A 59-year old 70 kg man with Parkinson's disease and rheumatoid arthritis is scheduled for total hip replacement. He takes aspirin, prednisone, and L-dopa chronically. Blood pressure is 170/95 mmHg, pulse is 82 bpm, temperature is 37 degrees centigrade, hemoglobin is 9.4, and fasting blood sugar is 180 mg/dl.
I. Rheumatoid arthritis
1. What special anesthetic problems are anticipated in patients with rheumatoid arthritis?
II. Drug therapy
1. How does L-dopa medication influence anesthetic management?
2. Should it be discontinued preoperatively?
3. What is the significance of his aspirin and steroid medication?
4. Should he receive preoperative steroids?
5. Why is his fasting blood sugar elevated?
6. What kind of preoperative evaluation is needed for anesthesia?
III. Significance of anemia
1. Should this patient be transfused preoperatively? Why or why not?
2. Compare the type and screen to type and crossmatch.
The type determines ABO and Rh antigen status, and the screen detects red cell antibodies. To determine ABO type, the patient's red cells are tested against Anti-A and Anti-B reagents. To determine red cell antibodies, the patient's serum is tested against group A and group B red blood cells. While the type takes about fifteen seconds, blood availability is about five minutes. The crossmatch requires about forty-five minutes.
3. What are some infectious disease markers that are tested?
Syphillis, alanine aminotransferase, antibody to hepatitis B surface antigen, hepatitis B core antigen, hepatitis C virus, HIV-1, HIV-2, Human T-cell Lymphocyte Virus I and II.
4. What kind of blood is used for an emergency?
Incomplete antibody testing may be required. This includes type-specific, uncrossmatched or partially uncrossmatched blood, or type O, Rh negative, uncrossmatched blood. O-negative red cells are preferable to O-negative whole blood, as they contain only a small plasma volume and should not have a significant amount of hemolytic antibodies.
I. Choice of anesthesia
1. The surgeon wants hypotensive anesthesia. Do you agree with this?
2. What are some contraindications of hypotensive anesthesia?
3. Does this influence the selection of maintenance technique and agents? Explain.
4. Does the use of methacrylate influence your choice?
1. Does hypotensive anesthesia require intraarterial pressure monitoring?
2. What are alternatives and their relative reliability?
3. What are some other monitors used for hypotensive anesthesia?
4. Why are they used?
I. Difficult intubation
1. After smooth induction with thiopental and pancuronium, you are unable to visualize the cords. What is your plan of action?
2. When is tracheostomy indicated?
3. What would you do if premature ventricular contractions were seen during laryngoscopy?
4. Compare intratracheal and intravenous lidocaine.
IV. Massive blood loss
1. During the procedure, blood loss becomes acutely significant. What are your criteria for transfusion?
2. Compare red blood cell to whole blood transfusion.
Red blood cells are available as stored with citrate, phosphate, and dextrose-adenine, or CPDA-1 units, as deglycerolized, leukocyte-poor, or as washed. CPDA-1 blood has a hematocrit of about 55% in a volume of about 300 ml. Leukocyte-poor cells are used for chemotherapy patients, or those with prior febrile transfusion reactions. Washed cells are for those with severe allergic reactions. Red cells are useful for increasing oxygen-carrying capacity, and for volume expansion.
Whole blood is rare, has a hematocrit of about 35%-40%, and has a volume of about 500 ml. It is indicated for increasing oxygen-carrying capacity and for correcting hypovolemia associated with shock.
2. How should red cells be given?
Normal saline is the best diluent, although any isosmolar non-calcium solution can be used. A filter of 170 mcm should be used, and a warmer is used if more than two units are to be given over a short period of time. Hypertonic solutions like 5% glucose can cause hemolysis or cell clumping, and or calcium-containing solutions like Lactated Ringer's solution cause clot formation.
3. Should fresh frozen or platelets be given with packed red cells?
No. There is no need to add platelets to prevent coagulopathy with even massive blood transfusion or cardiopulmonary bypass.
4. What are the indications for giving fresh frozen plasma?
Deficiencies of factors II, V, VII, IX, X, and XI, reversal of coumadin, diffuse bleeding in patients with massive blood transfusion over one blood volume, antithrombin III deficiency, and immunodeficiencies.
4. Compare the cost/benefit ratio of albumin and fresh frozen plasma.
5. How is fresh frozen plasma made?
Human blood is centrifuged, separated, and frozen within six hours of donation. Thirty percent of factors V and VIII may be lost, and this product should be used within twenty-four hours of thawing. Also, only ABO-compatible plasma should be used, and a standard 170 mcm filter should be used.
