Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, MI, USA
Kidney disease can be divided into two main categories: acute kidney injury (AKI) and chronic kidney disease (CKD). AKI develops over hours or days and may be a result of toxicities, sepsis or acute urinary obstruction; these are high risk anesthesia patients and should be stabilized as much as possible before sedation or anesthesia. CKD which is more commonly encountered is the focus of this discussion.
Chronic kidney disease is a structural or functional disease of one or both kidneys which has been present for an extended period of time (weeks, months or years). CKD is progressive and irreversible and currently there are no effective treatments that significantly slow the disease process. This is predominately a disease of older animals and the prevalence increases with age and is a common disease seen in veterinary practice. There may be a known underlying disease process that initiates renal damage but in most cases an inciting cause cannot be identified. There are several hallmark changes that aid in the diagnosis of CKD and staging is recommended. The International Renal Interest Society (IRIS) uses renal function tests, proteinuria and blood pressure to stage the disease in cats and dogs on a scale of 1 to 4 (www.iris-kidney.com). This approach allows for individualized treatment at each stage.
The function of the kidneys include excretion of metabolic waste products, regulation of blood volume, extracellular blood volume, acid-base balance and red blood cell production; therefore, disease can have far reaching effects. The kidneys have the ability to maintain these functions even as nephrons become damaged; azotemia does not become apparent until 60–70% of the functional kidney tissue is damaged. A dog or cat may present with no obvious clinical signs of renal disease and may have normal blood work yet have only a small percentage of functional kidney tissue left: when these patients are challenged by anesthesia they make be "tipped" over into renal failure.
Abnormalities frequently encountered in these patients include an elevated blood urea nitrogen, elevated creatinine, and hypoproteinemia. Electrolyte abnormalities may be present with potassium (high or low) being highly relevant to anesthetic management. Metabolic acidosis, hypertension, anemia and dehydration may be present and some patients may experience nausea and vomiting. Other co-morbidities, for example diabetes mellitus, may be present, and in older patients the consequences of ageing and their impact on anesthetic management must also be considered.
These patients may require anesthesia for many reasons (e.g., planned dental and orthopedic procedures or in an emergency situation such as trauma). In addition to considering the effects of anesthesia on renal function, the impact of surgery must also be appreciated; surgical stimulus results in catecholamine, renin, arginine vasopressin (AVP) and aldosterone release leading to increased renal vascular resistance and decreased renal blood flow (RBF) and glomerular filtration rate (GFR). Similar responses are elicited by pain and fear. These responses can be significantly ameliorated by low stress handling and good analgesic protocols. Laparoscopic surgery increase intra-abdominal pressure resulting in direct venous compression, decreased cardiac output and increases in renin, aldosterone and AVP sufficient to cause oliguria in human patients.1
The kidneys receive 20–25% of the cardiac output and have a high oxygen consumption rate (higher than the brain on a per gram basis). General anesthesia commonly results in decreased cardiac output, hypotension (mean arterial pressure (MAP) < 60 mm Hg or systolic arterial pressure (SAP) < 90 mm Hg); in one report 22% of dogs and 33% of cats were hypotensive during elective procedures.2 Renal blood flow and GFR are directly related; in normal healthy patients GFR is stable over a wide range of systemic blood pressure (mean arterial pressure of 80–180 mm Hg) due to renal autoregulation. However, autoregulation may be different in the face of disease and hypotension should always be addressed.
There is no single recommended anesthetic protocol for dogs and cats with CKD; each one will require an individualized approach, however, some suggestions can be made.3 Goals of anesthetic management include maintaining normotension, isovolemia and good cardiac output to maintain perfusion of vital organs.
Patients with CKD should be stabilized as much as possible prior to surgery; this is possible when the procedure is elective but even in an emergency situation spending time prior to anesthesia to correct as many abnormalities as possible is time well spent. It is important to ensure patients are adequately hydrated and this may require intravenous fluid administration. If nausea and vomiting are present these will contribute to dehydration and are very unpleasant; anti-nausea and/or anti-emetic drugs such as ondansetron or maropitant may be indicated. Normal serum potassium should be < 5.5 mEq/L and must be checked as hyperkalemia can be life threatening. Hyperkalemia causes altered cardiac excitability, automaticity and conduction and can result in cardiac arrest. If the patient is dehydrated, 0.9% saline is indicated and may be all that is required as the fluid therapy will dilute serum potassium, correct fluid deficits and cardiovascular function and enhance renal perfusion and excretion. Metabolic acidosis enhances hyperkalemia and should be corrected; this may also respond to rehydration. Regular insulin (0.5–1.0 U/kg) and dextrose (1–2 g per unit of insulin) can be used to rapidly decrease serum potassium. In an emergency 10% calcium gluconate (0.5–1.0 mg/kg IV) can be given to protect the heart until other measures are put in place to decrease serum potassium.
