Anesthesia Oral Boards – Flashcards
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What are some of the side effects of lithium and its effects on anesthesia? How do you treat it?
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Side effects of lithium include, skeletal muscle weakness, seizure, AV conduction abnormality, widened QRS, hypotension, cognitive changes. Drugs that leads to lithium toxicity are: NSAIDS, ACE-Inhibitors, thiazide diuretics. Give sodium containing fluids to prevent excessive renal reabsorption of lithium. Lithium reduces anesthetic requirements and it can prolong effects of depolarizing and non depolarizing muscle relaxants.
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Extubation concerns for post thyroidectomy
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Post extubation concerns for post thyroidectomy are, tracheomalacia, hematoma, RLN injury, post intubation croup, and edema
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RLN
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A branch of the Vagus nerve. RLN provides sensory and motor innervations below the vocal cords. It supplies all laryngeal muscles except for the cricothyroid (adductor) muscle, which is innervated by the external branch of the superior laryngeal nerve. Bilateral injury results in stridor and complete closure of the vocal cords, which will require intubation. Unilateral injury is more common, which results in hoarseness of the voice
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SLN
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Superior laryngeal nerve is a branch of the Vagus nerve. It provides sensory and motor functions above the vocal cords. It has two branches, external and internal branch. External branch innervates the cricothyroid (adductor) muscle, and the internal branch provides sensory function to the epiglottis, arytenoids, and vocal cords. It's blocked by injecting 2-3cc of 1% lidocaine at the greater cornu of the hyoid bone.
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What is the differential diagnosis of post op inspiratory stridor, periorbital tingliness, restlessness
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These symptoms are consistent with hypocalcemia from inadvertent removal of the parathyroid gland. Symptoms usually occur 24 to 96 hours post thyroidectomy, but it can occur 1 to 3 hours after surgery. Other causes include post intubation croup, residual neuromuscular blockade (higher incidence in patients with myasthenia gravis), RLN injury, hypoglycemia, hypoxia, hypercapnia.
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What is the differential diagnosis for post op fever s/p thyroidectomy
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thyroid storm, thyrotoxicosis, malignant hyperthermia, neurolyptic malignant syndrome, undiagnosed pheochromocytoma,
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How do you treat malignant hyperthermia?
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First, I would alert the surgeon and stop procedure and the offending agents, volatile anesthetics, succinylcholine. Hyperventilate with 100% oxygen. Call for help. Administer dantrolene at 2.5mg/kg until symptoms subsides or to max dose of 10mg/kg. Initiate cooling measures, i.e. ice under axilla, groin, cooling blanket, cold crystalloids. Stop cooling if temp falls less than 38 C. Place a foley to monitor myoglobinuria, and arterial line for frequent ABG, electrolyte sampling. ABG in MH shows mixed metabolic and respiratory acidosis. Treat hyperkalemia with hyperventilation, bicarbonate, glucose/insulin, and calcium. • Bicarbonate 1-2 mEq/kg IV. • Insulin - For pediatric, 0.1 units/kg and 1 ml/kg 50% glucose or for adult, 10 units regular insulin IV and 50 ml 50% glucose. • Calcium chloride -10 mg/kg or calcium gluconate 10-50 mg/kg for life-threatening hyperkalemia. • Check glucose levels hourly Follow ETCO2, electrolytes, blood gases, CK, core temperature, urine output and color, coagulation studies. If CK and/or K+ rise more than transiently or urine output falls to less than 0.5 ml/kg/hr, induce diuresis to >1 ml/kg/hr and give bicarbonate to alkalanize urine to prevent myoglobinuria-induced renal failure.
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What is the post op care for malignant hyperthermia?
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Observe the patient in an ICU for at least 24 hours, due to the risk of recrudescence. Dantrolene 1 mg/kg q 4-6 hours or 0.25 mg/kg/hr by infusion for at least 24 hours. Further doses may be indicated. • Frequent ABG as per clinical signs • CK every 8-12 hours; less often as the values trend downward Follow urine myoglobin and institute therapy to prevent myoglobin precipitation in renal tubules and the subsequent development of Acute Renal Failure. CK levels above 10,000 IU/L is a presumptive sign of rhabdomyolysis and myoglobinuria. Follow standard intensive care therapy for acute rhabdomyolysis and myoglobinuria (urine output >2 ml/kg/hr by hydration and diuretics along with alkalinization of urine with Na-bicarbonate infusion with careful attention to both urine and serum pH values).
