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ASK THE EXPERTS: SPECIFIC MEDICAL CONDITIONS

In thyroid disease is it safe to practice anesthesia to a patient whose TSH rate is low and T4 normal? I have assumed that low TSH means hyperthyroidism. What is the best way to deal with such patient. The medical endocrinologist say only T4 is important, but I have had patients with cardiac arrhythmic trouble and only low TSH. Is there risk of thyroid storm post operative in such cases? —patricia.momblano@vertibrae.com

Dr. Keith Candiotti responds:

It is often possible to have a patient with a low TSH but a normal T4 level. Very often this may be the result of a subclinical hyperthyroidism or may be seen in a patient who is on a little too much synthroid. In a patient with a normal T4 and decreased TSH it is appropriate to check for the T3 level as so-called T3 toxicosis should be ruled out. If both the T4 and T3 levels are normal it is very unlikely that the patient has clinically significant hyperthyroidism even if the TSH is depressed. In that case scenario thyroid storm would be very unlikely.


What are the options to treat perioperative hypertension and tachycardia in a patient with 'COPD'. Nowadays this seems to be an all encompassing label but I am referring to the elderly long time smoker or miner with DOE and sputum. Spirometry shows some obstruction with limited/no reversibility. We have ruled out light anesthesia and we are talking sbp > 200 dbp>100 and hr >100 —jojaidev@hotmail.com

Dr. David Lubarsky responds:

Cardioselective Beta antagonists are useful in these cases. Esmolol has been used in patients with known COPD with no significant decrement in PFTs recorded with doses in the therapeutic infusion range. The potential perioperative cardiac protective effects of cardioselective beta antagonists is an added bonus.


Is regional anaesthesia advisable for a renal transplantation recipient? What are the absolute indications for the same? —acchimote@hotmail.com

Dr. David Lubarsky responds:

There is almost never an absolute indication for regional. It may indeed be a preferable technique in some or many cases, depending on your skill and appreciation of its physiologic benefits. At Duke University, it was routine to do renal transplantation (cadaveric, extraperitoneal, low incisions) with just an epidural. Living related transplants are another story and usually require general anesthesia.


Regarding premedication in patients with cardiovascular disease (CAD, arterial hypertension) we have 3 questions: Should ACE (angiotensin convert. enzyme) blockers be given on the day of surgery--

a. In patients scheduled for vascular surgery?
b. In patients scheduled for CABG with extracorporeal circulation?

Under what conditions should one reduce the dose of ACE inhibitors? —georg@vertibrae.com


Dr. Richard Prielipp responds:

The data from Coriat et al would suggest the following: If the indication for use of ACEI is to treat congestive heart failure [that is, for afterload reduction], the ACEI should be CONTINUED, even on the day of surgery. This is important to avoid "overloading" the heart in the perioperative period when large fluid shifts are likely.

By contrast, if the indication for ACEI is treatment of chronic hypertension, you MAY elect to omit them on the day of surgery. There is evidence that continued treatment with ACEI will likely result in more hypotension during anesthesia and surgery. You should be more vigilant, and prepared, to treat this hypotension in such patients.


In the emergency department, what is the best method to use for pain relief in a patient suspected of acute abdomen? —rozbeno@hotmail.com

Dr. Raymond Sinatra responds:

This is a particularly controversial question. The patient should be medicated very judiciously; given enough pain medication to provide some degree of comfort, but not enough to mask symptoms or precipitate hemodynamic instability. NSAIDs and even the safer Coxibs should be avoided, as they could increase risks of GI bleeding. I generally employ small doses of IV opioids, usually morphine 1-2mg PRN, maximum dose 10mg/hour. If the patient is hypovolemic or hemodynamically unstable, I generally substitute fentanyl 12.5-25mcg or hydromorphone 200mcg PRN, Acetaminophen up to 1000mg may also be administered to complement opioid analgesic effects.


What is the ideal anesthesia management for a patient with MI<3 month? —fama7@hotmail.com

Dr. David Lubarsky responds:

Patients with a recent MI should be evaluated and optimized for myocardial function and myocardium at risk. A dobutamine stress echo is a good test to ascertain the status. With good myocardial function and limited myocardium at risk for further ischemia, anesthesia and surgery can procees as dictated by the patient's other medical conditions. It is probably prudent to begin beta blockers, preferably a week before surgery (See the Poldermans et al. article reviewed on this site) If there are significant problems, a cardiology consultation can be sought to improve ejection fraction, optimize treatment for ischemia, or suggest further revasculatization alternatives.


What are the recommendations for management of pulmonary hypertension, such as a patient with right heart failure?

Dr. Richard Prielipp responds:

This is indeed a complex and challenging patient management issue. One must assume these patients are very fragile, and intolerant of the "usual" hypotension during the induction of anesthesia. Further exacerbating hemodynamic instability is the change in right heart preload associated with positive pressure ventilation. Extra caution is always warranted when dealing with patients with pulmonary artery pressures which exceed 50% of systemic artery pressure.

ETIOLOGY & PATHOPHYSIOLOGY:

It is useful to recall the equation for pulmonary vascular resistance (PVR), as noted below PVR = [(MPAP-LAP)/CO], Where MPAP = mean pulmonary artery pressure, LAP = left atrial pressure, and CO = cardiac output.

This equation can be rearranged to define the three major etiologies of pulmonary hypertension, by solving for MPAP:

MPAP = LAP + CO*PVR. Thus, the THREE major causes of pulmonary hypertension are:

  1. LAP (left atrial hypertension, such as chronic congestive heart failure, mitral stenosis);
  2. CO (severe increases in cardiac output, usually from longstanding intracardiac shunts); and
  3. PVR (increases in pulmonary vasoconstriction, such as primary pulmonary hypertension, COPD, etc).

High PVR increases right ventricular afterload, and cardiac output progressively falls as the disease progresses. The overall goal is to lower (or prevent increases) in PVR, maintain right ventricular contractility, and thereby sustain adequate systemic oxygen delivery.

INDUCTION AND MAINTENANCE OF ANESTHESIA:

No single agent or technique has proven superior in the setting of pulmonary hypertension. A smooth, very controlled induction and emergence are essential, with constant attention to factors which could increase MPAP. Five key principles are:

  • Keep the patients well (or "super") oxygenated, which helps dilate the pulmonary arteries,
  • Maintain optimal lung volumes (normal FRC) and avoid atelectasis, or hyperinflation of the lungs,
  • Avoid exogenous or endogenous release of catecholamines, which precipitates further pulmonary vasoconstriction,
  • Strive for metabolic and /or respiratory alkalosis of the blood, using judicious hyperventilation and bicarbonate as necessary, and
  • Keep patients normothermic.

Specific Vasodilator Therapy.

Selective pulmonary vasodilators may prove necessary in patients refractory to conventional management noted above. Invasive hemodynamic monitoring is a prerequisite to vasodilator therapy, for complications such as systemic hypotension, increased intrapulmonary shunt, right ventricular ischemia, and acute heart failure are potential adverse sequelae. Inhaled nitric oxide, or intravenous Flolan (epoprostenol) are two considerations of drugs with significant degrees of pulmonary selectivity. Older agents with less specificity for the pulmonary circulation include nitroglycerin, sodium nitroprusside, prostaglandin E1, isoproterenol, and nifedipine or other calcium-channel blocking drugs.

SELECT REFERENCES:

  1. Prielipp R. Right-sided heart failure and pulmonary hypertension. Pages 112 — 124. In: Manual of Anesthesia and the Medically Compromised Patient. Cheng EY, Kay J, eds. J. B. Lippincott Company, Philadelphia, 1990.
  2. Rubin LJ. Primary pulmonary hypertension. N Engl J Med 1997; 36:111-117.
  3. Bailey CL, Channick RN, Rubin LJ. A new era in the treatment of primary pulmonary hypertension. [Editorial] Heart 2001; 85(3):251-252.
  4. Hohn L, Schweizer A, Morel DR, et al. Circulatory failure after anesthesia induction in a patient with severe primary pulmonary hypertension. Anesthesiology 1999;91:1943-1945.

I have a case with two diseases, a severe aortic insufficiency and hip fracture. Should I perform the hip replacement or the aortic valve replacement first? —jose.llagunes@wanadoo.es

Dr. Katherine Grichnik responds:

The usual approach to a patient with two opposing medical problems is to address the problem which is most urgent or acute. In general, a hip fracture is considered an emergency situation, which usually requires urgent stabilization. However, severe AI may result in decompensated congestive heart failure. The best approach would be to consult with the cardiologist, the cardiac surgeon and the orthopedic surgeon to discuss the relative degree of severity of each problem including the feasibility and extent of surgery needed for each problem. I suspect that the decision will be to operate expediently on the hip and aggressively manage the aortic insufficiency perioperatively. When the hip fracture isstabilized and after a period of recovery, the surgery for the AI would beconsidered.


I have a 40 yr old, female patient, who requires an open cholecystectomy. She suffers from Multiple Sclerosis, but is reasonably stable and active at present. She has been told by a fellow sufferer "Never to have a General Anaesthetic". However, she is adamant that she does not wish to have a Local anaesthetic procedure. What is the current thinking regarding General Anaesthesia in Multiple Sclerosis?—paul.woodsford@btinternet.com

Dr. David Lubarsky responds:

There is no problem with general anesthesia exacerbating multiple sclerosis to my knowledge. Neuraxial blocks may exacerbate symptoms.


Do you have recommendations for literature on the treatment of pulmonary hypertension?—pzhw@mail.nbptt.zj.cn

Dr. Katherine Grichnik responds:

Pulmonary hypertension is defined as a pulmonary arterial pressure over 25 mm Hg mean, 35 mm Hg systolic and 15 mm Hg diastolic. The clinical result is a high resistance to RV outflow, low cardiac output, diminished arterial oxygenation and right ventricular pressure overload and failure. The treatment of pulmonary hypertension is dependent of the cause of the hypertension and the duration of the pulmonary hypertension (allowing an estimate of its reversibility).

Hypoxic Pulmonary Hypertension:

The causes include obesity, kyphoscoliosis, neuromuscular disorders, pleural fibrosis and s/p lung resection.

Arterial Obstruction:

The causes include anatomic arterial obstruction with platelet activation/vasoconstriction from diseases such as sickle cell anemia or coagulation disorders. Embolic phenomena such as thromboemboli, schistosomiasis and connective tissue disorders are also etiologies.

Pulmonary Venous Obstruction:

The cause is obstruction distal to the pulmonary venous system such as coarctation or supra-aortic stenosis. This is the most common type of pulmonary hypertension.

Left to Right Shunt:

The cause is Eisenmenger's syndrome with chronic high pulmonary flow due to conditions such as a patent ductus arteriosus or an intracardiac shunt.

Primary Pulmonary Hypertension (PPH):

The cause of PPH is unknown. There is no cure. This is a progressive disease leading to congestive heart failure and respiratory failure. Treatment of pulmonary hypertension due to a reversible cause is to institute therapy for (eg anticoagulation for emboli) the cause or surgery to repair (eg repair of an intracardiac shunt) a specific etiology. Otherwise therapy is directed at symptomatic treatment and attempts to decrease pulmonary pressure. PPH is much harder to treat. Treatments include vasodilators, diuretics, and calcium channel blockers. The most commonly used vasodilator is epoprostenol. It is a powerful endogenous vascular smooth muscle relaxer and an inhibitor of platelet aggregation. Anticoagulants, digoxin and oxygen are also used. The ultimate treatment is via heart-lung transplant.

A great review of this subject can be found at

http://www.mayo.edu/cme/rst/pulmhyp/mcgoon.html. Some of the above information about this subject is from this site.

Review Literature:

  1. O'Brien A, Rounds S. Pulmonary hypertension update. Comprehensive Therapy. 26(3):190-6, 2000 Fall.
  2. Archer S, Rich S. Primary pulmonary hypertension: a vascular biology and translational research "Work in progress". Circulation. 102(22):2781-91, 2000 Nov 28.
    Click here for abstract
  3. 3. Hankins SR. Horn EM. Current management of patients with pulmonary
  4. hypertension and right ventricular insufficiency. Curr Cardiol Rep 2000 May;2(3):244-51
    Click here for abstract
  5. 4. Krowka MJ. Pulmonary hypertension: diagnostics and therapeutics. Mayo
  6. Clinic Proceedings. 75(6):625-30, 2000 Jun.
  7. 5. Arroliga AC. Dweik RA. Kaneko FJ. Erzurum SC. Primary pulmonary
  8. hypertension: update on pathogenesis and novel therapies. Cleveland Clinic Journal of Medicine. 67(3):175-8, 181-5, 189-90, 2000 Mar
  9. 6. Barnette MS. Underwood DC. New phosphodiesterase inhibitors as
  10. therapeutics for the treatment of chronic lung disease. Current Opinion in Pulmonary Medicine. 6(2):164-9, 2000 Mar
    Click here for abstract
  11. 7. Voelkel NF. Tuder RM. Severe pulmonary hypertensive diseases: a
  12. perspective. European Respiratory Journal. 14(6):1246-50, 1999 Dec
    Click here for abstract
  13. 8. Rabinovitch M. Pulmonary hypertension: pathophysiology as a basis for
  14. clinical decision making. Journal of Heart & Lung Transplantation. 18(11):1041-53, 1999 Nov.


What do you know about the anesthetic management of patients suffering from Familial Periodic Paralysis?—panjwani786@hotmail.com

Dr. Katherine Grichnik responds:

The Anesthetic Implications of Familial Periodic Paralysis Familial Periodic Paralysis (FPP) is categorized as a myopathy. The periodic paralysis myopathies come in three forms, hypokalemic, normokalemic and hyperkalemic. The most common form is the FPP is the hypokalemic form of periodic paralysis.

Genetic research indicates that periodic paralyses are caused by mutations in the genes that control development of sodium and/or calciumion channels in the muscle membrane. DNA testing is available but unreliable for absolute diagnosis.

Hypokalemic FPP is an inherited disease, autosomal dominent. Attacks usually begin in the first or second decade and occur in both sexes. Attacks start out infrequently but may ultimately occur daily. Attacks last from minutes to days. The attacks are characterized by proximal weakness of the arms and legs (especially hips and shoulders) followed bydistal weakness, usually sparing smooth or cardiac muscle. However, bulbaror respiratory weakness can be fatal. Reflexes are decreased or absent. Patients can lose sensation in paralyzed limbs but are alert during attacks. Usually there is a fall in serum potassium during the attack. During this time there may be urinary retention of sodium, potassium, chloride and water. Attacks resolve suddenly with full recovery of muscle function, but with repeated attacks permanent paralysis mayoccur. Patients can have a positive Babinski's reflex.

Concurrent problems during an attack may include cardiac arrhythmiasdue to hypokalemia. Airway protection must be considered if bulbar and respiratory weakness occurs. Prevention is with acetozolamide and avoidance of triggering situations. Attacks may be triggered by ingestion of a high carbohydrate meal, with rest after exercise, by infusions ofglucose/insulin, stress and hypothermia. Treatment includes potassiuminfusion and treatment of cardiac arrhythmias.