5. No blood was available, and the patient was given ten units of type O red blood cells. Is it okay to now use type-specific blood?
6. What if the patient had been given two units of type O, Rh-negative, uncrossmatched blood?
The patient should not receive type-specific blood until the blood bank determines that the transfused anti-A and anti-B antibodies are low enough.
5. What are complications of massive blood transfusion?
Complications include coagulopathy from dilutional thrombocytopenia, lack of factors V and VIII, disseminated intravascular coagulation associated with hypoperfusion or hemolysis, hyperkalemia, citrate toxicity, acidosis, decreased 2,3 diphosphoglycerate and hence a decreased oxygen-carrying capacity, or hypothermia.
6. What would your management of blood products be?
7. By how much will one unit of red cells increase the hematocrit?
By about three percent.
V. Nitroprusside toxicity
1. During isoflurane anesthesia, the requirement for sodium nitroprusside increases. What is the significance of this?
2. What diagnostic tests would you want?
3. What therapy would you give?
I. Relaxant reversal
1. In the recovery room, while still on the ventilator, tidal volume is 250 ml, vital capacity is 500 ml, and inspiratory force is -13 cm H2O. What is your differential diagnosis?
2. How do you evaluate residual relaxation?
3. What are your criteria for adequate reversal?
4. Compare neostigmine with edrophonium.
5. Compare atropine and glycopyrrolate.
6. What is the basic anatomy and physiology of the parasympathetic system?
Preganglionic fibers originate from cranial nerves 3,7,9, and 10, and S2-4. They synapse close to the end-organ, releasing acetylcholine at both the presynaptic and postsynaptic terminals. Nicotinic receptors are located at the neuromuscular junction and ganglions, and muscarinic receptors are located at postganglionic receptor sites. The vagus nerve is the predominant nerve, acting at the heart, respiratory tree, spleen, liver, kidney, bladder, and the proximal intestine. It maintains visceral functions, acting to cause bronchoconstriction, miosis, increased secretions, bradycardia, and activation of the gastrointestinal system.
7. Describe the synthesis and metabolism of acetylcholine.
Acetylcholine is synthesized in the presynaptic mitochondria from acety-coA and choline, by the enzyme choline acetyltransferase. It is stored in vesicles and when released, acetylcholine is primarily metabolized by acetyl-cholinesterase, which is membrane-bound in the synaptic junction. This enzyme is also located on erythrocytes. There is also a plasma cholinesterase known as butyrylcholinesterase which also metabolizes acetylcholine. It is produced by the liver and has a minor role in metabolism.
8. Describe what neuromuscular blocking agents are, and when they are used.
They are drugs that interrupt transmission of the neuromuscular junction, and are used for tracheal intubation, to assist with mechanical ventilation, to optimize surgical exposure, to reduce the metabolic work of breathing, to manage status epilepticus, status asthmaticus or tetanus, or to treat increased intracranial pressure.
9. Describe how impulses are transmitted at the neuromuscular junction.
An impulse arrives at the prejunctional nerve ending, and an influx of calcium releases acetylcholine, which binds to the receptor sites at the postsynaptic junction. Ions move, causing muscle contraction. Once acetylcholine is metabolized by acetylcholinesterase, normal ionic gradients resume, leaving the neuromuscular junction in a nonpolarized, resting state.
10. How are the effects of nondepolarizing muscle relaxants reversed?
By using a reversal agent like the acetylcholinesterase inhibitors neostigmine, pyridostigmine, and edrophonium, more acetylcholine is available at the receptor side, because they inhibit the enzyme that breaks down acetylcholine. Physotigmine crosses the blood-brain barrier, and is not used to reverse paralysis. These agents are positively charged, have quaternary ammonium groups, are water soluble, and are excreted by the kidney.
11. How does one prevent side effects from these drugs?
Muscarinic side effects that could lead to bradycardia are prevented by the use of an anticholinergic agent like atropine or glycopyrrolate, depending on whether edrophonium or neostigmine is used, so that the duration of actions are similar.
II. Emergence delirium 1. Emergence from anesthesia is delayed, and the patient is very disoriented. What is your differential diagnosis?
Hypoxia, hypotension, pain, central anticholinergic syndrome.
2. What is your diagnostic approach?
3. What is your therapy?