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What do MH and NMS have in common?
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Both manifest with mental status changes, tachycardia, and muscle rigidity. Both result in metabolic acidosis, profound hypercarbia, and muscle rigidity.
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What is Hunt Hess Classification?
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It's a system used to classify the severity of non-traumatic subarachnoid hemorrhage. Grade 0 is unruptured. Grade 1-5 is associated with ruptured aneurysm. Grade 1 is ruptured but with minimal symptoms. Mininal headache and nuchal rigidity. Grade 2 is associated with moderate to severe headache, no nuchal rigidity. Grade 3 is a patient who is drowsy, confused, or exhibit mild focal deficit. Grade 4 represents stupor, hemiparesis, vegetative disturbances. Grade 5, patient is in deep coma, moribund, or decerebrate rigidity.
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What does pulmonary function test include?
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PFT includes Lung volumes Airway resistance Diffusion capacity Spirometry
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What are the causes of decrease in FRC
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Pregnancy Ascites Neonates GA Obesity Supine
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What causes an increase in closing capacity
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closing capacity is the sum of closing volume plus residual volume. It's at which small airway begins to close. Factors that increase closing capacity are Age Chronic bronchitis LVF Smoking Surgery Obesity
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What is pulmonary shunt? Why does it occur? What are some of the causes of pulmonary shunt?
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Pulmonary shunt occurs when there is perfusion without ventilation. It represents areas of the lung where gas exchange does not occur (dead space), 100% inspired oxygen is unable to overcome the hypoxia caused by shunting. It's the most common cause of increase in A-a gradient. Normal A-a gradient is 5-10mmHg on RA, 20-30 on 100%O2. When A-a gradient is greater than 350mmHg, intubation is required Causes of shunt: PTX, bronchospasm.
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Perioperative beta blockers should be continued if ...
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patients are already on beta blockers to treat symptomatic arrythmia, HTN, angina, and cardiovascular conditions
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Perioperative beta blockers should be started if....
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1. Patients undergoing intermediate or vascular surgery who are at high cardiac risk for CAD, DM, ischemic heart disease, compensated or prior heart failure, CRI, CVA. Note: uncertain: patients undergoing intermediate or vascular surgery with no clinical risk factors.
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Intermediate Risk Surgeries are...
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CEA, head and neck, orthopedics, intrathoracic, intraperitoneal, and prostate.
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High Risk Surgeries are...
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Emergent major operation, especially in the elderly, aortic or major vascular surgery, large fluid shifts/loss, peripheral vascular surgery.
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What are some of the protamine's side effects
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pulmonary HTN, anaphylactoid/anaphylactic reaction, hypotension, myocardial depression. Reversal of heparin or additional dosing of protamine should be guided by ACT or a heparin-protamine titration assay
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The patient is hypotensive, bradycardic after induction for CPB, what do you think is the cause?
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given the timing of the event, the most likely cause for hypotension and bradycardia are myocardial depression from induction agent or volatile anesthetics. Other causes could be MI, LVF, PTX, heart failure.
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What are the possible causes for post op bleeding after CABG?
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thrombocytopenia, thrombocytopathia, hypothermia, dilution of coagulation factors, inadequate heparin reversal.
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How would you determine the cause of post op bleeding?
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I would repeat and ACT, get PT/PTT/INR, fibrinogen and fibrinogen split products. Most common cause of post op bleed is thrombocytopathia. TEG would also help determine any coagulopathy. Depending on the results of the study, I would treat withFFP, cryoprecipitate, factor 7. If the results of these studies fail to determine the cause of post op bleed, then the patient should return to the OR.
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What is thromboelastogram and what are parameters?
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TEG measures the viscoelastic properties of blood during induced clot formation. R - Initial clot formation. Represents the intrinsic pathway. K and Alpha - Speed of clot formation. Represents thrombin and fibrin formation. MA - Strength of the clot, which reflects platelet number and function
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Patient in an MVA who is awake, intoxicated, and has an aortic dissection. What monitors would you use?
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In addition to the standard ASA monitors, I would place a 5 lead EKG to monitor ischemia, proximal (right) and distal arterial lines. Proximal arterial line would allow me to monitor cerebral and coronary perfusion pressures, while the lower arterial line would aid in monitoring renal, mesenteric, spinal cord, lower extremity perfusion, foley catheter, SSEP, PA catheter to assess cardiac function and fluid status, and aid in early detection of myocardial ischemia. TEE (detection of myocardial ischemia, extent of dissection, valve abnormality,, wall motion abnormality, and LVEDV). Esophageal and rectal temp probes for core and peripheral temp.