The hyperkalemic form of FFP is much rarer than the hypokalemic form.It seems to be associated with a mutation of the sodium channel in muscle membranes. Prevention is also with acetozolamide and avoidance of triggering situations. Triggers may be exercise, potassium infusions, metabolic acidosis, and hypothermia. Treatment is directed toward protection of the heart from high potassium levels (calcium) and reductionof serum potassium levels

Other problems/diseases which could occur with or be mistaken for this disease are listed:

  1. Andersen's syndrome: A distinct form of periodic paralysis with hyper or hypokalemia, with long QT syndrome and skeletal abnormalities.
  2. Thyrotoxic hypokalemic periodic paralysis? hypokalemic periodic paralysis which is associate with an overactive thyroid gland, especially found in Asian male patients
  3. Malignant hyperthermia ? Mutations in the same gene responsible for MH have been liked to FPP. The diseases may be allelic. Patients are thought to be at increased risk of MH.
  4. Parmyotonia congenital may be a form of hyperkalemic periodic paralysis which can produce muscle stiffness or rigidity and weakness in response to cold or activity.
  5. Pain, acetozolamide side effects or drug interactions, migranes, and cognitive dysfunction between attacks can occur.
  6. Other diseases may have brief episodes of paralysis include diabetes, Addison's disease, and renal insufficiency. These episodes may follow administration of glucose in these patients

The anesthetic management of patients with periodic paralysis first involves knowing the patient's history and their particular disease characteristics. The concurrent diseases must be ruled out (such as Andersen's disease). The primary goal of the anesthetic is to avoid events (perioperatively) that are known to precipitate muscle weakness. Electrolytes should be normalized, hypothermia should be avoided and frequent monitoring of the serum potassium level is indicated. The ECGshould be constantly monitored for signs of arrthymias. These patients can be considered at risk of MH, thus avoidance of MH triggers is indicated.Use of nondepolarizing muscle relaxants is thought to be acceptable,although abnormal sensitivity to these agents may be encountered and adequate muscle strength must be assured prior to extubation.

References:

  1. PG Barash, BF Cullen, RK Stoelting, eds. Clinical Anesthesia, 3rd Edition, Lippincott-Raven, Philadelphia, 1997
  2. RK Stoelting, SF Dierdorf, eds. Anesthesia and Coexisting Disease, 3rd Edition, Churchill Livingstone, New York, 1998
  3. Sillen A, et al : Identification of mutations in the CACNL1A3 gene in 13 families of Scandinavian origin having hypokalemic periodic paralysis and evidence of a founder effect in Danish families. Am J Med Genet. 69: 102-106, 1997.
  4. Jurkat-Rott K, et al: A calcium channel mutation causing hypokalemic periodic paralysis. Hum Molec Genet. 3: 1415-1419, 1994.
  5. Ptacek LJ, et al : Dihydropyridine receptor mutations cause hypokalemic periodic paralysis. Cell 77: 863-868, 1994.
  6. Lapie P, et al : Hypokalemic Periodic Paralysis: an atosomal dominant muscle disorder caused by mutations in a voltage-gated calcium channel. Neuromuscular Disorders 7:234-240, 1997.
  7. Ptacek LJ, et al: Periodic paralysis. In: Fauci AS, et al, eds. Harrison's Principles of Internal Medicine. 14th Ed. NYC, McGraw Hill, 1998
  8. Johnsen, Torsten; Familial Periodic Paralysis with Hypokalaemia, Danish Medical Bulletin, March 1981 Vol. 28 No. 1
  9. Sagild U.: Hereditary Transient Paralysis, Copenhagen: Munksgaard,1959.
  10. Talbott JH.: Periodic paralysis: a clinical syndrome. Medicine 20: 85-143, 1941.
  11. Engel AG.: Disorders of Voluntary Muscle, 5th ed. Chapter 25 "Metabolic and Endocrine Myopathies," Edinburgh: Churchill Livingstone, 1988.
  12. Links T et al; Permanent Muscle Weakness in Familial Hypokalemic Periodic Paralysis, Brain 1990.
  13. Gamstorp I: Disorders Characterised by Spontaneous Attacks of Weakness Connected with Changes of Serum Potassium; Genetics of Neuromuscular Disorders, pp 175-195 1989; Alan R. Liss Inc.
  14. Links ThP, et al; Familial Hypokalemic Periodic Paralysis; Cip-Cegevens Kononklijke Bibliotheek, Den Haag 1992 ISBN 90-9005053-1
  15. Swash M, Schwartz MS: Neuromuscular diseases: A practical approach to diagnosis and management; 2nd ed. "The Periodic Paralyses" pp 344-348 London; Springer-Verlagg 1988
  16. Riggs JE. Review of the periodic paralysis; Clinical Neuropharmacology 1989.
  17. Links T, et al; Improvement of muscle strength in familial hypokalemic periodic paralysis with acetazolomide; Journal of Neurology, Neurosurgery and Psychiatry 1988
  18. Monnier N, et al. Malignant-hyperthermia susceptibility is associated with a mutation of the alpha1- subunit of the human dihydropyridine-sensitive L-type voltage-dependent calcium-channel receptor in skeletal muscle. Am J Hum Genet. 60:1316-1325:1997
  19. Manning BM, et al : Novel mutations at a CpG dinucleotide in the ryanodine receptor in malignant hyperthermia. Hum Mutat. 11: 45-50, 1998.
  20. Manning BM, et al: Identification of novel mutations in the ryanodine-receptor gene (RYR1) in malignant hyperthermia: genotype-phenotype correlation. Am J Hum Genet. 62: 599-609, 1998.
  21. Levitt LP, Rose LI, Dawson DM: Hypokalemic periodic paralysis with arrhythmia. New Eng J Med. 286: 253-254, 1972.
  22. Sansone,V.; Griggs, R. C.; Meola, G.; Ptacek, L. J.; Barohn, R.;
  23. Iannaccone, S.; Bryan, W, Baker, N, Janas, SJ, Scott, W, Ririe D, Tawil R. : Andersen's
  24. syndrome: a distinct periodic paralysis. Ann Neurol. 42: 305-312, 1997.
  25. Abbott GW, Sesti F, Splawski I, Buck ME, Lehmann MH, Timothy KW, Keating, MT, Goldstein SAN. : MiRP1 forms I(Kr) potassium channels with HERG and is associated with cardiac arrhythmia. Cell 97: 175-187, 1999. PubMed ID : 10219239
  26. Abbott GW, Butler MH, Bendahhou S, Dalakas MC, Ptacek LJ, Goldstein SAN. : MiRP2 forms potassium channels in skeletal muscle with Kv3.4 and is associated with periodic paralysis. Cell 104: 217-231, 2001.
  27. Bulman DE, Scoggan KA, van Oene MD, Nicolle MW, Hahn AF, Tollar LL, Ebers GC. : A novel sodium channel mutation in a family with hypokalemic periodic paralysis. Neurology 53: 1932-1936, 1999. PubMed ID : 10599760
  28. Jurkat-Rott K, Mitrovic N, Hang C, Kouzmekine A, Iaizzo P, Herzog J, Lerche H, Nicole S, Vale-Santos J, Chauveau D, Fontaine B, Lehmann-Horn F. : Voltage-sensor sodium channel mutations cause hypokalemic periodic paralysis type 2 by enhanced inactivation and reduced current. Proc Nat Acad Sci. 97: 9549-9554, 2000. PubMed ID : 10944223
  29. Inshasi JS, Jose VP, van der Merwe CA, Gledhill RF Dysfunction of sensory nerves during attacks of HypoKPP. Neuromuscular Disorders; June 1999


Does the diagnosis of GERD contraindicate the use of an LMA in lower extremity out-patient surgery? Local opinions vary.—chas.beattie@mcmail.vanderbilt.edu

Dr. Beverly Philip responds:

There is a lot of variation. In general, if the patient has symptoms that are caused or worsened by lying down, that patient should have a protected airway, and not an LMA. however, there are a lot of ohter symptoms that patients report as "GERD." Once again, a good history is critical.


When should one perform an awake endotracheal intubation on the morbid obese patient?—doxacurio@hotmail.com

Dr. David Lubarsky responds:

There are no specific "rules" for when to perform an awake endotracheal intubation. The best approach is the most conservative one - anyone you think might be difficult should get one. It only takes one lost airway in a lifetime to outweigh all the extra time and patient inconvenience of an awake fiberoptic. In our own program of gastric bypass on morbidly obese patients, we differentiate between truncal obesity with little to no airway redundant tissue and a "good" airway using Mallimpati class versus others. We generally feel comfortable with a rapid sequence induction for Mallimpati Class 1 and 2 and no redundant tissue or history suggestive of airway compromise. For those with any potential airway compromise from excess tissue (physical exam, history of difficult intubation, history of snoring, sleep apnea, etc.) or for those with Mallimpati Class 3 or 4, we usually will perform an awake fiberoptic intubation.


We have a patient in our ICU who has become a Ventilator Assisted Individual (VAI) since 27 Jul 2000. She is presently being ventilated in the SIMV+PS mode for the last four and a half months. The cause of her condition is compressive myelopathy cervical spine with atlanto-axial dislocation with high spinal injury (involving the phrenic nerve roots). Her spontaneous ventilatory effort is an absolute zero and she cannot maintain an existence without the ventilator. This is a big drain on the already meager resources of our institution. Please advise how to wean her off the ventilator and whether it will at all be possible?
drsadhan@caltiger.com

Dr. Douglas Coursin responds:

This is a tough situation. I am not sure what type of facility you are working in or what local or regional resources are available to you. In our center, after assessment by neurology, neurosurgery and possibly thoracic surgery (see below for discussion of phrenic nerve pacing), we would have performed a tracheostomy and placed this patient on our chronic ventilator ward. They would then have been placed in a nursing home, extended care facility or at home on a portable ventilator with home health care follow up (specially trained nurses and respiratory therapist to evaluate the patient and educate and assist the family).If this woman has irreparable or irreversible injury to C3-5, she is most likely ventilator dependent. Even if she has adequate accessory muscle activity to do some breathing, she will fail with time and/or be at extremely high risk for respiratory failure and or atalectasis and infection.In some situations at some centers, phrenic nerve pacing (sometimes bilaterally) may be tried. We have not done that for a number of years. In addition, the presence of a tracheostomy may make this difficult. The use of phrenic nerve pacing allows the patient some freedom from full time mechanical support. Some patients can be free of ventilation during the day for example, then rested at night on a portable ventilator.My suggestion is trach, chronic vent and referral of this patient if possible to a specialized center.
What is your opinion about the performance of lower extremity nerve blocks(specifically femoral and popliteal) under general anesthesia for postoperative pain management in an ambulatory surgery practice? Is there any published literature on this?
lalitajha@hotmail.com

Dr. Kathryn McGoldrick responds:

My personal opinion and philosophy is that it is safer to perform blocks with the patient awake. I have noticed several case reports in the literature recently of major neurologic complications following interscalene block performed with the patient under general anesthesia. There is nothing like an awake patient to complain of paresthesia, etc.


During GA for carotid endarterectomy one of my locums anesthesiologists saidthat if it took longer than 2 minutes to place the shunt glucose should beadministered since the brain uses it rapidly. Do you have any informationon this?
dmcclain@datasync.com

Dr. Katherine Grichnik responds:

After searching Medline, there were no randomized studies examining the effect of glucose administration if shunt insertion time was more than 2 minutes found. However, hyperglycemia is known to be a risk factor for poor outcome following stroke irrespective of diabetic status, although a definitive statement on causality cannot be made in the absence of randomized controlled trial data (quoted from reference 3). There is now overwhelming evidence to support the concept of hyperglycemia-induced cerebral damage in the acute phase of stroke, irrespective of whether the patient has previously diagnosed diabetes, unrecognized diabetes, impaired glucose tolerance, or "stress hyperglycemia," (quoted from reference 3) . However, the timing of the hyperglycemia surrounding cerebral ischemia and the adequacy of the remaining blood flow seem influence the effect of hyperglycemia on outcome (see reference 2). Thus, the effect of acute administration of glucose in this situation would depend on the patient's initial glucose level, how much cerebral ischemiais or has occurred and how good the remaining blood flow to the brain is.

Abstracts from Medline which are pertinent:

  1. Glucose solutions are associated with stroke occurrence during carotid endarterectomy: Preoperative risks predict neurological outcome of carotid endarterectomy related stroke. Sieber FE. Toung TJ. Diringer MN. Wang H. Long DM. Neurosurgery. 30(6):847-54, 1992 Jun.
    Click here for abstract
  2. However, the influence of hyperglycemia on cerebral ischemia is controversial: Blood glucose and stroke. Nagi M, Pfefferkorn T Haberl RL. Nervenarzt. 70(10):944-9, 1999 Oct
  3. Click here for abstract
  4. A well written paper discussing this topic: the abstract and introduction are included as they are both pertinent to this question:Glucose Potassium Insulin Infusions in the Treatment of Acute Stroke Patientswith Mild to Moderate Hyperglycemia: The Glucose Insulin in Stroke Trial (GISTScott, Jon F. BM, BS; Robinson, Gina M. RGN; French, Joyce M. BSc; O'Connell,Janice E. MB, ChB; Alberti, K.G.M.M. MD; Gray, Christopher S. MD Stroke:Volume 30(4) April 1999 pp 793-799
  5. Click here for abstract

What do you do with an incomplete spinal during a total knee? When performing a total knee, sometimes the spinal is inadequate and the patient can contract the quads and the patella moves. In some patients, the patella is difficult to evert and I THINK it is related to an incomplete spinal. In some cases, I can insert a plastic spacer, all looks well and then a while later, the spacer can no longer be inserted into theknee because of tightness. The anaesthesiologist usually administers Diprivan which causes the situation to occasionally get worse because the patient gets confused and appears to affect muscle tone. Do you agree that the use of a general is best, or are there better choices?mmessieh@aol.com

Dr. Francine D’Ercole responds:

In my practice over the past 10 years delivering orthopedic anesthesia there has been only a few (about three or four) incidents I recall of a 'completely' failed spinal. Usually the spinal was associated with an 'isobaric' localanesthetic which may have an unpredictable onset. A general anesthetic was performed after a failed spinal had occurred (that is, after waiting 30-45minutes). However, after emergence the patient was brought to the recovery room with a full motor/sensory block below the T10 dermatome. A profound 'delay' is spinal anesthesia had occurred. The etiology of this scenario is theoretical and may be associated with an a typical CSF volume especially common in geriatric patients. There is a place for 'isobaric' vs hyperbaric spinal anesthesiae specially in patients with a cardiac history who may not tolerate a high sympathectomy but the benefit/risk(s) need to be decided by the anesthesiologist.In the case you describe there is evidence a spinal anesthetic was successful,however, the 'level' may not have been high enough to provide optimal conditions. If this is true there should be NO sensory level between T10 and L2 dermatomes. An example may include: a hyperbaric spinal placed in the sittingposition with a delay in recumbent positioning resulting in a saddle block ormostly saddle block.ASRA (American Society of Regional Anesthesiology) recommendations for spinalanesthesia include:
  • Do not re-dose local anesthetics (LA) immediately after an inadequate or failed spinal anesthetic is administered. A second dose of LAmay be neurotoxic and predispose the patient to transient radicular irritation(TRI) or cauda equina.

