concentration. It therefore reflects glycemic control over the previous 1 to 2 weeks. While this does tend to give a more reliable indicator of glycemic control compared to spot glucose checks.
And therefore can provide useful information prior to anaesthesia. Well-controlled diabetics can have elevated levels, and uncontrolled diabetic animals can have normal levels. This is particularly true in cats, where fructosamine concentrations are often unchanged until the blood glucose concentration constantly exceeds 20 milli per litre.
And it can also be influenced by stress hyperglycemia. Therefore, assessment of fructosamine concentrations should be done only as part of a complete assessment of the patient. Where patients are hyperglycemic, particular attention needs to be paid to a patient's hydration status.
The automatic diuresis which occurs when blood glucose levels are more than 12 to 14 milli per litre can lead to dehydration and may influence the stability of intraoperative blood pressure. Provision of fluid therapy prior to anaesthesia may be required to correct any pre-existing dehydration, with the amount and rate of fluid administration being determined by the degree of dehydration and hyperglycemia. Fluid therapy is then often continued throughout the perianesthetic period.
A balanced isotonic crystallo solution such as Hartmann's solution is usually suitable, although depending upon the patient's serum potassium level, supplementation with potassium chloride may also be indicated. Care should be taken, however, not to use potassium supplemented fluids during anaesthesia where fluid boluss may be required. Procedures which require sedation or anaesthesia do need to be timed carefully in a diabetic patient.
It is generally recommended that anaesthesia is scheduled for first thing in the morning. This will reduce the need for a prolonged period of fasting and will allow the patient to resume a normal routine as soon as possible. It also likely allows a longer period of monitoring within the hospital environment prior to discharge.
If this is not possible, an alternative is to perform procedures in the afternoon. This allows a patient to receive their normal feed and insulin in the morning before undertaking an adequate period of fasting, usually between 4 to 6 hours following the morning feed before anaesthesia commences. Controlled diab patients rely on regular meals timed with the insulin administration.
It is therefore important that an accurate history is gained from the owner to enable clinicians to understand the normal feeding times and dosing schedule of insulin for that individual. This routine is obviously disrupted with pre-anesthetic fasting. A period of pre-anesthetic fasting is recommended to decrease the amount of food and liquid in the stomach, thus hopefully reducing the risk of vomiting or regurgitating in the perioperative period.
And therefore they should also help reduce the aspiration risk. This recommendation still holds true for diabetic patients, despite their needs for regular meals. There are numerous recommendations as to how to manage pre-anesthetic dose of insulin and subsequent glucose, although very little evidence to support one methodology over another.
Most suggestions rely on measurement of a spot blood glucose on the morning of surgery, with subsequent insulin dosing being tailored to the patient based upon its result. One canine study comparing administration of either 25% or 100% of the patient's insulin dose the morning of anaesthesia found that both regimes resulted in unpredictable blood glucose concentrations, neither resulting in glycaemic values within an acceptable range. A more recent study compared 4 groups.
Firstly, 12 hours fasting with insulin at half of its normal dose. Then 6 hours of fasting with a half insulin dose. Thirdly, 12 hours fasting with a full insulin dose, and finally 12 hours fasting with no insulin administered.
This study found no difference between baseline blood glucose and intraoperative values in all groups apart from the group which received no insulin. In this group, there was a significant increase of intraoperative blood glucose concentration compared to baseline. This suggests that in diabetic patients who are hypoglycemic on the day of surgery, they may benefit from administration of insulin rather than withholding it.
One example of a suggested pre-anesthetic insulin protocol which I commonly use is illustrated in the table on this slide and is based upon a spot blood glucose measurement taken the morning of anaesthesia. This is based on the assumption that the patient will be undergoing anaesthesia as the first patient on the surgical list. During anaesthesia, fluctuations in blood glucose can occur as a result of a number of things including efficacy of medical management, degree of patient stress response, disruption of feeding and exercise pattern, changes in basal metabolism, type and complexity of surgery, any perioperative medications which may have been administered.
And the presence of infection. Therefore, it is generally recommended that blood glucose is monitored regularly in the perioperative period in diabetic patients, usually every 30 to 60 minutes. The frequency of monitoring does to some extent depend upon the initial value and how well controlled the condition is.
The main concern for clinicians is the avoidance of hypoglycemia, especially as the clinical signs will likely be masked by sedative and anaesthetic agents. In the human field in the past, it was typically seen as acceptable to have a mild permissive hyperglycemia. However, in recent times this has fallen out of favour as the use of bedside monitors have improved ease of monitoring and severe hyperglycemia is potentially associated with a worse outcome and good glycaemic control seeming to improve the short-term outcome.
In veterinary medicine, there is not much evidence as to whether hyperglycemia should be avoided as strictly as it is in humans. The optimal target blood glucose during anaesthesia has not been defined. In the absence of this evidence, as we've said before, it is probably reasonable to assume that avoidance of extremes of hypo or hypoglycemia, while trying to maintain a blood glucose in a range which is considered normal for that individual, seems sensible.
Handheld glucometers designed for medical use can be inaccurate in veterinary medicine, particularly at the low end of the scale, which can equate to a value of 20 to 40% or 1 to 2 millimoles per litre, lower than the actual blood glucose concentration. Veterinary specific glucometers are now available, with the most widely available in the UK being the Alpha track. These have been calibrated and validated for use on dogs and cats.