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Would you perform a rapid sequence induction in an awake trauma patient who's intoxicated?
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Despite the increased risk for aspiration associated with intoxication, I would not perform a rapid sequence induction. My goals in this patient with aortic dissection, intoxication, possible cervical and internal injuries, is to securely secure the airway while avoiding hemodynamic instability (HTN can propagate the aortic dissection or cause rupture. Hypotension would result in myocardial ischemia), decrease the risk of aspiration, and injury to the cervical spine. To achieve these goals, I would preoxygenate the patient with 100% oxygen, administer anti-emetic and aspiration prophylaxis (zofran, metoclopromide, non-particulate antacid), provide in-line stabilization, apply cricoid pressure, and induce with etomidate, fentanyl, lidocaine, and succinylcholine. After induction, I'd place a double lumen endotracheal tube and confirm with lung auscultation, EtCO2, and fiberoptic scope
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The technician says that signal is lost on SSEP after aortic clamp. What would you do?
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Assuming stable anesthesia and institution of partial bypass, I'd optimize the patients hemodynamics, ask the perfusionist to increase the pump flow distal to the aortic clamp. If this were unsuccessful, I'd ask the surgeon to release the clamp, ensure adequate hypothermia (32 C), and consider withdrawing 10-15 ml of CSF from the lumbar drain with a target ICP of 5-15mmHg, and consider pharmacological intervention.
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What pharmacological interventions that can reduce the incidences of spinal cord ischemia?
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corticosteroids, calcium channel blockers, naloxone, dextrorphan.
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What hemodynamic changes that occur with placement of aortic cross-clamp?
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cardiovascular changes are variable depending on the location of the cross-clamp. Some of the effects of the cross-clamp are decrease in cardiac output, decrease in ejection fraction, decrease in renal blood flow and distal perfusion. Proximal effects of cross-clamp are increase in afterload, left ventricular pressure, central venous pressure, and pulmonary occlusion pressure.
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What are the metabolic changes that occur with aortic cross-clamp?
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There's an increase in mixed venous oxygen saturation, metabolic acidosis, decreased total body oxygen consumption, and increase in catecholamine release. All of these changes increase the risk of myocardial ischemia and heart failure, as well as distal ischemia.
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when would you extubate the patient?
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Extubation shouldn't be attempted until neuromuscular blockade is fully reversed, until the patient is hemodynamically stable, has no signs of metabolic derangements, and normothermia has been achieved. If none of these criteria are met, then I would not extubate the patient.
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what ventilation mode would you recommend?
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If the patient is not making any respiratory effort and assuming the lung compliance is normal, then I would place the patient on volume limited AC or SIMV. If the patient is making repiratory effort, then I would place the patient on a weaning mode, SIMV with PS and PEEP.
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What ventilation mode would you recommend for a patient who has undergone repair of aortic dissection?
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If the patient is not making any respiratory effort then I would place the patient on pressure control. Given the length of surgery, amount of fluid shift, all can reduce pulmonary compliance secondary to pulmonary edema.
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The patient persists to bleed a few hours after surgery. The surgeon suggest giving protamine. Would you do it?
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First I would investigate and treat the underlying cause, which could be thrombocytopathia, the most common cause of post op bleeding. Others include hypothermia, thrombocytopenia. I would repeat an ACT, PT/PTT/INR, fibrinogen, fibrin split product before giving another dose of protamine. If the ACT is prolonged, then I would give protamine, recognizing that protamine can cause paradoxical bleeding.
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How does hypothermia result in coagulopathy?
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In mild hypothermia (33-37C), the defect is in platelet aggregation and adhesion, but coagulation enzymes are normal. Below 33C, both platelet function and coagulation enzymes are affected. TEG is a good tool in detecting coagulopathy in mild hypothermia, and both TEG and PTT can be used to detect coagulopathy in hypothermia below 33 deg.
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What are some of the causes of delayed awakening from anesthesia? What would you do?
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Stroke from intraop cerebral ischemia, embolism, or hemorrhage. Other causes are residual neuromuscular blockade, residual sedation or narcotics, hypothermia, metabolic and electrolyte derangements, and hypoglycemia. I would ensure oxygenation and ventilation and review all medications given. Perform a focused physical exam, and reverse medications given. If unsuccessful, I'd consult a neurologist and get a CT scan of the head.