If anemia is present it is usually long standing and well tolerated; however, if bleeding is expected and the hematocrit is < 20% or Hb is < 7 g/dl transfusion should be considered. Pre-oxygenation via face mask is recommended.4
Decreasing stress, fear and pain are important and can be achieved with sedatives, tranquillizers, analgesics and low stress handling techniques.
A baseline blood pressure should be measured prior to anesthesia; CKD patients may be hypertensive and renal autoregulation may be altered (shifted to a higher range); in these patients a drop in blood pressure that would be tolerated by healthy patients may result in a significant decrease in RBF.
Acepromazine can be used if hypovolemia has been corrected. Low doses (0.01–0.03 mg/kg) and usually adequate and avoid the potential hypotension secondary to vasodilation seen with higher doses. There is some data in dogs suggesting acepromazine may offer renal protection.5 Alpha-2 adrenergic agents should be avoided as their effects on the kidney are unpredictable.6 Benzodiazepines (diazepam and midazolam) have minimal renal and cardiovascular effects; however, their effects are unpredictable and some animals become excited. Benzodiazepines are idea for co-administration at induction to reduce the dose of induction agent. Opioids should be incorporated and even for non-painful diagnostic procedures they are valuable because of their sedating properties, minimal cardiovascular effects and anesthetic sparing effects.
Injectable induction agents should be used; mask induction with inhalant agents is stressful and also requires a "large dose" which will cause cardiovascular depression. Propofol and alfaxalone are good choices but ketamine should be avoided as it will stimulate sympathetic activity. The dose of induction agent will be decreased if co-administered with a benzodiazepine.
Although isoflurane is less metabolized that sevoflurane this is a theoretical advantage. Anesthetic sparing techniques should be used (e.g., opioids, local anesthetic blocks) to minimize their effects.
Intraoperative use of "low dose dopamine" infusion is no longer advocated and has not been shown to provide renal protection; however, inotropes may be used to support cardiac output. Some CKD patients may benefit from mannitol induced diuresis;3,6 and suggested doses are 0.5–1.0 g/kg over 20 minutes.
Intraoperative monitoring is routine but should focus on blood pressure and if hyperkalemia is a concern the ECG should be closely monitored.
Chronic kidney disease patients may be challenging to anesthetize but with careful planning they can be well managed without further renal insult if the pathophysiology of the disease and the effects of anesthetic drugs on the kidney are understood.
References
1. Morgan G, Mikhali M, Murray M. Renal physiology and anesthesia. In: Morgan G, Mikhail M, Murray M, eds. Clinical Anesthesia. 4th ed. Columbus, OH: McGraw-Hill Medical; 2005:662–78.
2. Gordon AM, Wagner AE. Anesthesia-related hypotension in small animal practice. Vet Med. 2006;101(1):22–26.
3. Bednarski R, Grimm K, Harvey R, et al. AAHA anesthesia guidelines for dogs and cats. J Am Anim Hosp Assoc. 2011;47(6):377–385.
4. McNally EM, Robertson SA, Pablo LS. Comparison of time to desaturation between preoxygenated and nonpreoxygenated dogs following sedation with acepromazine maleate and morphine and induction of anesthesia with propofol. Am J Vet Res. 2009;70(11):1333–1338.
5. Boström I, Nyman G, Kampa N, Häggström J, Lord P. Effects of acepromazine on renal function in anesthetized dogs. Am J Vet Res. 2003;64(5):590–598.
6. Schroeder C. Renal disease. In: Snyder L, Johnson R, eds. Canine and Feline Anesthesia and Co-existing Disease. Ames, Iowa: Wiley-Blackwell; 2015:116–28.