  • Alternatively, a general anesthetic (GA) is appropriate if the patient is hemodynamically intact (minimal evidence of sympathectomy). Ifthe surgical procedure is of short duration a mask GA or laryngeal mask isappropriate if the spinal is partial/inadequate or short-lived (shorter than theprocedure). A failed spinal or a longer surgical procedure may require a GAwith endotracheal intubation or laryngeal mask with a 'balanced' anesthetictechnique. A balanced anesthetic may include the combination of: an inductionagent such as propofol, propofol infusion, narcotics, benzodiazepines,inhalational agents, muscle relaxants. The muscle relaxants administered with a 'secure airway' would provide the motor relaxation necessary for surgery in a safecontrolled manner. If blinded, you should be unable to determine the differencebetween motor blockade afforded by successful spinal anesthesia when compared togeneral anesthesia with muscle relaxants.

    If surgery is already underway part of the goal, especially for total jointsurgery, is to assure the patient NOT have awareness or the perception of painduring surgery.

The acute 'confusion' you describe is not from propofol alone;rather, it is inadequate anesthesia during a very stimulating portion of thesurgery (a.k.a.: acute profound pain causing a temporary delirious state with anattempt to manage discomfort with propofol). If 'break-through' discomfortoccurs temporizing with mask GA is appropriate until this portion (reaming themost stimulating) is complete. If mask GA or propofol bolus is not quite enoughto get the patient comfortable in a 'reasonable' amount of time then the airwayneeds to be secured in conjunction with a deep general anesthetic. Theanesthesiology-surgery TEAM needs to define 'reasonable' with patient safety thefirst priority; not three extra minutes of efficiency afforded by an abruptintubation. An abrupt induction for intubation with a residual spinalsympathectomy may not be tolerated by patients with coexisting cardiopulmonary disease. The surgical team may need to pause until a deeper level of anesthesia is SAFELY achieved.Addressing operating room efficiency, assuming spinal anesthesia is effectiveand successful 90-95% of the time for total knee surgery. Then, you should nothave to endure the time for emergence after a full general anesthetic most ofthe time. I would graciously accept the 5% occasional intraoperativeinconvenience afforded by an overall quality productive system.


Please tell me the incidence of nerve damage after brachial plexus block by interscalene approach. — P. Raghavendra Rao

Dr. Francine D’Ercole responds:

I do not recall anyone publishing the incidence of nerve damage after an interscalene block. Neurologic complications after shoulder surgery remains largely unstudied, except for case reports. However, there is an important reference for anyone who performs interscalene(IS) blockade, especially for shoulder surgery.The article below describes neurologic complications after total shoulder arthroplasty.

  • Lynch NM, Cofield RH, Silbert PL, Herman RC. Neurologic complications after total shoulder arthroplasty. J Shoulder and Elbow Surgery 1996;5:53-61. click here for abstract

The authors report a 4% frequency of neurologic injuries following shoulder(total arthroplasty) surgery in a retrospective study reviewing 417 cases in 368patients undergoing total shoulder arthroplasty. An IS block was used in only47 of the cases.The authors noted most injuries occurred at the level of the upper and middletrunks of the brachial plexus (BP). The presumed mechanism of injury wastraction on the BP occurring during surgery. No axillary or local nerve injurieswere identified which is contrary to reports in the literature. Risk factorsincluded: surgical approach, operative time, a chemotherapeutic agent.Additional comments include the difficulty in identifying an etiology forneurologic complications in patients receiving an IS block for shoulder surgery,since the site of needle insertion approximates the level where the deficitsusually occur at the level of the upper or middle trunks.


Our orthopedic surgeons state that if geriatric fractured hips are not operated on quickly (within 24-48 hours) that they will often developp neumonia and die as a result. Is there any data to support this claim? —keatswrx@golden.net

Dr. Francine D’Ercole responds:

To date NO meta-analysis has been completed to describe clinical outcomes with recommended treatment for hip fractures. The timing of surgery remains controversial. Evidence that a delay in operating leads to increase morbidity is inconclusive. In general, early surgery is indicated in premorbidly fit patients, where as surgery should be delayed if correctable comorbidities are present.Reiterated, delay in fracture fixation in elderly patients who were physiologically stable on admission, significantly increases morbidity and mortality. However, surgery performed within 72 hours on patients with acute medical illnesses in addition to their fractures was associated with a higher death rate.A publication by JD Zuckerman [2], a prospective study which included 367 patients, concluded that a delay of more than two calendar days after admission is an importantpredictor of mortality within one year for the elderly who have a hip fracture,cognitively intact, walking, living at home before fracture.

References:

  1. Lyons AR. Clinical outcomes and treatment of hip fractures. Am J Med. 1997 Aug 18; 103(2A):51S-64S.
    Click here for abstract
  2. Zuckerman JD. J Bone Joint Surgery Am. 1995 Oct;77(10):1551-6

What is your advice concerning the treatment of orchiodiny (testicular pain)? — faberbox@hotmail.com

Dr. Richard Rosenquist responds:

The treatment of testicular pain is highly dependent on the presumedetiology of the pain. Is it something that began after trauma, surgery, vasectomy, orchiectomy or spontaneously? Is it a dull aching pain? Is it related to physical or sexual activity? Is it associated with numbness or hypersensitivity? The treatments might range from support to medications including tricyclic anti-depressants, anti-seizure medications, oranalgesics, injections, surgery or psychologically based treatments. The pain literature does not have a great deal to offer in this area at the present time. We are currently designing a joint study with the department of Urology at the University of Iowa to begin to provide a better definition of the types of testicular pain, the potential treatments and the long term outcome of the treatments. We hope that this will allow us to be more successful in treating these very difficult pain problems in the future.


Is there an increased risk of air/fluid emboli in a patient undergoing a hysteroscopy who has a history of mitral valve prolapse? —BRoehm7925@aol.com

Dr. David Lubarsky responds:

Increased risk is associated with venous pressure and surgical technique. A well managed patient with MV prolapse should be well-replete with fluids prior to anesthesia, The risk may even be reduced, as attention is now being paid to fluid status


In our country [Spain], we don't have experience in the perioperative management of patients with hemoglobin-s anemia (drepanocytic a.).Could you send my recommended references or protocols? We start now to receive patients with this, until recently, "exotic" disease. — J.Serra

Dr. David Lubarsky responds:

Assuming you are speaking about Hgb S (Sickle Cell Disease and Trait), I suggest Stoelting and Dierdorf's Anesthesia and Co-Existing Disease, p.401-403, Third Edition, published by Livingstone Publishers.


I would like to ask question about high block. In my hospital we had a 15 year old boy came to the OR for debridement in his leg. We decided to use a spinal block for this operation. We had a successful block with 0.5% isobaric marcaine 3.2 ml, and then level of block rose to T1. Blood pressure was dropping, but we were able to support this with ephedrine. However, the patient became very anxious, even after we reassured him. We assessed that ventilation was adequate. should this patient be sedated to reduce his anxiety? What is the best way to manage this patient? —pui_vech@yahoo.co

Dr. David Lubarsky responds:

Interestingly, I had a similar case where the use of 3cc isobaric 0.5% marcaine resulted in an unexpectedly high block. I have never had that problem with isobaric 2% lidocaine. The anxiety was related to the inability to sense breathing. Diaphragmatic excursion is absolutely sufficient in a young person absent chest musculature. However, one cannot sense one's chest moving up and down, so anxiety and dyspnea (defined as awareness of each respiration) result. Sedationi with non-vasodilating drugs would be appropriate, with support of ventilation as required.


We have noticed higher incidence of post operative nausea and vomiting in breast surgery patients in post operative patients. Is there a reason for this? —jyotsna_punj@yahoo.com

Dr. Kathryn McGoldrick responds:

There is definitely a very high incidence of PONV in breast surgery patients. Perhaps it is because many of the patients are both young and female—two groups known to be at higher risk for PONV. Also, some hormonal factors may be operative.


Do different concentrations of oxygen in the post operative period have any effect on post op nausea and vomiting? —jyotsna_punj@yahoo.com

Dr. Kathryn McGoldrick responds:

I am unaware of any randomized, prospective studies on the effect of different concentrations of oxygen on PONV. Recently, studies have shown that increased concentrations of oxygen intraoperatively may be associated with a reduced incidence of postoperative infection in patients having bowel surgery.


What are contraindications for regional (spinal) anesthesia? Sepsis? Fever? How high of fever is a contraindication for subarachnoid block? Is WBC or Fever a criteria ? Is a negative blood culture a "green light"?—david35off@aol.com

Dr. David Lubarsky responds:

This is a matter of some debate. There are no documented incidents of meningitis in an adult to my knowledge related to placement of an epidural/spinal. A old Boston Childrens' Hospital study done on pediatric patients presenting for fever of unknown origin, receiving a spinal tap, and then testing positive for sepsis, were followed for subsequent development of meningitis. One of several age range groups followed had a slightly higher incidence. Therefore, given the lack of proven outcome benefits in most studies of regional vs. general, I would weigh this potential risk against the potential benefit of a spinal/epidural. A negative blood culture would definitely be a "green light" in my opinion.


I recently had a patient aspirate during induction of anesthesia. Could you tell me what you feel is appropriate action when this happens so I can compare it to what was done for this patient? —Crna1990@aol.com

Dr. David Lubarsky responds:

Supportive therapy is the primary approach. Aspiration is discussed in all major textbooks, and I would suggest looking in any text for a full discussion.Prophylactic antibiotics are not indicated (wait for culture positive sputum),nor are steroids, nor is immediate bronchoscopy unless particulate aspiration has occurred. Suctioning the endotracheal tube immediately following the eventis wise. Minor tracheal lavage is often done, but probably not efficacious as acid damage has occurred by the time this is employed, and distal damage is more problematic. Aspiration may worsen over 24 hours, so extubation should only occur if the patient has a large amount of pulmonary reserve. For the same reason, observation for at least 24 hours is mandatory, preferably with pulseoximetry monitoring.


I am a 2nd year Anesthesiology resident. In our hospital, we are using epidural morphine for post-operative pain control. We give 2-3 mg morphine in 10 cc nss or sterile water. One of our patients, female, 70 years old, ASA 2, had a cholecystectomy under GA. We placed an epidural catheter approximately 6-7 cm in the epidural space. The next day when I was giving epidural morphine, the patient complained of pain instead of the usual cold sensations. The pain was localized in the subcostal area right side. Can you provide any explanation of this? What reference can you suggest in finding out the incidence of pain during the administration of epidural morphine?

drtotoboy@hotmail.com

Dr. Richard Rosenquist responds:

There are a host of reasons for a patient to complain of pain during an epidural injection, depending on where the catheter is inserted andwhere the tip is located. It is common for older adults to develop either neuroforaminal narrowing or central canal narrowing leading to "spinalstenosis". In some elderly patients receiving epidural injections, thereis a sudden increase in hydraulic pressure that can produce pain. This may also be seen in patients who have had prior back surgery. It is also possible for the catheter tip to exit the spinal canal via a neuroforamen.The large volume of injectate may create some localized pressure on a nerveroot or expand tissue outside of the spinal canal resulting in pain. I amnot aware of any specific reference giving the incidence of pain duringepidural injection. I will say that if the patient has an unusual paincomplaint or rapid onset of numbness, the injection should be stopped. Thecatheter may need to be withdrawn slightly or replaced altogether to correct the problem.


What are the recommendations for administering regional anesthetics to patients taking plavix, pletal and ticlid (all anti-plateletinhibitors)? —Ron Olson MD abillue@usa.net

Dr. David Lubarsky responds:

We generally recommend being off Plavix for 7 days, but our thoracic anesthesia colleagues performing both thoracic epidurals and paravertebral blocks like to see them off for 11 days. Some vascular surgeons will do a case without discontinuing it, if necessary, but then we do not perform regional anesthetics.There is no definitive answer as to safety. I've never heard of pletal - please feel free to resubmit with a generic name and we'll try to find it.We treat ticlid about like aspirin, stop it for 5 days if possible, but generally don't worry about it if there is a good reason to be on it.
What is the current thinking regarding the appropriateness of regional techniques for patients with peripheral neurological syndromes? I recently decided not to use my usual technique of epidural anaesthesia in a wheelchair-bound patient with severe diabetic neuropathy for Fem-pop bypass, purely to protect myself from 'hassle' later on. Is this reasonable? —jyotsna_punj@yahoo.com

Dr. Francine D’Ercole responds:

The decision may need to be based on a Benefit versus Risk scale. I agree peripheral neurologic states may not afford you with accurate patient feedback necessary to identify a parathesia. However, alternative regional techniques may include isobaric spinal anesthesia (assuming agents such as lovenox, plavix, pletal are not part of the patients regime). The benefit may be reducing morbidity in a patient who may not tolerate general anesthesia.

Reference:

  • Roger A, Walker N, et al. Reduction of postoperative mortality and morbidity with epidural or spinal anesthesia: results from overview of randomized trials. BMJ 2000; 321: 1-12.

What is the effect of catecholamines on:
  1. Venous grafts after coronary artery bypass grafting (CABG)?
  2. The post-transplant heart?
    k_sanky@yahoo.com

Dr. Katherine Grichnik responds:

This is very difficult question to answer, as there is not much literature that has been written about these specific questions. The pattern of catecholamine elevation perioperatively has been addressed in previous studies. In upper abdominal surgery, epinephrine (E) increases and remains elevated for 3-12 hours postoperatively [1,2] whereas norepinephrine (NE) may stay elevated for 72 hours. Coronary artery bypass surgery (CABG) is associated with exaggerated hormonal and inflammatory responses occurring during and after cardiopulmonary bypass (CPB) and continuing for 12 h or longer [11]. There are markedly increased concentrations of plasma catecholamines and stress-related hormones [11]. Cheng, et al. found that E increased 300% over baseline levels in the first 3 hours after surgery in CABG patients [4]. Parker et al. have suggested that elevated mean arterial pressure (MAP) with emergence and in the early postoperative period is associated with high total NE concentration in patients undergoing lower extremity revascularization [5]. Further, they found that hypertension in the postoperative period is associated with persistently elevated NE concentration [5]. This group also found an increase incidence of myocardial infarction and death in those with increased postoperative catecholamine concentrations in the vascular surgery patient population [5].

Mitigation of the postoperative endocrine response may be of clinical benefit in patients undergoing CABG surgery [11]. Release of catecholamines, specifically NE, is associated with increases in systemic vascular resistance and arterial pressure, and suppression of the sympathetic nervous system response could have beneficial effects on fibrinolysis, sensitivity of platelets to E, left ventricular function, and coronary artery vasoconstriction [11]. However, outcome data from cardiac surgical patients, relating adverse events to modulation of the postoperative endocrine response, are limited .

The concern about the effect of catecholamines on saphenous vein grafts relates to concern about graft function [11]. Spasm of arterial and venous graft conduits can occur both during harvesting and after the graft is connected [12]. After a coronary artery bypass graft is connected, spasm can cause major problems with myocardial perfusion. To select the best pharmacologic agent to prevent or reverse vasoconstriction in a graft requires an understanding of the reactivity of that particular type of graft to vasoconstrictor and vasodilator agents [12]. Rosenfeldt et al. review the current state of knowledge about the reactivity of arterial and venous grafts to vasoconstrictor and vasodilator agents [12]. They describe the practical application of this knowledge in the operating room and in the postoperative care.