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Would you place an epidural in this patient with aortic aneurysm?
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Assuming there are no contraindications and coagulopathy, I would place an epidural for this patient. Epidural provides excellent post op pain control. It improves respiratory function, GI motility, graft patency, and attenuation of stress response. Epidural has complications, which include epidural hematoma, abscess, menigitis, headache, and interference with spinal cord monitoring. Heparin: Since this patient will be anticoagulated with heparin therapy intraop, I would start the heparin therapy an hour after the epidural is placed. I would pull the catheter only after normalization of coagulation status.
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Induction for patient with CAD, aortic stenosis +/-aortic aneurysm...
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Given the patient's (leaky aneurysm, CAD, AS, HTN), It's important to maintain hemodynamic stability during induction. Hypertension and tachycardia can result in cerebral vascular event such as stroke, propagation or rupture of aneurysm, myocardial ischemia, and heart failure. On the other hand, hypotension can be just as detrimental. Patients with CAD and AS rely on diastolic aortic pressure to provide adequate coronary perfusion. Therefore, and arterial line would allow me to more quickly identify and treat changes in blood pressure.
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How can you provide renal protection during aortic cross-clamping?
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The best method to protect renal perfusion is by maintaining hemodynamic stability and intravascular volume. Other methods include preconditioning with intermittent cross-clamping or the internal iliacs prior to aortic cross-clamping, and or use mannitol, dopamine, fenoldapam. All of theses drugs increase renal perfusion and blood flow, however, they have not been shown to improve outcome in aortic surgery.
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Are renal protective strategies necessary when the proximal aortic cross-clamp is infrarenal?
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Yes. Even when aortic cross-clamp occurs below the renal arteries, it can increase renal vascular resistance, decreasing renal blood flow. Other contributing factors include surgical trauma to the renal arteries and the embolization of the artherosclerotic debris to the kidneys.
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BP increases and ST segment depression occurs after supraceliac aortic cross-clamp. What are the steps to alleviate this problem?
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1. I would alert the surgeon to release the clamp immediately. 2. provide 100% oxygen and ensure adequate ventilation, and optimize hemodynamic variables. If the ST depression improves, then 3. lower the BP using SNP or NTG and ask the surgeon to slowly reclamp. 4. and look out for hypertension and ST changes. 5. My goal is to reduce the afterload enough to avoid cardiac ischemia, while at the same time provide adequate coronary and distal perfusion. 6. To this end, I would administer inotropes and vasodilators while monitoring EKG, SSEP, MEP,and TEE, and both proximal and distal arterial BP.
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How does SNP work?
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SNP enters the RBC, an nonenzymatic reaction results in the release of NO and CN ions. These CN ions can combine with Thiosulfate, metHgb to form thiocyanate and cyanometHgb. It can bind to cytochrome oxidase which impairs tissue oxygen utilization. The impairment of oxygen utilization results in metabolic acidosis and CN toxicity, cardiac arrythmias, tachyphylaxis, and increased venous oxygen content. The risk of developing CN toxicity is minimal if the dose doesn't exceed 0.5mg/kg/h.
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What is the treatment for SNP toxicity?
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First, stop the infusion, then administer 100% oxygen. Administer sodium thiosulfate, amyl nitrate, or sodium nitrate. These drugs remove the CN ions from the circulation, so they are unavailable to bind to cytochrome oxidase.
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What preparations are needed prior to release of aortic cross-clamp?
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Prior to the release of aortic cross-clamp, I would 1. discontinue vasodilators, 2. replace fluid blood loss by administering fluids/blood guided by TEE. I would correct any electrolyte and metabolic derangements, and coagulopathies. Anticipating persistent decrease in SVR and severe hypotension, I would have vasopressors and crystalloid available.
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After release of aortic-cross clamp, the BP drops to 82/40. Is this expected?
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Yes. The hypotension is caused by washout of vasoactive and cardiodepressant mediators, combined with distal pooling of blood. In this case, I would initiate fluid boluses, provide 100% oxygen and ensure ventilation, administer vasopressors, place the patient in t-berg position. Other causes include, myocardial ischemia, LVF, dysrrhythmias, PTX, acid-base or electrolyte derangements. If hypotension persists, then I would ask the surgeon to reapply the clamp and attempt another release.
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Urine output is only 20cc over the past 2 hours in the ICU. How would you evaluate and manage this situation?