It is recommended to use veterinary specific monitors where possible. But despite this, regardless of the monitor used, it is important to ensure that the same glucometer is used for measurements on a single patient to ensure consistency. If documented, treatment for hypoglycemia, that is where the blood glucose level is equal to or below 3.5 milli per litre, should be instigated promptly.
This is usually achieved via an infusion of a dextrose solution, either usually at a 2.5% or 5% concentration, a starting rate of 2 mL per kilogramme per hour. The concentration and infusion rate can then be tailored to the individual based upon their response to treatment.
Using concentrations of dextrose higher than 5% are not recommended, especially if they are to be administered via a peripheral vein, as the hyper osmolarity of the solution can result in phlebitis. Infusions should be stopped or at least reduced when the blood glucose reaches approximately 140 millimo per litre and 16.5 millimo per litre in dogs and cats respectively.
Because at this level, glycosuria and osmotic diuresis will occur. Dextrose infusions may have to be continued into the recovery period if the animal does not eat and return to its normal. Or feeding an insulin regime promptly.
Treatment of documented hyperglycemia may not be required. Depending upon the degree of any documented hyperglycemia, clinicians may opt to treat this perioperatively with either short acting IV or IM neutral insulin, or with a proportion of the patient's own longer acting insulin. However, while permissive hyperglycemia is likely not to be ideal, the metabolic consequences of such hyperglycemia in cats and dogs generally are slow in onset and offset.
Therefore, providing that there are no other major metabolic derangements in the patient, especially if some insulin has been administered prior to starting the procedure, it is unlikely that complications will occur in such a short period of time. Thinking now specifically about what anaesthetic protocol to use for these patients. Many clinicians tend to become very focused on what anaesthetic protocol is best.
As you said, this is particularly true for patients with concurrent disease. However, as has hopefully been suggested above and on the previous slides, the assessment, management, and stabilisation of the patient. Along with preparation, are more important than the specific drugs which should be used.
Use of specific anaesthetic agents is probably of less importance compared to avoiding any stress response inducing factors, including pain, hypertension, hypoxemia, hypothermia, hypercapnia, and inadequate levels of anaesthesia. Having said this, there are some general guidelines for anaesthetic agent choice. It is often advised that short acting anaesthetic agents are used for diabetic patients in order to allow a rapid recovery and resumption of eating on recovery.
Additionally, some anaesthetic agents are known to have an effect on glucose homeostasis, either in a positive or a negative manner. The best example of this is the alpha 2 agonists, which are known to antagonise insulin secretion, resulting in an increased blood glucose concentration. Other agents such as ketamine are known to increase sympathetic tone, and it's therefore probably wise to avoid use of these agents in diabetic patients.
Conversely, use of opioid analgesia can help produce not only hemodynamic but also hormonal and metabolic stability. This is achieved through blockade of the sympathetic nervous system and HPA access, which can help abolish the hyperglycemia seen in normal patients and may be of benefit in the diabetic patient. Similarly, use of local anaesthetic techniques are also shown to reduce the perioperative stress response with similar metabolic effects.
Gold standard perianesthetic care should be provided throughout. Key considerations include management of patient temperature and analgesia. This should continue into the recovery period, including, most importantly, performing regular pain assessments with analgesic treatment as required.
This is particularly crucial for diabetic patients as we wish for them to have a rapid recovery, to allow a prompt return to a normal feeding and insulin regime. Close monitoring of the diabetic patient is advocated, with standard anaesthetic monitoring tools used. Of particular importance is blood pressure monitoring.
Although diabetes is a risk factor for hypertension in dogs, but not cats, it has actually been shown that during anaesthesia, diabetic dogs are more likely to become hypotensive than non-diabetic dogs. This is thought to be due to hypovolemia, secondary to hyperglycemia induced osmotic diuresis. It highlights the need to consider pre and perianesthetic fluid therapy alongside careful blood pressure monitoring to allow any hypertension to be documented and treated promptly.
We've already mentioned that diabetic patients have an increased risk of infections. Therefore, while not strictly to do with anaesthesia, we do need to be considerate of the fact that strict aseptic techniques should be performed in the perianesthetic period, with consideration of appropriate perioperative antimicrobial therapy for any invasive procedures. Once a diabetic patient recovers from anaesthesia, it is recommended to feed a small amount of food as soon as is practical.
This is especially important if the patient has not eaten for a prolonged period of time and has received all or part of their insulin dose. It is sensible to continue regular monitoring of blood glucose until the time that the patient eats, although the frequency of monitoring is generally reduced. I usually suggest monitoring blood glucose every 2 hours in the recovery period until the patient eats.
The overall goal is to return the patient to their normal feeding and insulin dosing schedule as soon as is possible following anaesthesia. For example, if a patient undergoes a procedure in the morning, is then fed a small meal on recovery, they should return to their normal routine that evening. Hopefully this webinar has provided you with an overview and the basics for anaesthetic management of the diabetic patient.
Anaesthesia of any patient with an endocrine disease such as diabetes mellitus should focus on medical stabilisation of the condition, where possible, prior to commencing. All comorbidities should be considered with their underlying pathophysiology alongside the patient requirements for the specific procedure for which they are to undergo. This will hopefully ensure a minimal impact of the anaesthesia on the underlying patient condition.
Using a basic gold standard anaesthetic approach, ensuring provision of appropriate analgesia should help the patient to recover and return to normal function as quickly as possible.