Attention is also being turned to the hypercoagulable state as a cause of graft failure [13]. Tuman et al has suggested that decreasing the stress response (in part from elevated catecholamines) may decrease a postoperative hypercoagulable state, which may decrease the incidence of graft thrombosis [6]. Although there are some exciting new modalities for preventing graft disease, the difficulty in transposing animal data to humans and the uncertainty of the biologic similarities of in vitro and in vivo endothelial cell biochemistry makes any immediate solution to vein graft failure unlikely [13]. Therefore an even greater increase in the use of arterial grafts in the near future seems likely [13].

The effect of catecholamines on venous bypass grafts is difficult to separate from what the effect is on the heart and the hemodynamic status of the patient as a whole. For example, in a low cardiac output (LCO) state, exogenous catecholamine administration may be necessary to achieve an adequate MAP to allow for graft perfusion and thus adequate myocardial perfusion. A side effect of elevated catecholamines on venous bypass grafts may include the effect of hypertension on graft stress, which may lead to bleeding. There is also a suggestion that some instances of LCO syndrome is in part caused by the very catecholamines used to treat LCO. This could also lead to poor venous graft flow and perhaps to thrombosis and/or graft failure.

We must remember that many transplanted hearts may have already suffered a myocardial injury due to catecholamines [8]. Brain death of the donor has been noted to be preceded by hypertension and corresponding elevations in serum catecholamine levels [10]. Catecholamine levels may fall shortly after brain death. Thus a donor heart can be exposed to excessive catecholamines. The resulting myocardial injury may be more pronounced or apparent the longer the patient is kept alive after neurological injury. The injury can be described as a focal myocardial necrosis characterized by contraction band necrosis [8]. Thus, a donor heart may arrive with both an injury and perhaps with a need for exogenous catecholamine administration due to down regulation of myocardial adrenergic receptors after catecholamine exposure.

The need for use of additional exogenous catecholamines in the post transplant period is dependent on a number of factors including (but not limited to) the condition of the heart at the time of procurement, duration of cardiac ischemia, effectiveness of the solution used to preserve the heart in transport, duration of cardiopulmonary bypass after reperfusion, exposure of the recipient’s circulation to prior catecholamine therapy (especially milrinone) and haemostatic abnormalities requiring pressor support to maintain MAP. Clearly, the least amount of catecholamine use, the better for the transplanted heart (or any heart for that matter). However, it is neither possible nor feasible to exclude catecholamines in the post bypass period after transplant in many patients. The tradeoff is a possible myocardial injury versus hemodynamic stability. It is prudent of limit the catecholamine dosage to that needed for the desired hemodynamic effect.

Another interesting twist is the persistent elevation of atrial natriuretic factor (ANF) after transplantation [9]. The interaction of cyclosporine with vascular smooth muscle and endothelial cells leading to increased sensitivity to vasopressor hormones and increased circulating levels of endothelin may be the most likely explanation for the chronic elevation of ANF plasma levels [9]. In this context, ANF may play a key role in moderating the side effects of cyclosporine treatment [9].

References:

  1. Young JB, et al. Dissociation of sympathetic nervous system and adrenal medullary responses. Am J Physiol 1984;247:E35-E40
    Click here for abstract
  2. Dorman T, et al. Effects of clonidine on prolonged postoperative sympathetic response. Crit Care Med 1997;25:1147-52
    Click here for abstract
  3. Sun LS, et al. Crit Care Med 1997;25:1930-3
  4. Cheng DCH, et al. JTCVS 1996;112:755-64
  5. Parker SD, et al. Catecholamine and cortisol responses to lower extremity revascularization: correlation with outcome variables. Perioperative Ischemia Randomized Anesthesia Trial Study Group. Crit Care Med 1995;23:1954-61
    Click here for abstract
  6. Tuman K et al. Effects of epidural anesthesia and analgesia on coagulation and outcome after major vascular surgery. Anesth Analg 1991;73:696-704
    Click here for abstract
  7. Papp L, et al. Arvosi Hetilap 1999;140:179-85
  8. Baroldi G, et al. J Heart & Lung Transplantation 1997;16:994-1000
  9. Masters RG, et al. Neuroendocrine response to cardiac transplantation. Canadian Journal of Cardiology. 1993;9:609-17
    Click here for abstract
  10. Powner DJ et al. J Heart & Lung Transplantation. 1992;11:1046-53
  11. Plunkett, J, et al. Urine and plasma catecholamine and cortisol concentrations after myocardial revascularization. Modulation by continuous sedation. Multicenter Study of Perioperative Ischemia (McSPI) Research Group, and the Ischemia Research and Education Foundation (IREF). Anesthesiology 1997;86:785-796
    Click here for abstract
  12. Rosenfeldt, et al. Pharmacology of coronary artery bypass grafts. Annals of Thoracic Surgery. 1999;67:878-88
    Click here for abstract
  13. Mills NL, Everson CT Current Opinion in Cardiology. 1995:10:562-8

How does one approach a patient whose pulse oximetry is in the low 90s just prior to induction of anesthesia without any abnormalities in CXR or physical, especially in a young patient who is a heavy smoker but who has no history of lung disease? What benefit is there in routinely recording pulse oximetry in the preop assessment clinic?
— Shanthi Rajendran shanthi@peoplepc.com

Dr. Katherine Grichnik responds:

A low preoperative SpO2 deserves an investigation as to why it has occurred. There are multiple reasons that a patient may have a low SpO2 preoperatively:

  • Machine error
  • Abnormal hemoglobinopathy
  • IV dye administration
  • fingernail polish
  • probe movement
  • excessive light conditions
  • excessive venous pulsations
  • Multiple medical conditions may also lead to arterial hypoxemia, including:
  • Decompensated pulmonary edema and congestive heart failure
  • Sickle cell anemia
  • Diseases with intrapulmonary shunting (such as bronchoalveolar carcinoma and congenital AV shunting)
  • Congenital heart disease with intracardiac shunting
  • Pneumonia
  • Alveolar hypoventilation syndrome with obesity
  • Severe COPD

An arterial blood gas using a co-oximeter if necessary should be done to confirm or disprove a low SpO2 reading. Serious pulmonary and cardiac diseases should be sought. If heart disease is suspected, a cardiac work-up including transthoracic echo to detect intracardiac lesions may be useful. I believe that routinely recorded SpO2 in the preoperative assessment clinic is very useful. An abnormal finding can thus be investigated in the preoperative time period instead of risking the possibility of a cancelled or delayed case as the result of this finding just before surgery.


A patient had a dural tap with a first attempt. An epidural catheter was successfully placed at another level for post op pain control. The following day the patient developed a post dural puncture headache. Conservative treatment is commenced for 24 hours, but without improvement. An epidural bloodpatch is the next consideration. Can it be given via the existing catheter?
pretoriu@home.com

Dr. Richard Rosenquist responds:

The answer is yes. The blood patch can be given via the existing catheter. There is no good data to compare the success rates of injecting via the needle as compared to injecting via the catheter, but it has definitely been performed successfully.


We are six anesthesiologists performing a large volume of surgery for one surgeon and one procedure. We have had varying rates of PONV even though the anesthesia technique is always the same. Overall PONV rate is about 3%. We would like to have a scientific look at our individual rates. How many cases do we need to study to document a significant difference or lack of it? Is there a simple reference?
— R Rajendran MB


Dr. Katherine Grichnik
responds:

This is an answer from one of our statisticians:

The answer depends on what you are trying to compare. That is, PONV rates in which different groups? To find sample required, the investigator must specify the alternative PONV rate expected. Also, with such a small incidence rate, finding a difference will require very large samples. For example, to show a difference in rates from 3% down to 1.5% would require 1650 subjects in each of 2 groups (at alpha=0.05 and 80% power in 2-tailed test). To distinguish between 3% and 6% would require 800 subjects per group. A good reference with sample size tables is Joseph L. Fleiss, Statistical Methods for Rates and Proportions, 2nd Edition. New York: John Wiley and sons, 1981



Can you please help me to find information about:
  • anesthesia and acute alcoholism

  • anesthesia and chronic alcoholism

— Dr Marc Reynvoet marc.reynvoet@groeninghe.be

Dr. Katherine Grichnik responds:

The best place to start is a general textbook such as Anesthesia and Coexisting Disease, edited by RK Stoelting, SF Dierdorg and RL McCammon (Churchill Livingstone, New York). The chapter on "Diseases of the Liver and Biliary Tract" covers the anesthetic implications of acute and chronic alcoholism. A Medline search yielded the other references below:

  1. Spies C. Anesthesiologic aspects of chronic alcohol abuse. Ther Umsch, 2000 Apr, 57:4, 261-3
    Click here to view abstract

  2. Fiset L, Leroux B, Rothen M, Prall C, Zhu C, Ramsay DS. Pain control in recovering alcoholics: effects of local anesthesia. J Stud Alcohol 1997 May 58:3 291-6
    Click here to view abstract

  3. Fassoulaki A, Farinotti R, Servin F, Desmonts JM. Chronic alcoholism increases the induction dose of propofol in humans. Anesth Analg 1993 Sep 77:3 553-6
    Click here to view abstract

  4. Temes R, Feteiha M, Mapel D, Crowell R, Ketai L, Wernly J. Esophageal rupture after regional anesthesia: report of two cases. J Clin Gastroenterol 1999 Jun 28:4 360-3
    Click here to view abstract


  5. Sadeghi P, Zacny JP. Anesthesia is a risk factor for drug and alcohol craving and relapse in ex-abusers. Med Hypotheses 1999 Dec 53:6 490-6
    Click here to view abstract


  6. Orr DL 2d, Glassman AS. Conversion phenomenon following general anesthesia. J Oral Maxillofac Surg 1985 Oct 43:10 817-9
    Click here to view abstract


  7. Patel R, McArdle JJ, Regan TJ. Increased ventricular vulnerability in a chronic ethanol model despite reduced electrophysiologic responses to catecholamines. Alcohol Clin Exp Res 1991 Oct 15:5 785-9
    Click here to view abstract


  8. Swerdlow BN, Holley FO, Maitre PO, Stanski DR. Chronic alcohol intake does not change thiopental anesthetic requirement, pharmacokinetics, or pharmacodynamics. Anesthesiology 1990 Mar 72:3 455-61
    Click here to view abstract


  9. Newman LM, Curran MA, Becker GL. Effects of chronic alcohol intake on anesthetic responses to diazepam and thiopental in rats. Anesthesiology 1986 Aug 65:2 196-200
    Click here to view abstract

  10. Stubbs CD, Slater SJ. Ethanol and protein kinase C. Alcohol Clin Exp Res 1999 Sep 23:9 1552-60
    Click here to view abstract


  11. Shapira Y, Lam AM, Paez A, Artru AA, Laohaprasit V, Donato T. The influence of acute and chronic alcohol treatment on brain edema, cerebral infarct volume and neurological outcome following experimental head trauma in rats. J Neurosurg Anesthesiol 1997 Apr 9:2 118-27
    Click here to view abstract


  12. Adams ML, Cicero TJ. Alcohol intoxication and withdrawal: the role of nitric oxide. Alcohol 1998 Aug 16:2 153-8
    Click here to view abstract


  13. St Haxholdt O, Krintel JJ, Johansson G. Pre-operative alcohol infusion. The need for analgesic supplementation in chronic alcoholics. Anaesthesia 1984 Mar 39:3 240-5
    Click here to view abstract


Do you have any suggestions to reduce the incidence of post cardiac bypass upper extremity neuropathies? We see 10 to 15 of these a year (1000 heart cases/yr - arms tucked to the side, thumbs up, egg crate padding). Most are temporary but some end up requiring carpal tunnel or ulnar transposition surgeries.
— Charles Spivak, MD Sleeper987@aol.com

Dr. Katherine Grichnik responds:

Injury (clinically apparent and subclinical) to the brachial plexus may occur in up to 87% of patients after CABG using symmetric and asymmetric sternal retraction. Clinical plexopathy has been reported to be between 12% and 37.5% of patients. Studies have revealed conflicting results, in part due to the methods used to assess brachial plexus injury. Studies have used detailed neurological examinations, somatosensory evoked potentials (SSEPs), and electromyogram examination. Patients thought be more at risk include those with diabetic neuropathies, those with preexisting neurological disorders elderly patients, those who had repeated internal jugular cannulation attempts, the use of an automated blood pressure cuff, those who had a long cardiopulmonary bypass time and those patients who are significantly over ideal body weight. Injury occurs with both symmetric sternal retraction and asymmetric sternal retraction (used for internal mammary harvest) and occurs bilaterally. Reasons postulated for the nerve bundle injuries include nerve stretch, nerve compression and nerve injury due to penetration of the nerves by a fractured first rib after sternotomy.

Various interventions have been tried to reduce the incidence of brachial plexus injury. A hands-up (HU) position (arms behind the head and elevated above the level of the table) as opposed to an arms at the side (AAS) position has been investigated [1]. The authors found that both positions resulted in decline of SSEPs, but that the AAS position resulted in a higher incidence of postoperative ulnar symptoms. Various types of retractors (Ankeney, Pittman, Favalaro, Canadian, Rultract, etc) are also used clinically, with the goal of reducing brachial plexus injury. In the above referenced study, the HU position with the Pittman sternal retractor offered a modest decrease in brachial plexus injury. Other interventions would be to try to modify the risk factors identified above.

Reference:

  1. Jellish SW, Blakeman B, Warf P, Slogoff S. Hands-Up Positioning During Asymmetric Sternal Retraction for Internal Mammary Artery Harvest: A Possible Method to Reduce Brachial Plexus Injury. Anesth Analg 1997 Feb;84(2):260-5
    Click here for abstract


What is the risk of Candidal infection in the postoperative patient?

Dr. Douglas Coursin responds:

Candida spp is the fourth most common cause of blood-borne infections in the United States. This is a dramatic increase over the past several decades when it was previously almost unknown. Invasive candidiasis and candidemia are life-threatening complications for critically ill patients. Diagnosis of such infections is often challenging. In addition, various unusual and frequently resistant candidal species other than Candida albicans are occurring more commonly in immunosuppressed and critically ill perioperative patients.

There are a host of risk factors for patients developing candidal sepsis. These include immunosuppression, the presence of indwelling catheters, particularly Hickman and central venous catheters, utilization of broad-spectrum antibiotics, prolonged hospitalization, and perforation of a viscus. Patients who are immunosuppressed, have invasive monitoring performed, and receive broad-spectrum antibiotics are at particularly high risk. Empiric therapy is considered appropriate when patients have more than three sites colonized or when they have even a low number of colonies of fungi present on peritoneal fluid analysis. Historically, amphotericin B was the main antifungal agent for candidal species. However, the more recently developed azole, fluconazole, is frequently used both prophylactically and for therapy for sensitive organisms. However, the selection of resistant organisms and development of resistance is a real problem with the azole compounds. In the past, there has been major concern over the side effect problems associated with amphotericin B, particularly the rapid development of renal insufficiency as well as other systemic side effects. Most recently, liposomal-entrapped amphotericin and colloidal suspensions of amphotericin have been developed which are far less nephrotoxic. However, there is no difference in the effective doses that can be given. The liposomal and colloidal suspensions are dramatically more expensive than generic amphotericin. Patients also usually require pretreatment with Tylenol, Demerol, and sometimes corticosteroids prior to the infusion of any ampho B preparation.

Fungal infections are here to stay. We need to be vigilant for the development of fungal infections in immunosuppressed and high risk patients. We also need to judiciously use anti-microbials to limit the development of resistance to fungi or fungal colonization of our critically ill patients.