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low urine output following aortic surgery has a high mortality, therefore I would aggressively evaluate and treat this oliguria. First I would examine the patient and review the PA catheter data, vital signs, fluid administration and blood transfusion history, and medication administered. Then I would check the foley catheter for signs of kinking or obstruction. If there are no signs of obstruction, the I would administer a fluid bolus challenge. If there are no apparent cause for oliguria, then I would order serum and urine electrolytes to calculate the frational excretion of sodium and consider a nephrology consult.
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Patient has an epidural. He is now awake from surgery, but he can't move his legs. What do you think could be the cause and what would you do?
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This is very concerning. There could be several causes. 1. epidural/spinal hematoma with spinal cord compression, 2. intrathecal epidural catheter, 3. neurological injury from poor spinal cord perfusion. I would perform a neurologic exam, check the local anesthetic concentration and infusion rate, aspirate the catheter to look for CSF, discontinue the epidural infusion, and consider CT/MRI and neurological consult.
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How does surgical dissection and aortic cross-clamping increase the risk of spinal corad ischemia?
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clamping of the aorta can cause spinal cord hypoperfusion. Blood supply of anterior spinal cord is supplied by anterior spinal artery, which arises from basilar and vertebral artery, and is supplied by 6-10 radicular arteries arising off the aorta at variable locations. Artery of Adamkiewicz originates from T-9-12.
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SCPP...
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Spinal cord perfusion pressure is Diastolic aortic pressure - CSF or or CVP, whichever is greater. Placement of the clamp causes cerebral hyperemia with subsequent increase in CSF pressure. Combined with decrease in diastolic aortic pressure, can lead to decreased spinal cord ischemia.
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Regional vs. GA in CEA
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While there's no evidence that either regional or GA is superior for CEA, my first choice would be regional anesthesia. Given the patients extensive cardiac history and recurrent embolic events, regional anesthesia has the advantage of hemodynamic stability, avoiding cardiac depression associated with general anesthesia, sympathetic response to laryngoscopy. Another advantage is that it allows for continuous neurological monitoring of an awake patient, which is considered the most sensitive method of detecting cerebral ischemia and aids in more selective carotid artery shunting.
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What are the disadvantages of regional anesthesia vs general anesthesia in CEA?
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The disadvantages of regional anesthesia in CEA is the limited access to the patient during the conversion to general anesthesia. It also requires patient cooperation.
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Which patients with CHF should be given beta blocker?
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Beta blockers should now be considered standard therapy in patients with New York Heart Association class II or class III heart failure who are hemodynamically stable, who do not have dyspnea at rest and who have no other contraindications to the use of these agents. Several large randomized, controlled mortality trials have been stopped early because of significant improvement in mortality rates in patients with heart failure who were given beta blockers in addition to angiotensin-converting enzyme inhibitors, diuretics and, sometimes, digoxin.
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What is normal digoxin level and what is associated with digoxin toxicity?
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Normal digoxin level is 0.5-2 ng/ml. Digoxin toxicity may result in EKG changes and/or arrhythmias, and is potentiated by hypokalemia, hypomagnesemia, and hypercalcemia. Digoxin toxicity may compromise the ability to monitor for cardiac ischemia, since even in normal range, it can have mild ST depression in multiple EKG leads.
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What are your primary concerns during induction and intubation for TEF repair?
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I have several concerns, including 1. aspiration, due to TEF, 2. gastric distension from either improper ETT placement or insufflation from positive pressure ventilation, 3. difficult intubation if intubating an awake and vigorous neonate, 4. hypotension from inability to feed, 5. inadequate ventilation from poor pulmonary compliance.
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How is decreasing FiO2 in an infant with PDA beneficial?
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By titrating the FiO2 to a PaO2 of 50-70mmHg reduces the risk of Retinopathy Of Prematurity. It also increases Hypoxic Pulmonary Vasoconstriction which decreases the left to right shunt that is causing pulmonary vascular congestion and volume overload of the heart.
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What are the risk factors for Retinopathy Of Prematurity? How do you avoid it?
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Birth weight < 1500g (3.3lbs), prematurity, mechanical ventilation, respiratory distress, hypoxia, acidosis. To avoid ROP, maintain oxygen saturation 87-95% and avoid major fluctuations in oxygen levels, anemia, hypercarbia,and acidosis.
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During dissection of ductus arteriosus, the infant becomes hypotensive and bradycardic. What's the most likely cause and what would you do?
