A 54-year old 60 kg woman is to undergo cervical laminectomy in the sitting position for osteoarthritic disease. She has an 80-pack year history of smoking cigarettes, and has been diabetic for fifteen years. Chronic medications include aspirin and chlorpropamide (Diabinese). Blood pressure is 140/80 mmHg, pulse is 76, respirations are 14, temperature is 37 degrees centigrade, and hemoglobin is 11gm/dl.
I. Pulmonary function
1. What is the significance of her smoking history to her anesthetic care?
2. Are pulmonary function tests required preoperatively? Why or why not?
3. You want these tests. Which would you expect to provide anesthetically relevant information? Explain.
4. Could preoperative pulmonary therapy make a difference for her? Explain.
1. Should this patient receive preoperative insulin on the morning of surgery?
2. How do you decide?
If she is noninsulin-dependent, and under good control, she is less likely to be metabolically unstable and have end-organ dysfunction. Those with a long history of poorly controlled diabetes, with complications like ketoacidosis, are more likely to arrive with an uncontrolled glucose requiring insulin preoperatively. . 3. What sequelae of diabetes might this patient have that would directly influence your anesthetic plan?
Pertinent sequelae of diabetes include evidence of coronary disease, hypertension, autonomic neuropathy, renal dysfunction, cardiomyopathy, gastroparesis, and atlanto-occipital dysfunction with decreased ability to extend the neck. Metabolic abnormalities include hypo- or hyperglycemia, hyperkalemia, ketoacidosis, and hypovolemia.
4. Can you evaluate these issues on the night before surgery?
Preoperative laboratories include glucose, electrolytes, blood urea nitrogen, creatinine, urinalysis, and electrocardiogram. If abnormalities are found, an arterial blood gas, ketones, osmolarity, calcium, phosphorus, and magnesium.
1. What is the mechanism for aspirin and nonsteroidal anti-inflammatory drugs' anticoagulation effects?
Aspirin inhibit platelet cyclooxygenase, impeding thromboxane A2 and platelet aggregation. The effect begins at about two hours after oral dose, and lasts for the life of the platelet, about seven to ten days. Nonsteroidals have a similar effect, but it lasts for only one to three days.
1. Would and end-tidal CO2 monitor and pulse oximetry obviate the need for an arterial catheter? Why or why not?
2. The patient has inadequate brachial and external jugular veins, so you attempt to insert a right atrial catheter via the internal jugular veins, but you are unable to pass the catheter on either side. Would you proceed with the case without a right atrial line?
II. Anesthetic induction
1. Is preoxygenation indicated in this patient? Why or why not?
2. Is it required in all patients?
Preoxygenation is important for all patients undergoing general anesthesia. Delivery of 100% oxygen denitrogenates the lungs, filling the functional residual capacity of the lungs with oxygen instead of nitrogen. This allows a period of time, about three to five minutes, for which the patient will not desaturate.
3. Would you choose midazolam for induction? Why or why not?
4. How do benzodiazepines cause amnesia?
They act on postsynaptic neurons, the receptor sites of which have two alpha and two beta subunits. Benzodiazepines bind the alpha subunits, and gamma-amino butyric acid, or GABA, an inhibitory neurotransmitter, binds the beta subunits. When benzodiazepines bind to their sites, it enhances the binding of GABA. Once GABA occupies its site, there is an influx of chloride ions into the neuron, causing hyperpolarization and inhibition.
5. Compare thiopental with midazolam induction.
Effects of thiopental: Effects of midazolam include anterograde amnesia, sedation, antiseizure effects, and unconsciousness and respiratory depression in high doses. There are no analgesic effects.
6. What are some differences between midazolam, diazepam, and lorazepam?
Midazolam is the most lipid soluble, therefore has the fastest onset. Lorazepam is the least lipid soluble, and has a slow onset and a long duration of action. Diazepam has two active metabolites that can produce sedation up to eight hours after dosage.
7. How do these drugs differ in their amnestic properties?
Lorazepam is a stronger amnestic agent that diazepam, and midazolam is also a strong amnestic, although it has a shorter duration than lorazepam.
8. How are benzodiazepines metabolized?
The liver metabolizes these drugs, through glucuronidation or oxidation, so its metabolism can be impaired in the elderly, and in those with liver disease. Diazepam has two active metabolites, lorazepam has none, and midazolam has one metabolite with minimal effects.
9. Name clinical uses of midazolam.
Preoperative sedation, intravenous sedation, induction and maintenance of anesthesia, and antiseizure effects.
9. The patient cannot extend her neck at the preoperative interview. What is your plan for airway management?
III. Anesthetic maintenance
1. What drugs would you use for maintenance if the surgeon requests induced hypotension? Explain your rationale.
2. Is nitrous oxide contraindicated in this case? Why or why not?
3. Would you use a muscle relaxant? Why or why not?
4. Would curare be your choice for relaxant? Why or why not?
5. You decide not to use curare. What will you use? Explain your rationale.
1. During induced hypotension to a mean arterial pressure of 65 mmHg, the pressure suddenly decreases to a mean arterial pressure of 40mmHg. What is your differential diagnosis?
2. The end-tidal CO2 also decreases. What is your differential diagnosis?
3. What is your treatment if air embolism is diagnosed?
1. During the case, the oxygen saturation falls from 99% to 95%. What is your interpretation?
2. What is your differential diagnosis?
3. What is your management?
1. In the recovery room, urine output is 10 ml/hr for two hours. What is your differential diagnosis?
2. Is "low-dose" dopamine a good first choice for treatment?
3. Explain dose-specific receptor affinity, and give an example.
Dose-specific receptor affinity refers to different concentrations of a drug resulting in a different receptor affinity. Dopamine and epinephrine are examples. Dopamine has dopaminergic effects below an infusion rate of 3 mcg/kg/min, has beta-1 effects between 3-10 mcg/kg/min, and alpha-1 effects at more than 10 mcg/kg/min. Epinephrine has beta-2 effects below 2 mcg/min, mixed alpha, beta-1 and beta-2 effects between 2-10 mcg/min, and alpha-1 effects above 10 mcg/min.
3. How would you manage?
II. Failure to awaken
1. Four hours after discontinuing a volatile anesthetic, the patient is still unresponsive. The pupils are small and central, and she has bilateral extensor plantar reflexes. Is this a cause for concern? Why or why not?
2. What is your differential diagnosis?
3. What is your management?