References:

  1. Munoz P, et al. Criteria used when initiating anti-fungal therapy against Candida spp in the ICU. International J Anti-Microb Agents 2000; 15:83-90.

  2. Verduyn LFM, et al. Nosocomial fungal infections: candidemia (Review). Diagn Microbiol Infect Dis 1999; 34:213-20.

  3. Dean DA, Burchard KW. Surgical perspective on invasive Candida infections (Review). World J Surg 1998; 22:127-34.


In my ICU, we are very concerned about the succinylcholine use in emergency intubation due to the fear of malignant hyperthermia. Should it be used as first relaxant drug?
— Alfredo Londono M.D allondon@epm.net.co

Dr. Douglas Coursin responds:

Historically, the depolarizing muscle relaxant succinylcholine (sux) has been used frequently for facilitation of intubation during rapid sequence inductions and in critically ill patients. With the development of faster onset aminosteroid nondepolarizers such as

rocuronium and rapacuronium, some experts have advised the routine avoidance of sux. Major concerns with the use of sux in the critically ill center primarily around the risk of life-threatening hyperkalemia in a multitude of clinical scenarios and secondarily the possibility of triggering a malignant hyperthermic response. Hyperkalemic responses secondary to sux may occur more frequently than initially realized. This is a definite risk factor in the following patients:

    • Patients with history of MH
    • Patients with crush injuries
    • Patients after 24 hours of an acute burn until it is completely healed
    • Patients with spinal cord transections, upper motor neuron lesions, and selected stroke and closed head injury patients
    • Individuals with intra-abdominal sepsis
    • Patients who are in renal failure (see text)
    • Patients who are already hyperkalemic prior to intubation
    • Patients with various muscular dystrophies (myotonia congenita or dystrophica)

There have been reports of unexpected hyperkalemia in critically ill patients. These may have been in patients who had an unrecognized neurologic or myopathic pathology or have received long term nondepolarizing agents and have changes in their neuromuscular junction, as well as changes in the receptor with a proliferation of extra-junctional receptors and conversion to a more juvenile receptor.

Furthermore, the use of sux in children remains open to debate and somewhat controversial. A number of years ago, the FDA recommended that sux not be used routinely in children but only in the case of life-threatening emergencies. Clearly, one must take into account the risk factors for hyperkalemia, malignant hyperthermia, and severe unexpected reactions in patients with selected myotonic states and muscular dystrophies.

Recently, Thapa and Brull from the Department of Anesthesiology at the University of Arkansas published an extensive review commentary on whether sux should be used in hyperkalemic patients with renal failure. In this in-depth discussion, they reviewed the pertinent literature on sux use in chronic or acute renal failure patients. Although it is somewhat open to debate, if the potassium is normal in the chronic renal failure patient, it is probably okay to use sux if needed. However, the acute renal failure patient is a very different situation. These people do not have the ongoing bowel exchange losses that are seen in chronic renal failure and, of course, they tend to have a greater rise in potassium which alters the intracellular to extracellular ratio of potassium and increases the risk of dysrhythmias. Therefore, the conclusion was that sux not be used in patients with acute renal failure in the operating room or the ICU. Thapa and Brull also went on to state they felt it was likely that with the availability of newer agents, succinylcholine will be used less frequently (but we have heard this before).

In summary, I use sux less commonly in the ICU than I used to before the newer agents. I also use it with respect and ask myself, is there some absolute or relative contraindication to sux in this patient? Finally, I am always careful about overestimating the feasibility of emergently intubating an unstable critically ill patient. With that said, I have a low threshold to do an awake intubation with appropriate topicalization and sympathetic stress modulation.

References:

  1. Thapa S, Brull S. Succinylcholine-induced hyperkalemia in patients with renal failure: an old question revisited. [Review] Anesth Analg 2000;91:237-41.
    Coursin DB, Prielipp RC. Use of neuromuscular blocking drugs in the critically ill patient. [Review] Crit Care Clin 1995; 11:957-81.Click here for abstract

I would like to know the clinical course of patients suffering from malignant hyperthermia.I recently had a patient who experienced malignant hyperthermia and now, eight months later, he is having an elevated CPK and muscular pain. Is a muscle biopsy indicated? What is the best treatment?
giubusti@hotmail.com

Dr. Katherine Grichnik responds:

Please see previous answers on malignant hyperthermia through our Ask the Experts Archives. A muscle biopsy is not an unreasonable thing to do in this situation, with a patient with clinical symptoms associated with MH. It would provide a definitive answer to your proposed diagnosis. A search for non-anesthetic causes for MH, such as heat exhaustion, may also be in order. If you truly think that MH is occurring, treatment with dantrolene is indicated. Search for and prevention of secondary problems such as acidosis and renal failure is indicated. Please call an international MH hotline to find answers to all of your questions. The number is 0011 315 428 7924. The website address is http://www.mhaus.org/index.html for the Malignant Hyperthermia Association of the United States.


What is the best way to manage, as an outpatient, a 70 yr old male with a history of St. Jude aortic valve replacement, currently on coumadin anticoagulation, who desires an epidural steroid injection for lumbar degenerative disc disease with herniation and radiculopathy? Would you check prothrombin time daily and then commence IV heparinization (which would require hospitalization) as the prothrombin time reached a certain INR? Or would you consider low molecular weight or SQ heparin as an outpatient?
—Albert Hinn, MD

Dr. Richard Rosenquist responds:

Any plan for altering the coagulation status of a patient with an indwelling artificial valve would need to be done in conjunction with the cardiologist. I suspect that admitting the patient to the hospital, converting to heparin, documenting a normal PTT prior to performing the injection and restarting the heparin one hour after the procedure would be

the safest way to approach it. If the cardiologist felt that normal coagulation could be tolerated for a longer period of time, merely stopping the coumadin, obtaining an INR of 1.4 and restarting the coumadin the evening after the injection would be the simplest. I am unsure if the SQ heparin will provide adequate anticoagulation for a valve. If it does and is used, the injection should be performed just prior to the time for the next dose and the dose should be held for one hour after the injection. I think that the risk of epidural hematoma in association with the use of low molecular weight heparin precludes the safe use of this medication. This is especially true of an outpatient procedure without consistent neurologic monitoring following the procedure.


One of our orthopaedic surgeons has been requesting that we include 20 mg of depomedrol in our femoral nerve blocks and claims it doubles the duration of the block. Does data exist to support this? If not, what are the legal implications of doing so? Is it enough to argue that depomedrol and local anesthetics are given epidurally and therefore should be safe for peripheral nerve blocks? Some members of our group are willing to try it, others refuse. What is your opinion?
— Alistair MacDonald

Dr. Francine J. D'Ercole responds:

The administration of systemic steroids (as compared to topical hydrocortisone) does not go without side effects. At our institution, the most common diagnosis for avascular necrosis of the hip requiring free-fibular vascular graft vs. hip arthroplasty is systemic steroid exposure. The steroid exposure may be a one-time or multiple exposure regardless of dosage. This effect of steroids may be an accumulative effect. Realize, this fact is difficult to prove or disprove.

It is true epidural depomedrol is used for the conservative management of radicular pain or herniated disc, however, the risk-benefits for steroids administration in this scenario is indicated and appreciated in the literature. However, the risks and benefits of using steroids to extend the long-acting effects of a peripheral nerve block for any appreciable length of time have not been well documented or supported by the literature. Example: after total knee arthroplasty would you delay the initiation of PCA-narcotics for 1-2 hours? Big deal!

The following questions to consider include:

  • Will the adjuvant (steroid) significantly change the outcome or postoperative management in the patient population?
  • Will administration of this adjuvant go without increased risk?
  • What is the scientific basis to determine dosage?
  • Do you have IRB (institution review board) approval for a scientific, well-designed
  • study?
  • How do you defend your position if a medicolegal situation arises without well-documented literature support?
  • And — what about mechanisms…?

I have done a literature search and have identified (zero) publications. Should you be challenged, I recommend awaiting references or at the least (1) reasonable publication in a peer-reviewed journal. The risk benefits far outweigh the indication not to.


I have heard of the possibility of a reflex Breuer-Luckhart or Brewer-Luckhart laryngospasm being caused by parasympathetic stimulation, such as noxious stimulation under light mask anesthesia, for example during a D&C. Is there a reference that gives more detail on this?
— Paul E. Hess

Dr. Katherine Grichnik responds:

The sensory innervation of the larynx originates from two branches of each vagus nerve, the superior laryngeal nerve and the recurrent laryngeal nerve. The motor innervation by the recurrent laryngeal nerve comes from each vagus nerve, except the cricothyroid muscle, which is innervated by the external (motor) branch of the superior laryngeal nerve from each vagus nerve. A sacral parasympathetic stimulation could be associated with a parasympathetic response in the larynx (via the vagus), although I am not aware that a specific association had been identified or named. I was unable to find either Breuer-Luckhart or Brewer-Luckhart laryngospasm in the literature.


How would you optimally manage post dural puncture headache?
— Chandrashekar K. Kolvekar

Dr. Peter D. Dwane responds:

Authorized treatments for post dural puncture headache (PDPH) can be found in any of the standard Anesthesia texts. The most important initial step in the treatment of PDPH is the ruling out of other treatable, but life threatening, causes of headache such as preeclampsia, subarachnoid hemorrhage, and meningitis. Once the diagnosis of PDPH is defined, then a variable period of time, dependent on the local resources and customs as well as the needs of the patient and of the medical team, should be devoted to conservative treatment. This conservative therapy time period lasts from zero to two or more days, and would include bed rest (with bathroom privileges), oral caffeine, and analgesics. At the end of this time it is appropriate to offer the patient an epidural blood patch (EBP) which is initially effective in at least 90% of cases; over time, the long term effectiveness of EBP approaches 70%. Should the headache recur with a similar severity to that which warranted the initial EBP, it can be repeated. It has been my experience that for most patients that, when the headache recurs they decide to not request another blood patch, but rather to allow time to resolve the situation.


How does one approach a patient whose pulse oximetry is in the low 90s just prior to induction of anesthesia without any abnormalities in CXR or physical, especially in a young patient who is a heavy smoker but who has no history of lung disease? What benefit is there in routinely recording pulse oximetry in the preop assessment clinic?
— Shanthi Rajendran shanthi@peoplepc.com

Dr. Katherine Grichnik responds:

A low preoperative SpO2 deserves an investigation as to why it has occurred. There are multiple reasons that a patient may have a low SpO2 preoperatively:

  • Machine error
  • Abnormal hemoglobinopathy
  • IV dye administration
  • fingernail polish
  • probe movement
  • excessive light conditions
  • excessive venous pulsations
  • Multiple medical conditions may also lead to arterial hypoxemia, including:
  • Decompensated pulmonary edema and congestive heart failure
  • Sickle cell anemia
  • Diseases with intrapulmonary shunting (such as bronchoalveolar carcinoma and congenital AV shunting)
  • Congenital heart disease with intracardiac shunting
  • Pneumonia
  • Alveolar hypoventilation syndrome with obesity
  • Severe COPD

An arterial blood gas using a co-oximeter if necessary should be done to confirm or disprove a low SpO2 reading. Serious pulmonary and cardiac diseases should be sought. If heart disease is suspected, a cardiac work-up including transthoracic echo to detect intracardiac lesions may be useful. I believe that routinely recorded SpO2 in the preoperative assessment clinic is very useful. An abnormal finding can thus be investigated in the preoperative time period instead of risking the possibility of a cancelled or delayed case as the result of this finding just before surgery.


A patient had a dural tap with a first attempt. An epidural catheter was successfully placed at another level for post op pain control. The following day the patient developed a post dural puncture headache. Conservative treatment is commenced for 24 hours, but without improvement. An epidural bloodpatch is the next consideration. Can it be given via the existing catheter?
pretoriu@home.com

Dr. Richard Rosenquist responds:

The answer is yes. The blood patch can be given via the existing catheter. There is no good data to compare the success rates of injecting via the needle as compared to injecting via the catheter, but it has definitely been performed successfully.


We are six anesthesiologists performing a large volume of surgery for one surgeon and one procedure. We have had varying rates of PONV even though the anesthesia technique is always the same. Overall PONV rate is about 3%. We would like to have a scientific look at our individual rates. How many cases do we need to study to document a significant difference or lack of it? Is there a simple reference?
— R Rajendran MB


Dr. Katherine Grichnik
responds:

This is an answer from one of our statisticians:

The answer depends on what you are trying to compare. That is, PONV rates in which different groups? To find sample required, the investigator must specify the alternative PONV rate expected. Also, with such a small incidence rate, finding a difference will require very large samples. For example, to show a difference in rates from 3% down to 1.5% would require 1650 subjects in each of 2 groups (at alpha=0.05 and 80% power in 2-tailed test). To distinguish between 3% and 6% would require 800 subjects per group. A good reference with sample size tables is Joseph L. Fleiss, Statistical Methods for Rates and Proportions, 2nd Edition. New York: John Wiley and sons, 1981



Can you please help me to find information about:
  • anesthesia and acute alcoholism

  • anesthesia and chronic alcoholism

— Dr Marc Reynvoet marc.reynvoet@groeninghe.be

Dr. Katherine Grichnik responds:

The best place to start is a general textbook such as Anesthesia and Coexisting Disease, edited by RK Stoelting, SF Dierdorg and RL McCammon (Churchill Livingstone, New York). The chapter on "Diseases of the Liver and Biliary Tract" covers the anesthetic implications of acute and chronic alcoholism. A Medline search yielded the other references below:

  1. Spies C. Anesthesiologic aspects of chronic alcohol abuse. Ther Umsch, 2000 Apr, 57:4, 261-3
    Click here to view abstract

  2. Fiset L, Leroux B, Rothen M, Prall C, Zhu C, Ramsay DS. Pain control in recovering alcoholics: effects of local anesthesia. J Stud Alcohol 1997 May 58:3 291-6
    Click here to view abstract

  3. Fassoulaki A, Farinotti R, Servin F, Desmonts JM. Chronic alcoholism increases the induction dose of propofol in humans. Anesth Analg 1993 Sep 77:3 553-6
    Click here to view abstract

  4. Temes R, Feteiha M, Mapel D, Crowell R, Ketai L, Wernly J. Esophageal rupture after regional anesthesia: report of two cases. J Clin Gastroenterol 1999 Jun 28:4 360-3
    Click here to view abstract


  5. Sadeghi P, Zacny JP. Anesthesia is a risk factor for drug and alcohol craving and relapse in ex-abusers. Med Hypotheses 1999 Dec 53:6 490-6
    Click here to view abstract


  6. Orr DL 2d, Glassman AS. Conversion phenomenon following general anesthesia. J Oral Maxillofac Surg 1985 Oct 43:10 817-9
    Click here to view abstract


  7. Patel R, McArdle JJ, Regan TJ. Increased ventricular vulnerability in a chronic ethanol model despite reduced electrophysiologic responses to catecholamines. Alcohol Clin Exp Res 1991 Oct 15:5 785-9
    Click here to view abstract


  8. Swerdlow BN, Holley FO, Maitre PO, Stanski DR. Chronic alcohol intake does not change thiopental anesthetic requirement, pharmacokinetics, or pharmacodynamics. Anesthesiology 1990 Mar 72:3 455-61
    Click here to view abstract


  9. Newman LM, Curran MA, Becker GL. Effects of chronic alcohol intake on anesthetic responses to diazepam and thiopental in rats. Anesthesiology 1986 Aug 65:2 196-200
    Click here to view abstract