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The most likely cause would be traction on the lung, resulting in hypoxemia, increase in shunt. I would manually ventilate with 100% oxygen, verify the accuracy of the monitors, and evaluate the EKG, airway pressures, and tidal volume. I would ask the surgeon to release the traction until hemodynamics improve. I would also assess blood/fluid loss and determine any correction is necessary, and administer atropine to correct any persistent bradycardia.
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What is neutral temperature as it relates to the neonate?
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Neutral temperature is the ambient temperature at which oxygen consumption is minimized. Avoiding increased oxygen utilization, acidosis, glucose consumption is important in a sick neonate. Neurtral temperature for a premie is 34C, 32C for term, and 28C for adults.
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How do infants maintain heat?
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The primary mechanism for heat generation for an infant is nonshivering thermogensis from brown adipose tissue metabolism. Nonshivering thermogensis results in increased in oxygen consumption and heat production. This process is limited in premies and sick infants who are deficient in brown fat stores. Therefore it is important to keep normothermia in premies and sick infants in the perioperative period.
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What are some of the causes of serizure in infants?
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Some of the causes of seizures in infants are intracranial hemorrhage, hypoxic-ischemic encephalopathy, hypocalcemia, hypoglycemia, hypomagnesemia, obstetric related infection (TOxoplasmosis, Rubella, CMV, Herpes).
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How do anesthetics affect MEP?
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MEP monitors the functional integrity of the descending motor pathways in the anterior spinal cord, which may show a decreased in amplitude and increase in latency with the use of opioids, sedative hypotics, and volatile anesthetics. These signals may also represent spinal cord ischemia. With MEPs increase in latency is not reliable, but decrease in amplitude 50-80% is considered significant. Since MEP is more sensitive than SSEP to singal suppresion from volatile anesthetics, TIVA is often used. MEP may be monitored with two twitches.
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What is the disadvantage of MEP?
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MEP is not yet considered standard of care for neuromuscular monitoring. The associated risks are scalp burns, bite injury, seizures, cardiac arrhythmias, cost, and anesthetic restrictions. It shouldn't be used for patients with cochlear implants, active seizures, or vascular clips in the brain.
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How do anesthetics affect SSEP?
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SSEP monitors the functional integrity of the ascending sensory pathway of the posterior spinal cord, which may show decreased in amplitude and increase in latency with anesthetic suppression. Narcotics have the least effect on SSEPs. Anesthetic suppression, hypothermia, hypoxia, hypotension, hypercarbia all produce similar changes to those seen with spinal cord ischemia.
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How do you assess this patient's pulmonary/cardiac status?
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First, I would start by conducting a focused history and physical to determine the extent and severity of any pulmonary/cardiac disease. More specifically, I would attempt to identify signs and symptoms of ( ), such as ( ), and obtain relevant history, such as ( ). Given the risks associated with this surgery, I would order a (CXR, PFT, EKG, Echo, stress test, CBC, BMP, ABG...)
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Would you order a PFT?
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I would order a PFT. While PFTs are not warranted in all preoperative patients with pulmonary disease, I believe they would be indicated this patient with (long standing smoking history, who is hypoxic on room air, and is about to undergo a surgical procedure associated with increased risk of postoperative pulmonary complications).
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Wouldn't a history and physical provide enough information?
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Although a history and physical would provide most of the needed information, PFTs would provide additional information concerning the type and severity of the disease, baseline pulmonary function, and the presence of reversible component. I would also order an ABG to identify CO2 retention and severity of his pulmonary disease.
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What are some of the alcohol withdrawal symptoms?
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Patients with chronic alcoholism will develop tremulousness within 6-8 hours, hallucinations and seizures starting at 24-36 hours, and delirium tremens within 72 hours. Signs and symptoms of DTs are, fever, tachycardia, hypertension, confusion, perceptual distortions, agitation, autonomic instability.
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How would you evaluate patient for alcohol withdrawal symptoms?
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I would obtain a history of his alcohol consumption, including type, frequency and quantity of alcohol consumed. Then I would perform a physical exam looking for signs of chronic alcoholism, such as cirrhosis, hepatic enchephalopathy, cardiomyopathy, gait disturbance, Wernecke-Korsakoff syndrome. To this end, I would order CBC, BMP, coags, LFTs, CXR, EKG, serum glucose, if not already ordered. I would initiate administration of a benzodiazepine for alcohol withdrawal prophylaxis.
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What concerns do you have in someone with chronic alcohol abuse?
