Answering your questions: Sedating and anesthetizing patients that have organ system dysfunction


Answering your questions: Sedating and anesthetizing patients that have organ system dysfunction

What agents and monitoring devices might be better in these patients? This anesthesiologist tells you how to handle common situations.
Jul 01, 2005

Q: Based on the results of physical examination and routine screening tests, what constitutes dysfunction of such severity to warrant a change in routine sedation or anesthetic protocols?

Preanesthetic evaluations can reduce morbidity by alerting a clinician to take action to optimize a patient's preoperative status and perioperative management. In my opinion, preanesthetic evaluations should initially include only a thorough history and physical examination. When abnormalities are found in the history and during the physical examination, additional diagnostic tests should be performed to confirm and measure these findings. When no abnormalities are identified in the history or during physical examination and a complete blood count, serum chemistry profile, and urinalysis are nevertheless performed, the likelihood of obtaining an abnormal test result is high, but I think the clinical relevance of an abnormal result under these circumstances is questionable.1 We get into trouble if we make erroneous laboratory results the problem.

For example, a threefold increase in liver enzyme activity on a serum chemistry profile may suggest that something (e.g. trauma, inflammation) has caused enzymes to leak out of liver cells; however, this does not tell us much about liver function or the liver's ability to metabolize anesthetic agents. Without supporting evidence, I probably wouldn't change my anesthetic protocol.

However, the decision to alter my protocol is obvious if I am already looking for changes in liver function based on the patient's history and physical examination findings, and the tests reveal decreased albumin and blood urea nitrogen concentrations. Such abnormalities suggest decreased liver function.

Another situation that requires a change in anesthetic management would be any elevation in the serum creatinine concentration. If it is determined that renal azotemia is present, we know that well over half of kidney function is gone. Measures I would take in response include

  • Eliminating any prerenal azotemia component and electrolyte abnormalities (e.g. potassium) before anesthesia
  • Maintaining a diuresis throughout the perioperative period by using a higher fluid administration rate (15 to 20 ml/kg/hr) and monitoring urine output (oliguria is less than 1 to 2 ml/kg/hr)
  • Monitoring anesthetic depth more closely and making appropriate changes more frequently to avoid excessive anesthetic agent administration.

With regard to changes in the use of specific anesthetic agents, ketamine is generally avoided in cats with renal disease since recovery may be unnecessarily prolonged because of decreased renal elimination. I also avoid alpha2 agonists, such as xylazine and medetomidine, in any patient with systemic disease, as cautioned by their labels. Dramatic changes in oxygen delivery to the tissues can occur in healthy patients after administering alpha2 agonists,2-5 and compromised patients should not be challenged when alternatives are available. Instead, I premedicate with opioids intravenously so I can avoid tranquilizers, decrease my induction agent dosages, and decrease vaporizer settings intraoperatively.

Any hepatic, renal, cardiovascular, pulmonary, or central nervous system dysfunction in a patient should elicit a proportional response when making decisions about the patient's anesthetic management. If I can reasonably use a measure that may improve preoperative patient status and perioperative management, I should take that measure.

Q: Is intravenous induction safer than mask induction in dogs or cats with cardiac or respiratory disease?

The concentrations of inhalant anesthetics required for mask induction cause cardiorespiratory depression (i.e. peripheral vasodilation, hypercapnia) similar to or greater than that associated with most intravenous induction agents. Moreover, mask inductions are usually more expensive than injectable inductions, and environmental pollution is unavoidable.

Perceived advantages of mask inductions include the following:

  • Inhalation anesthetics can be easily eliminated from the body with ventilation; they are not nearly as dependent on redistribution and metabolism for recovery as most injectables are.
  • The change in anesthetic depth is typically gradual compared with boluses of intravenous induction agents, giving the patient time to compensate for cardiovascular changes.
  • Intravenous access is not required (though it is ideal before any anesthetic induction).

I have switched from intravenous to mask induction when the premedication effect was much greater than I expected. In this situation, mask induction is possible by using vaporizer settings no higher than 1% isoflurane or 2.5% sevoflurane.