  10. Stubbs CD, Slater SJ. Ethanol and protein kinase C. Alcohol Clin Exp Res 1999 Sep 23:9 1552-60
    Click here to view abstract


  11. Shapira Y, Lam AM, Paez A, Artru AA, Laohaprasit V, Donato T. The influence of acute and chronic alcohol treatment on brain edema, cerebral infarct volume and neurological outcome following experimental head trauma in rats. J Neurosurg Anesthesiol 1997 Apr 9:2 118-27
    Click here to view abstract


  12. Adams ML, Cicero TJ. Alcohol intoxication and withdrawal: the role of nitric oxide. Alcohol 1998 Aug 16:2 153-8
    Click here to view abstract


  13. St Haxholdt O, Krintel JJ, Johansson G. Pre-operative alcohol infusion. The need for analgesic supplementation in chronic alcoholics. Anaesthesia 1984 Mar 39:3 240-5
    Click here to view abstract


Do you have any suggestions to reduce the incidence of post cardiac bypass upper extremity neuropathies? We see 10 to 15 of these a year (1000 heart cases/yr - arms tucked to the side, thumbs up, egg crate padding). Most are temporary but some end up requiring carpal tunnel or ulnar transposition surgeries.
— Charles Spivak, MD Sleeper987@aol.com

Dr. Katherine Grichnik responds:

Injury (clinically apparent and subclinical) to the brachial plexus may occur in up to 87% of patients after CABG using symmetric and asymmetric sternal retraction. Clinical plexopathy has been reported to be between 12% and 37.5% of patients. Studies have revealed conflicting results, in part due to the methods used to assess brachial plexus injury. Studies have used detailed neurological examinations, somatosensory evoked potentials (SSEPs), and electromyogram examination. Patients thought be more at risk include those with diabetic neuropathies, those with preexisting neurological disorders elderly patients, those who had repeated internal jugular cannulation attempts, the use of an automated blood pressure cuff, those who had a long cardiopulmonary bypass time and those patients who are significantly over ideal body weight. Injury occurs with both symmetric sternal retraction and asymmetric sternal retraction (used for internal mammary harvest) and occurs bilaterally. Reasons postulated for the nerve bundle injuries include nerve stretch, nerve compression and nerve injury due to penetration of the nerves by a fractured first rib after sternotomy.

Various interventions have been tried to reduce the incidence of brachial plexus injury. A hands-up (HU) position (arms behind the head and elevated above the level of the table) as opposed to an arms at the side (AAS) position has been investigated [1]. The authors found that both positions resulted in decline of SSEPs, but that the AAS position resulted in a higher incidence of postoperative ulnar symptoms. Various types of retractors (Ankeney, Pittman, Favalaro, Canadian, Rultract, etc) are also used clinically, with the goal of reducing brachial plexus injury. In the above referenced study, the HU position with the Pittman sternal retractor offered a modest decrease in brachial plexus injury. Other interventions would be to try to modify the risk factors identified above.

Reference:

  1. Jellish SW, Blakeman B, Warf P, Slogoff S. Hands-Up Positioning During Asymmetric Sternal Retraction for Internal Mammary Artery Harvest: A Possible Method to Reduce Brachial Plexus Injury. Anesth Analg 1997 Feb;84(2):260-5
    Click here for abstract


What is the risk of Candidal infection in the postoperative patient?

Dr. Douglas Coursin responds:

Candida spp is the fourth most common cause of blood-borne infections in the United States. This is a dramatic increase over the past several decades when it was previously almost unknown. Invasive candidiasis and candidemia are life-threatening complications for critically ill patients. Diagnosis of such infections is often challenging. In addition, various unusual and frequently resistant candidal species other than Candida albicans are occurring more commonly in immunosuppressed and critically ill perioperative patients.

There are a host of risk factors for patients developing candidal sepsis. These include immunosuppression, the presence of indwelling catheters, particularly Hickman and central venous catheters, utilization of broad-spectrum antibiotics, prolonged hospitalization, and perforation of a viscus. Patients who are immunosuppressed, have invasive monitoring performed, and receive broad-spectrum antibiotics are at particularly high risk. Empiric therapy is considered appropriate when patients have more than three sites colonized or when they have even a low number of colonies of fungi present on peritoneal fluid analysis. Historically, amphotericin B was the main antifungal agent for candidal species. However, the more recently developed azole, fluconazole, is frequently used both prophylactically and for therapy for sensitive organisms. However, the selection of resistant organisms and development of resistance is a real problem with the azole compounds. In the past, there has been major concern over the side effect problems associated with amphotericin B, particularly the rapid development of renal insufficiency as well as other systemic side effects. Most recently, liposomal-entrapped amphotericin and colloidal suspensions of amphotericin have been developed which are far less nephrotoxic. However, there is no difference in the effective doses that can be given. The liposomal and colloidal suspensions are dramatically more expensive than generic amphotericin. Patients also usually require pretreatment with Tylenol, Demerol, and sometimes corticosteroids prior to the infusion of any ampho B preparation.

Fungal infections are here to stay. We need to be vigilant for the development of fungal infections in immunosuppressed and high risk patients. We also need to judiciously use anti-microbials to limit the development of resistance to fungi or fungal colonization of our critically ill patients.

References:

  1. Munoz P, et al. Criteria used when initiating anti-fungal therapy against Candida spp in the ICU. International J Anti-Microb Agents 2000; 15:83-90.

  2. Verduyn LFM, et al. Nosocomial fungal infections: candidemia (Review). Diagn Microbiol Infect Dis 1999; 34:213-20.

  3. Dean DA, Burchard KW. Surgical perspective on invasive Candida infections (Review). World J Surg 1998; 22:127-34.


In my ICU, we are very concerned about the succinylcholine use in emergency intubation due to the fear of malignant hyperthermia. Should it be used as first relaxant drug?
— Alfredo Londono M.D allondon@epm.net.co

Dr. Douglas Coursin responds:

Historically, the depolarizing muscle relaxant succinylcholine (sux) has been used frequently for facilitation of intubation during rapid sequence inductions and in critically ill patients. With the development of faster onset aminosteroid nondepolarizers such as

rocuronium and rapacuronium, some experts have advised the routine avoidance of sux. Major concerns with the use of sux in the critically ill center primarily around the risk of life-threatening hyperkalemia in a multitude of clinical scenarios and secondarily the possibility of triggering a malignant hyperthermic response. Hyperkalemic responses secondary to sux may occur more frequently than initially realized. This is a definite risk factor in the following patients:

    • Patients with history of MH
    • Patients with crush injuries
    • Patients after 24 hours of an acute burn until it is completely healed
    • Patients with spinal cord transections, upper motor neuron lesions, and selected stroke and closed head injury patients
    • Individuals with intra-abdominal sepsis
    • Patients who are in renal failure (see text)
    • Patients who are already hyperkalemic prior to intubation
    • Patients with various muscular dystrophies (myotonia congenita or dystrophica)

There have been reports of unexpected hyperkalemia in critically ill patients. These may have been in patients who had an unrecognized neurologic or myopathic pathology or have received long term nondepolarizing agents and have changes in their neuromuscular junction, as well as changes in the receptor with a proliferation of extra-junctional receptors and conversion to a more juvenile receptor.

Furthermore, the use of sux in children remains open to debate and somewhat controversial. A number of years ago, the FDA recommended that sux not be used routinely in children but only in the case of life-threatening emergencies. Clearly, one must take into account the risk factors for hyperkalemia, malignant hyperthermia, and severe unexpected reactions in patients with selected myotonic states and muscular dystrophies.

Recently, Thapa and Brull from the Department of Anesthesiology at the University of Arkansas published an extensive review commentary on whether sux should be used in hyperkalemic patients with renal failure. In this in-depth discussion, they reviewed the pertinent literature on sux use in chronic or acute renal failure patients. Although it is somewhat open to debate, if the potassium is normal in the chronic renal failure patient, it is probably okay to use sux if needed. However, the acute renal failure patient is a very different situation. These people do not have the ongoing bowel exchange losses that are seen in chronic renal failure and, of course, they tend to have a greater rise in potassium which alters the intracellular to extracellular ratio of potassium and increases the risk of dysrhythmias. Therefore, the conclusion was that sux not be used in patients with acute renal failure in the operating room or the ICU. Thapa and Brull also went on to state they felt it was likely that with the availability of newer agents, succinylcholine will be used less frequently (but we have heard this before).

In summary, I use sux less commonly in the ICU than I used to before the newer agents. I also use it with respect and ask myself, is there some absolute or relative contraindication to sux in this patient? Finally, I am always careful about overestimating the feasibility of emergently intubating an unstable critically ill patient. With that said, I have a low threshold to do an awake intubation with appropriate topicalization and sympathetic stress modulation.

References:

  1. Thapa S, Brull S. Succinylcholine-induced hyperkalemia in patients with renal failure: an old question revisited. [Review] Anesth Analg 2000;91:237-41.

  2. Coursin DB, Prielipp RC. Use of neuromuscular blocking drugs in the critically ill patient. [Review] Crit Care Clin 1995; 11:957-81.Click here for abstract

What is the best way to manage, as an outpatient, a 70 yr old male with a history of St. Jude aortic valve replacement, currently on coumadin anticoagulation, who desires an epidural steroid injection for lumbar degenerative disc disease with herniation and radiculopathy? Would you check prothrombin time daily and then commence IV heparinization (which would require hospitalization) as the prothrombin time reached a certain INR? Or would you consider low molecular weight or SQ heparin as an outpatient?
—Albert Hinn, MD

Dr. Richard Rosenquist responds:

Any plan for altering the coagulation status of a patient with an indwelling artificial valve would need to be done in conjunction with the cardiologist. I suspect that admitting the patient to the hospital, converting to heparin, documenting a normal PTT prior to performing the injection and restarting the heparin one hour after the procedure would be

the safest way to approach it. If the cardiologist felt that normal coagulation could be tolerated for a longer period of time, merely stopping the coumadin, obtaining an INR of 1.4 and restarting the coumadin the evening after the injection would be the simplest. I am unsure if the SQ heparin will provide adequate anticoagulation for a valve. If it does and is used, the injection should be performed just prior to the time for the next dose and the dose should be held for one hour after the injection. I think that the risk of epidural hematoma in association with the use of low molecular weight heparin precludes the safe use of this medication. This is especially true of an outpatient procedure without consistent neurologic monitoring following the procedure.


I would like to know the clinical course of patients suffering from malignant hyperthermia.I recently had a patient who experienced malignant hyperthermia and now, eight months later, he is having an elevated CPK and muscular pain. Is a muscle biopsy indicated? What is the best treatment?
giubusti@hotmail.com

Dr. Katherine Grichnik responds:

Please see previous answers on malignant hyperthermia through our Ask the Experts Archives. A muscle biopsy is not an unreasonable thing to do in this situation, with a patient with clinical symptoms associated with MH. It would provide a definitive answer to your proposed diagnosis. A search for non-anesthetic causes for MH, such as heat exhaustion, may also be in order. If you truly think that MH is occurring, treatment with dantrolene is indicated. Search for and prevention of secondary problems such as acidosis and renal failure is indicated. Please call an international MH hotline to find answers to all of your questions. The number is 0011 315 428 7924. The website address is http://www.mhaus.org/index.html for the Malignant Hyperthermia Association of the United States.


One of our orthopaedic surgeons has been requesting that we include 20 mg of depomedrol in our femoral nerve blocks and claims it doubles the duration of the block. Does data exist to support this? If not, what are the legal implications of doing so? Is it enough to argue that depomedrol and local anesthetics are given epidurally and therefore should be safe for peripheral nerve blocks? Some members of our group are willing to try it, others refuse. What is your opinion?
— Alistair MacDonald

Dr. Francine J. D'Ercole responds:

The administration of systemic steroids (as compared to topical hydrocortisone) does not go without side effects. At our institution, the most common diagnosis for avascular necrosis of the hip requiring free-fibular vascular graft vs. hip arthroplasty is systemic steroid exposure. The steroid exposure may be a one-time or multiple exposure regardless of dosage. This effect of steroids may be an accumulative effect. Realize, this fact is difficult to prove or disprove.

It is true epidural depomedrol is used for the conservative management of radicular pain or herniated disc, however, the risk-benefits for steroids administration in this scenario is indicated and appreciated in the literature. However, the risks and benefits of using steroids to extend the long-acting effects of a peripheral nerve block for any appreciable length of time have not been well documented or supported by the literature. Example: after total knee arthroplasty would you delay the initiation of PCA-narcotics for 1-2 hours? Big deal!

The following questions to consider include:

  • Will the adjuvant (steroid) significantly change the outcome or postoperative management in the patient population?
  • Will administration of this adjuvant go without increased risk?
  • What is the scientific basis to determine dosage?
  • Do you have IRB (institution review board) approval for a scientific, well-designed
  • study?
  • How do you defend your position if a medicolegal situation arises without well-documented literature support?
  • And — what about mechanisms…?

I have done a literature search and have identified (zero) publications. Should you be challenged, I recommend awaiting references or at the least (1) reasonable publication in a peer-reviewed journal. The risk benefits far outweigh the indication not to.


I have heard of the possibility of a reflex Breuer-Luckhart or Brewer-Luckhart laryngospasm being caused by parasympathetic stimulation, such as noxious stimulation under light mask anesthesia, for example during a D&C. Is there a reference that gives more detail on this?
— Paul E. Hess

Dr. Katherine Grichnik responds:

The sensory innervation of the larynx originates from two branches of each vagus nerve, the superior laryngeal nerve and the recurrent laryngeal nerve. The motor innervation by the recurrent laryngeal nerve comes from each vagus nerve, except the cricothyroid muscle, which is innervated by the external (motor) branch of the superior laryngeal nerve from each vagus nerve. A sacral parasympathetic stimulation could be associated with a parasympathetic response in the larynx (via the vagus), although I am not aware that a specific association had been identified or named. I was unable to find either Breuer-Luckhart or Brewer-Luckhart laryngospasm in the literature.


How would you optimally manage post dural puncture headache?
— Chandrashekar K. Kolvekar

Dr. Peter D. Dwane responds:

Authorized treatments for post dural puncture headache (PDPH) can be found in any of the standard Anesthesia texts. The most important initial step in the treatment of PDPH is the ruling out of other treatable, but life threatening, causes of headache such as preeclampsia, subarachnoid hemorrhage, and meningitis. Once the diagnosis of PDPH is defined, then a variable period of time, dependent on the local resources and customs as well as the needs of the patient and of the medical team, should be devoted to conservative treatment. This conservative therapy time period lasts from zero to two or more days, and would include bed rest (with bathroom privileges), oral caffeine, and analgesics. At the end of this time it is appropriate to offer the patient an epidural blood patch (EBP) which is initially effective in at least 90% of cases; over time, the long term effectiveness of EBP approaches 70%. Should the headache recur with a similar severity to that which warranted the initial EBP, it can be repeated. It has been my experience that for most patients that, when the headache recurs they decide to not request another blood patch, but rather to allow time to resolve the situation.