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Chronic alcohol abuse has multisystemic effects, including CNS depression resulting in an increase in MAC requirement, tolerance to other drugs, cognitive impairment, cerebral atrophy, cerebellar degeneration, and peripheral neuropathy. Other concerns are cardiomyopathy, cirrhosis, GI bleeding, nutritional deficiency, hypoglycemia, thrombocytopenia, electrolyte abnormalities, and acute withdrawal symptoms.
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What are the risks of poor perioperative glucose control?
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Patients with poor perioperative glucose control are at risk for impaired would healing, increased rates of surgical infections, and osmotic diuresis. Poor glucose control has been associated with worse neurological outcome following traumatic brain injury.
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What blood sugar would be acceptable to proceed with surgery?
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The recommendation is to achieve a glucose level of < 180mg/dL. I would not delay the case for a glucose of 220mg/dL. However, with an increased risk of impaired would healing, increased rates of surgical infection, and potential osmotic diuresis, I would administer regular insulin in an attempt to lower plasma glucose while avoiding hypoglycemia. This will require frequent glucose sampling intraoperatively for tight glucose control.
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What are the manifestations of autonomic neuropathy?
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Clinical manifestations of autonomic neuropathy include gastroparesis, painless MI, peripheral neuropathy, HTN, orthostatic hypotension, impotence, resting tachycardia.
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What are your concerns with giving sodium bicarbonate to correct metabolic acidosis?
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My concerns with giving sodium bicarb. are 1. it increases additional CO2, which diffuses into cells and result in worsening intracelluar acidosis, 2. increase in additional CO2 results in shift of hemoglobin dissociation curve to the left, which increases Hgb's affinity to oxygen, 3. it results in hypokalemia, and 4. hyperosmolar state due to excess in sodium. Unless the metabolic acidosis is life threatening, pH <7.1, it's best to avoid giving sodium bicarbonate as a treatment of metabolic acidosis.
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So how do you treat severe metabolic acidosis?
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I would hyperventilate and keep PaCO2 < 30. I would obtain serum lactate, serum and urine ketones, blood alcohol level, measure urine output, BUN/Cr to identify acute renal failure. Then I would initiate appropriate treatment to address the underlying causes.
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What are the causes of post op blindness? What would you do? And what would you tell the patient and the family?
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Post op blindness is caused by anterior and posterior ischemic optic neuropathy, rentinal artery occlusion, and cortical blindness. Most likely cause is result of impaired oxygen delivery. To this end, I would immediately assess the patient and correct any metabolic derangements, elevate the head of the bed to facilitate venous drainage, ensure adequate BP, hemoglobin, oxygenation, and cardiac function. In discussion with the patient and the family, I would assure that all precautions were taken to minimize this risk, and everything would be done to appropriately assess and treat the patient, including an urgent ophthalmology consult.
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What is Posterior Ischemic Optic Neuropathy?
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PION is blindness caused by impaired oxygen delivery resulting in irreversible nerve damage. It occurs at 24-48 hours after surgery. Physical findings are painless vision loss, visiual field defects, lack of light perception, or complete vision loss. It carries a poor prognosis.
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What patients are at risk of developing PION?
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Patients who undergoes spine surgery longer than 6.5 hours and blood loss more the 45% of estimated blood volume have a strong association with Posterior Ischemic Optic Neuropathy. Some of the contributing factors include intraoperative hypovolemia, anemia, hypotension, hemodiluation, hypoxia, ocular pressure, prolonged surgery, and blood loss.
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How would you evaluate a patient for pneumonectomy?
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I would start by conducting a history and physical exam to identify signs and symptoms of cardiac and pulmonary disease. I would also focus on airway exam, exercise tolerance, and renal function. To evaluate the severity of the patient's pulmonary disease, the risk of pulmonary complications, and his tolerance of pneumonectomy, I would order PFTs, and EKG, CXR, and/or a CT, and an ABG; assess his exercise tolerance with stair climbing or a 6 min walk test, or exercise SpO2; and estimate his ppoFEV1%. If his ppoFEV1 were <40%, I would order a DLCO, V/Q scan, a VO2 max, and TTE to evaluate RV function. Patients with a ppoFEV1% <40% are at high risk of right heart failure following pneumonectomy.
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How would you evaluate this patient's cardiac status?
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I would perform a history and physical examination focusing on the patient's CAD, previous MI, HTN, DM, and all related surgical and pharmacological interventions (PTCA, stents). This would include a review of previous medical records and tests related to cardiac function. More specifically, I would like to determine the severity of his CAD, affected coronary vessels, and whether he's medically optimized. In the absence of signs and symptoms suggestive of myocardium at risk, I wouldn't require and additional testing prior to surgery, other than a 12-lead EKG.