One of our orthopaedic surgeons has been requesting that we include 20 mg of depomedrol in our femoral nerve blocks and claims it doubles the duration of the block. Does data exist to support this? If not, what are the legal implications of doing so? Is it enough to argue that depomedrol and local anesthetics are given epidurally and therefore should be safe for peripheral nerve blocks? Some members of our group are willing to try it, others refuse. What is your opinion? — Alistair MacDonald

Dr. Francine J. D'Ercole responds:

The administration of systemic steroids (as compared to topical hydrocortisone) does not go without side effects. At our institution, the most common diagnosis for avascular necrosis of the hip requiring free-fibular vascular graft vs. hip arthroplasty is systemic steroid exposure. The steroid exposure may be a one-time or multiple exposure regardless of dosage. This effect of steroids may be an accumulative effect. Realize, this fact is difficult to prove or disprove.

It is true epidural depomedrol is used for the conservative management of radicular pain or herniated disc, however, the risk-benefits for steroids administration in this scenario is indicated and appreciated in the literature. However, the risks and benefits of using steroids to extend the long-acting effects of a peripheral nerve block for any appreciable length of time have not been well documented or supported by the literature. Example: after total knee arthroplasty would you delay the initiation of PCA-narcotics for 1-2 hours? Big deal!

The following questions to consider include:

  • Will the adjuvant (steroid) significantly change the outcome or postoperative management in the patient population?
  • Will administration of this adjuvant go without increased risk?
  • What is the scientific basis to determine dosage?
  • Do you have IRB (institution review board) approval for a scientific, well-designed
  • study?
  • How do you defend your position if a medicolegal situation arises without well-documented literature support?
  • And — what about mechanisms…?

I have done a literature search and have identified (zero) publications. Should you be challenged, I recommend awaiting references or at the least (1) reasonable publication in a peer-reviewed journal. The risk benefits far outweigh the indication not to.


I have heard of the possibility of a reflex Breuer-Luckhart or Brewer-Luckhart laryngospasm being caused by parasympathetic stimulation, such as noxious stimulation under light mask anesthesia, for example during a D&C. Is there a reference that gives more detail on this? — Paul E. Hess

Dr. Katherine Grichnik responds:

The sensory innervation of the larynx originates from two branches of each vagus nerve, the superior laryngeal nerve and the recurrent laryngeal nerve. The motor innervation by the recurrent laryngeal nerve comes from each vagus nerve, except the cricothyroid muscle, which is innervated by the external (motor) branch of the superior laryngeal nerve from each vagus nerve. A sacral parasympathetic stimulation could be associated with a parasympathetic response in the larynx (via the vagus), although I am not aware that a specific association had been identified or named. I was unable to find either Breuer-Luckhart or Brewer-Luckhart laryngospasm in the literature.


How would you optimally manage post dural puncture headache? — Chandrashekar K. Kolvekar

Dr. Peter D. Dwane responds:

Authorized treatments for post dural puncture headache (PDPH) can be found in any of the standard Anesthesia texts. The most important initial step in the treatment of PDPH is the ruling out of other treatable, but life threatening, causes of headache such as preeclampsia, subarachnoid hemorrhage, and meningitis. Once the diagnosis of PDPH is defined, then a variable period of time, dependent on the local resources and customs as well as the needs of the patient and of the medical team, should be devoted to conservative treatment. This conservative therapy time period lasts from zero to two or more days, and would include bed rest (with bathroom privileges), oral caffeine, and analgesics. At the end of this time it is appropriate to offer the patient an epidural blood patch (EBP) which is initially effective in at least 90% of cases; over time, the long term effectiveness of EBP approaches 70%. Should the headache recur with a similar severity to that which warranted the initial EBP, it can be repeated. It has been my experience that for most patients that, when the headache recurs they decide to not request another blood patch, but rather to allow time to resolve the situation.


Are there any preoperative guidelines on DMD (Duchenne muscular dystrophy)? We will be starting with DMD patients on scoliosis reconstruction. We have our own preoperative guidelines for scoliosis, maar none specifically for the DMD. With regards to the nature of the operation and ( of course ) the pulmonary condition of the patient, do you ventilate your patient postoperatively? —Sibarani-Ponsen, R.D.

Dr. Katherine Grichnik responds:

Duchenne’s Muscular Dystrophy (DMD) is a psuedohypertrohpic muscular dystrophy in which the lack of production of dystrophin weakens the muscle cell membrane and may allow increased calcium into the cell. Skeletal muscle is most obviously affected but smooth muscle and cardiac muscle may also be involved. This disease has a variable but progressive course characterized by painless degeneration and atrophy of muscles with loss of muscle function. The disease is sex-linked and clinically appears in males. Weakness occurs by ages 2-5 and many patients are wheelchair-bound by age 12. Due to axial muscle imbalance, kyphoscoliosis occurs. Many patients die between the ages of 15-25, usually from CHF, or pneumonia.

Anesthetically, patients may present for surgery such as scoliosis surgery. These patients are challenging to care for and have an increased incidence of morbidity and mortality. Patients may have problems with many organ systems including those listed.
Respiratory: decreased muscle function and kyphoscoliosis, restrictive lung disease, ineffective cough with chronic infections, Cardiac: 605 have myocardial degeneration characterized by dysrhythmias, decreased LV contraction, papillary muscle dysfunction, right heart failure, and a loss of R waves in the lateral precordial leads GI—delayed gastric emptying, impaired swallowing

Preoperative assessment must focus on the known physiological effects of DMD and optimization of the patient’s respiratory and cardiac status prior to surgery.

Anesthetic care can be complicated by adverse events such as cardiac arrest and postoperative ventilatory failure. Succinylcholine is contraindicated due to the occurrence of cardiac arrest, rhabdomyolysis and hyperkalemeia with its administration. There is a controversy about whether these patients are at risk for malignant hyperthermia as well. Anesthetic agents may have unanticipated profound myocardial depressant effects.

Postoperatively the patients must be monitored closely for cardiac and pulmonary dysfunction. The decision about when to extubate these patients is an individual decision and must be based on the complexity of the operative course and on the return of adequate neuromuscular function postoperatively. A period of ventilatory support and intensive respiratory therapy postoperatively can be anticipated.

Reference:

  1. Barash PG, Cullen BF and Stoelting RK eds. Clinical Anesthesia 3rd Edition 1997: Lippincott-Raven, Philadelphia.

Are there any case reports in the literature involving a diagnosis of quadriplegia due to anterior spinal artery syndrome after a patient undergoes a cervical spinal cord decompression/laminectomy?
—kasarda@aol.com

Dr. John Keifer responds:

Greenberg's Handbook of Neurosurgery defines Anterior Spinal Cord Syndrome (AKA anterior spinal artery syndrome) as cord infarction in the region supplied by the anterior spinal artery. This may result from occlusion of the spinal artery or compression of the anterior cord (e.g. by dislocated bone fragment or by traumatic herniated disc). The syndrome presents as bilateral paraplegia and dissociated sensory loss (loss of pain and temperature sensation {spinothalamic tract} and preserved posterior column function {two point discrimination, position sense and deep pressure sensation). In view of the etiology of this syndrome, I suppose it is conceivable that such a lesion could occur in association with cervical laminectomy, if the if the reason for decompression was trauma or herniated disc. In order for the operation itself to cause the lesion, I suppose that something could occur intraoperatively to compromise the anterior spinal circulation.

References:
  1. Svensson LG, Von Ritter CM, Groeneveld HT, Rickards ES, Hunter SJ, Robinson MF, Hinder RA. Cross-clamping of the thoracic aorta. Influence of aortic shunts, laminectomy, papaverine, calcium channel blocker, allopurinol, and superoxide dismutase on spinal cord blood flow and paraplegia in baboons. Annals of Surgery 1986 Jul;204(1):38-47
  2. Murata T, Ohhata K, Tsujikawa S, Sumimoto T, Kitano S, Shirahata N, Hakuba A, Choi SK [A case of spontaneous spinal epidural hematoma presenting Brown-Sequard syndrome]. [Japanese] No Shinkei Geka - Neurological Surgery 1984 Sep;12(10):1195-200

What is off CPB cardiac surgery?
—Venkatesan Kumaresh

Dr. Katherine Grichnik responds:

Off-pump cardiac surgery is performance of coronary artery bypass grafting without cardiopulmonary bypass. This involves slowly positioning the heart with pads in the pericardial cradle to obtain access to the diseased coronary artery, stabilization of a small section of the heart around the area to be grafted with a cardiac stabilization device ,and grafting an internal mammary artery or a vein graft to the coronary artery. If a vein graft is used, then a partial aortic occlusion clamp is also used to create the proximal anastomosis of the vein graft to the aorta for perfusion. Benefits are: the avoidance of cardiopulmonary bypass, possible decrease in adverse neurological outcomes, possible decrease in adverse end-organ (lungs, kidneys, mesentery) outcomes, possible decreased inflammatory response, possible shorter operations, possible shorter intubations and ICU stays, possible shorter hospitalizations. Risks are: hemodynamic instability during heart positioning and clamping of the coronary artery to be grafted, challenges of maintaining normothermia, and a steep learning curve for the surgeon and anesthesiologist. This technique is being performed with increasing frequency in the United States.


Are there any case reports in the literature involving a diagnosis of quadriplegia due to anterior spinal artery syndrome after a patient undergoes a cervical spinal cord decompression/laminectomy?
—kasarda@aol.com

Dr. Francine D'Ercole responses:

I am unaware of any cases associated with cervical laminectomy. However, the following references were found crossing anterior spinal artery syndrome with cervical spine and laminectomy.

References:

  1. Foo D, Rossier AB, Cochran TP. Complete sensory and motor recovery from anterior spinal artery syndrome after sprain of the cervical spine. case report. European Neurology 1984;23(2):119-23.
  2. Kowalske KJ, et al. Spinal cord injury syndrome with motor sparing in the absence of all sensation. Archives of Physical Medicine & Rehabilitation 1991 Oct ;72(11):932-4.

How can I handle patients with sore throat postextubation who have to breathe by mouth. Is there anything new?
—Dr. Alberto Balderas


Dr. Katherine McGoldrick responds:

My favorite remedies are tea with honey and a humidifier at the bedside. Unfortunately, to date we have no "high-tech" solution to this very real problem.


In recent years spinal anesthesia seems to be becoming the first option for C/section in many obstetrics anesthesia services. On the other hand, PDPH is day by day becoming a more important problem, legally and medically. PDPH is, with any needle, more common with spinal than epidural anesthesia. Spinal anesthesia is faster, cheaper, and easier but, in my mind, does not provide better anesthesia than epidural. What is your opinion?
—Dr. Luis Valenzuela


Dr. Peter Dwane responds:

You are quite right. Spinal anesthesia for Cesarean section has increased significantly over the last 10-15 years. For my first 20 years of practice, the only regional anesthetic most of my colleagues and I used for C/sections was epidural anesthesia. Almost a dozen years ago I began using spinal anesthesia because of the advent of small, 25 gauge, spinal needles. But it wasn't until two years after that, when I added intrathecal fentanyl to this spinal technique, that I became "sold" on spinals for C/sections.

There have been other parallel developments, such as the recognition that the increased risk of difficult intubation with or without aspiration reduced the incidence of elective general anesthetics for C/section. Also, the incidence of C/sections has increased during this time.

From my point of view, spinals have at least four advantages over epidurals for most C/sections:
  • a lower failure rate than epidurals
  • no risk of local anesthetic toxicity
  • the ability to repeat the spinal if the initial block fails (if the anesthetic level is non-existent or too low)
  • more rapid onset of block, with shorter time in the operating room.

In addition, I see an advantage regarding the risk of PDPH. With epidural anesthesia, risk of PDPH is approximately 0.5 - 1.0 % in the hands of experienced anesthesiologists; when using a 25 GA pencil-point needle, the incidence is about 1-2%. However, in my opinion, the severity and duration of the PDPH is significantly less with the new solid-tipped needles, and this more than balances the increased incidence of PDPH with subarachnoid block.

Vincler et al [1] state that the Obstetric Anesthesiologist is at greater risk of being sued for minor injuries including headache, pain during anesthesia, back pain and emotional distress than are nonobstetric anesthesiologists. But factors other than injury likely cause patients to sue. They may be unhappy with their care and/or have unrealistic expectations of their labor and delivery experience. Therefore, it may be especially important to establish a good relationship with obstetric patients, and to take time to discuss risks, complications, and expectations of planned procedures.

But Seeberger et al [2] reported, in favor of spinal anesthesia, that it took less time to achieve sufficient spread of block, and there was a significantly lower incidence of incomplete sensory block at level L5/S1, incomplete motor block, and pain during surgery.

What I can say for sure is that in the three years that our obstetric anesthesia group has been practicing, the seven of us routinely use spinal anesthesia as our first choice. And we usually only use epidural anesthesia if a catheter is in place when the decision to go to C/section has been made. In this time we have not had any legal problems, although we have had a number of PDPHs, a few of which need an epidural blood patch. I feel that a good patient-doctor relationship will alleviate many of the legal issues. As well, attention to making sure that the patients' expectations are realistic is also useful.

References:

  1. Vincler LA, Chadwick HS. Medicolegal Issues in Obstetric Anestheisa. In Obstetric Anesthesia Principles and Practice: Chesenut DH ed, 2nd ed. Mosby 1999: 559-76.
  2. Seeberger MD, Lang ML, Drewe J, Schneider M, Hauser E, Hruby J. Comparison of spinal and epidural anesthesia for patients younger than 50 years of age. Anesthesia & Analgesia. 78(4):667-73, 1994.

Is there any information about reactions to sevoflurane, such as sneezing or eye inflammation? One of my friends has a very bad reaction when he uses this product.
—Dr. Momblano

Dr. Beverly Philip responds:

There is no pattern of sneezing or eye inflammation associated with sevoflurane that I am aware of. The collection of symptoms that Dr. Momblano describes appears to represent an environmental allergy. The individual involved may wish to explore that path, including latex allergy.


A 5 year old boy with tetralogy of fallot and palliative shunt (2 years ago) has been admitted in hospital for head trauma and massive epidural hematoma in CT scan. The patient was conscious and had cyanosis (peripheral and central) and clubbing. Hemoglobin was 17 mg/dl and vital signs were stable. Could you recommend the best choice of drug for induction of anesthesia in this patient. May we use ketamine for induction? And what can I do for better oxygenation in the postoperative period despite the use of phenylephrine and beta blockers and increasing FIo2? And is PEEP useful?
—Nasser Yeganeh

Dr. Cote responds:

This sounds like a board examination question. Obviously for some reason this child had not had corrective surgery so one is left with a cyanotic child who is still at risk for acute deterioration should right ventricular outflow tract obstruction occur (a Tet spell) although the risk is less in the presence of a shunt. With two years passage it is clear that the shunt is inadequate if the child it cyanotic and has a high hemoglobin value. The most important issue here is to remember the basic physiological goal, which is to maintain peripheral vascular resistance so as not to encourage right to left shunting, and to avoid anything which reduces pulmonary blood flow (hypercabia, hypoxia). In addition, if we are dealing with a head injury in a child, we must to maintain cerebral perfusion pressure. Your suggestion for a ketamine induction is exactly what I would choose. The phenylephrine would maintain peripheral vascular resistance and the beta blockers may be useful to relief a tet spell should one occur. PEEP may not be helpful since it would decrease pulmonary blood flow and increase central venous pressure which would in turn decrease cerebral perfusion pressure (CPP=MAP-CVP). Also this child should have normal lungs and one would not expect additional benefit from PEEP. The best bet is to maintain a full vascular volume and administer supplemental oxygen.