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Would you allow parents to accompany the child into the OR?
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There some evidence that suggest parental presence for induction reduces the anxiety in a child older than 4 years of age. This is true when both parent and child have relatively calm demeanor as baseline. However, there's also evidence that the presence of an anxious parent during induction results in anxious child, I would not allow the parent into the OR in this child with asthma and worsening stridor.
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What is respiratory papillomatosis and how would you treat it?
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Respiratory papillomatosis is a benign laryngeal papilloma caused by HPV. It's self limiting, however if left untreated, it can cause complete airway obstruction. The treatment is serial CO2 laser ablation until regression. Some papillomatosis will require adjunct therapy, such as interferon alpha, , ribavirin, or acyclovir.
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What are the advantages and disadvantages of caffeine-halothane muscle contracture test?
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The advantage of the caffeine-halothane contracture test is that if helps to identify affected family members and gives greater anesthetic choices in the future, assuming the test is negative. The disadvantages of the test is that it's a surgical procedure, expensive, and not many centers around the country conducts the test. The child has to be older than 7 years of age.
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What are some of the ventilatory options for surgical procedures performed around the vocal cords?
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The options are 1. armored ETT with spontaneous respiration, 2. intermittent apnea - intermittent ventilating without a secure airway, 3. intermittent jet ventilation. Both intermittent apnea and intermittent jet ventilation has advantage of decreasing the risk of airway fire, however, the disadvantage is an unsecured airway. Supraglottic jet ventilation is not ideal for patients with decreased chest wall compliance (obesity, restrictive lung disease, gastric distention), or inhibit full exhalation (severe COPD, laryngospasm, glottic lesions, and interarytenoid scarring).
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What are the complications associated with supraglottic jet ventilation?
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Some of the complications associated with jet ventilation are 1. misalignment of the gas jet to the glottic inlet resulting in poor ventilation and/or gastric distention, 2. barotrauma (pneumomediastinum, subcutaneous emphysema, pneumothorax).
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What are the steps taken during an airway fire?
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I would immediately alert the OR staff and the surgeon, discontinue oxygen supply from the airway, remove the ETT, and if the fire persists, flood the field with saline. The I would mask ventilate with 100% O2 and perform direct laryngoscopy to assess the airway for damage and remove any debris. If the fire had reach the interior of the ETT, I would consider bronchial lavage and fiberoptic assessment of the more distal airways. I would delay extubation for 24 hours given the risk of developing airway edema. I would consider serial CXR, short term high-dose steroids, and pulmonary consult.
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What is the DDx for an intubated patients has hypoxia and increased airway pressures?
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Hypoxia with increased airway pressures in an intubated patient is consistent with airway obstruction or decreased lung compliance. Some of the causes are bronchospasm, pleural effusion, pulmonary edema, acute lung injury, mucous plug, kicked ETT, right main stem intubation, or PTX.
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Patient for transphenoidal resection of pituitary tumor. What information would you like to know preop?
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In addition to conducting a history and a physical examination, I would like to know the size of the tumor and any supracellar extension, which would result in neurological deficits. Also, I'd like to know if it's a hormone secreting tumor, and if there were any associated symptoms such as Cushing's or acromegaly? Furthermore, I would assess the airway, IV access, and the extent and severity of any co-existing diseases.
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What are the effects of hormone secreting tumor?
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Excessive secretion of growth hormone in the prepubertal patients result in gigantism and in adult patients acromegaly. Acromegalic patients experience skeletal and soft tissue overgrowth, which results in large hand, feet, nose, mandible, tongue, soft palate, tonsils, and epigottis. Acromegaly is also associated with cardiomegaly, HTN, accelerated atherosclerosis, vocal cord paralysis, OSA, arthritis, insulin resistance, and glottic stenosis.
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You see PVCs soon after infiltration of local anesthetic. What do you think is the cause and what would you do?
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Most likely cause of PVCs after infiltration of local anesthetic is the result of the injection of epinephrine containing local anesthetic or use of cocaine pledgets. I would provide 100% oxygen, check BP and EKG for myocardial ischemia. I would then treat any HTN or significant arrhythmias. Other causes of PVCs include hypoxia, cardiac ischemia, air embolism, electrolyte abnormalities, or anesthetic induce cardiac depression.