I am a CRNA with 18 years of practice. I had a case last week that was quite strange—a 35 y.o. male, 240 lbs., for knee arthroscopy. He had a history of hypertension (no rx). I put an epidural (25mls 2% xylocaine) in this patient. Dermatome level ~t8. The case lasted 40 minutes and was entirely uneventful until shortly after the tourniquet (TQ) went down. At this point, the patient complained of nausea. I noted his heart rate slowing to ~38 bpm. I told the patient to take a few deep breaths while I drew up, and I gave him a small amount of atropine (0.3mg). His heart rate briefly picked up to 50 bpm. Before the atropine even reached the patient, he went into asystole...nada...nothing. I assisted his respirations by mask, gave 1 mg atropine, and began CPR. I also gave him 0.5 mg of epinephrine which, after around 1 minute of asystole, finally brought back a rhythm (svt of 140 with pvc's) and a pressure of 240/140. Lidocaine & brevibloc brought his system back to normal. The patient was awake, talking, and saying he remembered everything. Very uneventful paar course. Lab, x-ray, EKG came up with nothing. Is this just big vagal response? The epidural didn't seem too high to inhibit the sympathetic system. Any ideas? —kc2302@aol.com

Dr. Francine D'Ercole responds:

Actually, this is a very common scenario. Conditions such as morbid obesity or a full-term gravida requiring placement in the supine position may restrict venous return into the Inferior Vena Cava (IVC); decrease return from the IVC into the right heart. This is precisely why a sponge or pillow is placed under the right hip during c-section to displace the weight of a gravid uterus (or in this case a large abdomen or pannus) from the IVC. Add to the mechanics of positioning the physiologic response of a central neuraxial block. Recall a T8 sensory block assumes a sympathectomy 4-6 levels higher, therefore, the sympathectomy actually occurred at T4-T2. In addition to lower extremity vasodilation, including the expansion of a large venous capacitance, cardioaccelerators may have been blunted.

The final insult occurred when the tourniquet (TQ) was lowered. Lowering the TQ shunts a percentage of the blood volume from a grossly vasodilated system into the exsanguinated extremity. The final result is a cycle of vasodilation with decreasing blood pressure, diminished venous return, diminished heart rate response. Also, I recommend reviewing cardiovascular reflexes especially the well described theory associated with this response known as the Bezold-Jarisch Reflex. Additionally, I recommend a slight right oblique position to displace the abdomen in obese patients when possible and anticipate with ample IV fluid hydration. During profound bradycardia and asystole associated with central blockade the first line drug should be epinephrine.



What is a safe level of TSH and T4 to use when performing surgery on a patient with hyperthyroidy if the surgery is not an emergency? Currently, we often use a controlled level of T4 but very low TSH when clinical symptoms of hyperthyroidism are present.  —Dr. PM

Dr. Grichnik responds:
If the free T4 and free T3 are in the normal range in a patient with intact pituitary function so that the TSH is accurate, a suppressed TSH in a non-elective procedure is usually acceptable for the procedure.



I have recently observed an adverse event which I do not fully understand. A 22 y.o. WF presented to the operating suite for cystoscopy secondary to an obstructed ureter. She had been hospitalized for 24 hours and was receiving hydration and insulin therapy. I did an induction with propofol and placed a laryngeal mask. Approximately 20 minutes into the case she had the sudden onset of ventricular fib rapidly progressing to asystole. Epinephrine and one defibrillation returned her to NSR, but she suffered anoxic injury and later, expired. Could you please offer some suggestions as to the etiology of the fibrillation? Will cardiac autonomic neuropathy lead to a similar pattern?  —Garry Stubbs


Dr. Grichnik responds:

Although I do not know the exact clinical history, laboratory values and EKG of the patient in question, it sounds as though the patient may have had an underlying intraventricular conduction defect. Autonomic neuropathy and QT variability are common in patients with diabetes mellitus. This may be exacerbated by electrolyte abnormalities. Please see the discussion below for a small literature review of the subject.

In a letter to the editor of the Lancet, Jermendy observed: "Those with increased QT dispersion (difference between the longest and shortest QT interval) are at a high risk of sudden unexpected death. Prolongation of the QT interval has been found to predict sudden death in coronary artery disease, alcoholic cirrhosis and apparently healthy individuals. Cardiac autonomic neuropathy is a well-recognized complication of diabetes mellitus, and its consequences include QT interval prolongation. The association of QT prolongation with sudden unexpected death has suggested a causal relation diabetic patients, although causality may be in dispute". [4]

Robillon et al. studied QT dispersion in diabetic versus nondiabetic patients, where they found that diabetic patients had greater QT variability. They postulated but did not prove an increased risk of sudden death and ventricular arrhythmias.[5]

Yotsukura and Ishikawa stated that ventricular arrhythmias are frequently observed in patients with diabetes mellitus. Ventricular arrhythmias may be increased with advancing severity of diabetes mellitus. [2] The incidence of ventricular arrhythmias is closely related to the occurrence of a disturbance of the autonomic nervous system.

Shehadeh and Regan state that the heart muscle can be independently involved in diabetic patients. In a study of diabetic versus nondiabetic children, those with diabetes were found to have a longer QRS duration. The voltage of the QRS complex for the last 40 ms was significantly lower in the diabetic group as compared to the nondiabetic children. The authors suggest that the findings imply that the children with diabetes mellitus frequently have intraventricular conduction disturbances regardless of glycemic control condition. [6]

Oka-Manabe et al examined a 63-year old diabetic man who had complete AV block with bifid T waves. The patient had marked QT variability. This condition was partially corrected by potassium repletion, and ventricular pacing. [1] Some have observed magnesium deficiency in patients with diabetes mellitus, with adverse clinical consequences. [3]

References:
  1. Oka-Manabe S, et al. Prominent bifid T waves observed in the QT prolongation caused by complete atrioventricular blockade in a hypokalemic diabetic patient. J of Electrocardiology 32:289;1999
  2. Yotsukura M and Ishiawa K. Arrhythmias in patients with metabolic disease. Nippon Rinsho-Japanese Journal of Clinical Medicine 54:2202;1996.
  3. Rude RK. Magnesium deficiency and diabetes mellitus. Causes and effects. Postgraduate Medicine. 92:222;1992
  4. Jermendy, G. QT prolongation and sudden unexpected death. Lancet 343:742; 1994.
  5. Robillon JF, et al. Diabetes and Metabolism 25:419;1999
  6. Shehadeh A and Regan TJ. Cardiac consequences of diabetes mellitus.Clinical Cardiology 18:301;1995



My orthopedic surgeon has stated that after doing lumbar laminectomy, he would like to insert an epidural catheter and infuse bupivacaine with fentanyl postoperatively. Does this pose any extra risk of infection or faster absorption of local anesthetic in the operative site? As he prefers to insert the epidural catheter through ligamentum flavum where he has just removed lamina, will the drug not diffuse back?  —Dr. S.A. Azeez Pasha


Dr. Francine J. D'Ercole responds:

There are two questions regarding the intraoperative placement of an epidural catheter placed by the surgeon under direct visualization in the operative field prior to wound closure.

The first question is, is there any "extra" risk of infection? To date, I am unaware of any large study to determine the increased risk for patients having intraoperative placement of a catheter when compared to those patients requiring spine surgery without a catheter. However, recall that the catheter is placed in a sterile field with the strict sterile technique. One could argue that there are case reports describing patients requiring non-spine surgery having epidural catheters who are at risk for immunosuppression and later develop (over weeks/months) a sterile epidural abscess associated with the presence of a foreign body (the catheter). Of course, this is rare. One would need to weigh the benefits versus risks for postoperative acute pain control.

The second question concerns absorption of local anesthetic and the integrity of a closed-field to prevent extravastion of local anesthetic. The best placed catheter may be under direct placement and supervision. In this case the surgeon has the best view. He knows precisely the length of catheter to advance into the epidural space and secures it through the ligamentum flavum. The surgical closure is adequate to support a closed-system to allow epidural analgesia. The usual rate of infusion required for this technique does not involve high plasma concentration level for local anesthetics with fentanyl. Consider, the surgeon may have a high rate of success with postoperative pain management with this technique or he would not bother to make the extra effort. You could ask about his outcome or success rate for postoperative pain management.



There was recently some discussion in our hospital about the high costs of using sevoflurane. I currently use isoflurane and I'm completely happy with this anesthetic. The main advantage is induction, which is fantastic with sevoflurane. On the other hand while using sevoflurane on minimal flow, the difference in costs is not so big, as isoflurane can also be used in this way. Are there big advantages in recovery time/nausea & vomiting/shivering/hangover effect/time to discharge between sevoflurane and isoflurane? Where can I find evidence-based researches on this subject?  —Piotr Konopka

Dr. Beverly Philip responds:

The cost difference between the inhaled anesthetics for maintenance at minimal flows is not much. Times to eye opening are only a couple of minutes different between them. I think that the best argument for using sevo in my ambulatory practice because of the side effect profile difference: less drowsiness AFTER awakening and less nausea. The latter difference persisted for 24 hrs- for this I use the reference Philip et al. Anesth Analg 1996; 83:314-19.

Differences in discharge times have been hard to show [between any drugs] because discharge times may depend largely on the facility's recovery processes, overshadowing the effect of the drugs used. That said, it is my unsubstantiated observation that I can discharge patients within a 1/2 hour after their 1/2 hr sevo general anesthetic, but I can't do that with iso. Sevo is not the only way to get this result, but not iso.



I had as a patient a young, active duty Marine who was scheduled for facial scar revision and open septorhinoplasty. In October 1999, he was involved in a military training accident resulting in significant facial trauma (loss of an eye, Lefort fracture, etc.) which apparently resulted in a "bedside tracheostomy." The wife of the patient states that he had an "allergy to anesthesia gases." Reviewing the surgeon's discharge summary, the trauma surgeon stated that "when the anesthesia gases were turned on, the patient developed severe bronchospasm resulting in bilateral chest tubes." This event took place in California and we are located in North Carolina. We phoned the anesthesia provider who apparently did the case, but, ironically, he couldn't recall the specifics. Even more ironic is the fact that the surgeon remembered it vividly and simply stated, hey, I'm no anesthesiologist but when [anesthesia] turned on the gases, the guy decompensated. I performed my case using only TIVA. Are you familiar with ANY cases of paradoxical bronchoconstriction to volatiles? Allergy to volatiles? If so, is there a mechanism by which one may be evaluated for this? We owe it to the patient and family to prove or dispel the "allergy theory." Incidentally, there was NEVER an MH suspicion.  —Don Fontenot

Dr. Grichnik responds:

This patient may have had an underlying component of asthma or reactive airways disease. It is conceivable that the intubation and not the "anesthesia" caused severe bronchospasm. Further, the patient may have reacted to an intravenous drug such as an antibiotic with the timing of the bronchospasm coinciding with the onset of anesthetic inhalational agent administration. Many of our intravenous agents release histamine, also a possible etiology. The patient may have had a URI at the time, predisposing him to bronchospasm. Other case reports have noted bronchospasm with vagus nerve stimulation [1]. The etiology of the bronchospasm may be related to sympathetic nervous blockade, histamine release, or anaphylaxis [2]. Mechanical obstruction in the anaesthesia delivery-system and tracheal tube may be mistaken for bronchospasm [3]. An interesting abstract about bronchospasm is copied here [4]: With the aid of a computer-based anaesthetic record-keeping system, anaesthetics complicated by bronchospasm during anaesthesia at the Karolinska Hospital were retrieved. The incidence of bronchospasm was calculated in groups characterized by various variables. In total, 246 cases of bronchospasm in 156,064 anaesthetics were retrieved. This corresponds to one case in 634 anaesthetics or 1.7 per 1000 patients. High incidence figures were seen in the age group 0-9 years (4.0/1000) when the patients showed a respiratory infection (41.1/1000), a pathological preoperative ECG (24.3/1000), an obstructive lung disease (21.9/1000), were classified as belonging to ASA class III (23.8/1000), if a tracheal intubation was performed (9.1/1000) or a rectal anaesthesia (35.7/1000) was given. In the age group 50-69 years (1.8/1000), high incidence figures were seen when there was an airway obstruction (8.8/1000), an obstructive lung disease (7.7/1000), a previous myocardial infarction (5.4/1000), a bronchoscopy (7.6/1000) or a mediastinoscopy (7.8/1000) was performed. Most of the cases had no history of allergy or asthma recorded in the anaesthetic form. In this series the triggering factor more often seemed to be of mechanical origin.

It sounds like the patient had a bronchospastic episode which coincided with anesthetic agent administration. There are no specific reports of bronchospastic reactions to inhalational agent administration which I could find. However, I think it was prudent to conduct a TIVA anesthetic!

References:

  • Intraoperative bronchospasm induced by stimulation of the vagus nerve. Anesthesiology. 88(6):1675-7, 1998 Jun.
  • Otani S. Tokioka H. Fujii H. Tanaka T. Kosogabe Y. Morita K. Hirakawa M. A case of severe bronchospasm under epidural anesthesia with fentanyl. Masui - Japanese Journal of Anesthesiology. 46(10):1378-81, 1997 Oct.
  • Aarhus D. Soreide E. Holst-Larsen H. Mechanical obstruction in the anaesthesia delivery-system mimicking severe bronchospasm. Anaesthesia. 52(10):992-4, 1997 Oct
  • Olsson GL. Bronchospasm during anaesthesia. A computer-aided incidence study of 136,929 patients. Acta Anaesthesiologica Scandinavica. 31(3):244-52, 1987 Apr.



    Is the Wilson Frame contraindicated for use in morbidly obese patients requiring prone position anesthesia? What are the cardiovascular effects of placing a morbidly obese patient under anesthesia prone on a Wilson frame?   —Barry Nathaniel Swerdlow

    Dr. D'Ercole responds:
    The Wilson frame is a frame usually indicated for those patients requiring spine surgery/instrumentation in the prone position. The weight limit for the frame is tagged on the frame 'not to exceed 300 lbs'. Alternatively, chest pads could be used. In the morbidly obese patient my practice avoids general anesthesia (GA) whenever the possibility of employing a regional technique exists. If GA is the definitive anesthetic plan the surgeon and patient must be informed there may be the possibility the patient will not be able to tolerate ventilation (usually secondary to high PAP) exacerbated by positioning. Examples include:
    1) exaggerated lithotomy common in RP Prostatectomy
    2) lateral position common in total hip replacement
    3) prone position for extensive spine surgery. Assuming the patient has no COPD, the FRC and VC in any morbidly obese patient will be significantly decreased if placed in any position as cited above.

    If the 'attempt' to proceed with surgery is made as decided by risks/benefits the tolerance for ventilation would be determined by two questions. First, what is the ventilation profile in the patient in the supine position (PAP, O2 Stats, ability to manually ventilate with or without muscle relaxants, ABG, need for pressure-ventilator)? Based on the first question, the second question would be whether the patient could tolerate a different position for an extended time considering the first set of parameters will be significantly diminished. Remember this is a trial and you may cancel surgery at any time preferably prior to incision.

    Regarding the complete cardiopulmonary profile, remember compression of the inferior vena cava can be avoided if the patient is placed in the left lateral oblique (decrease weight on the right side by placing a sponge/pad under the right side). I recommend this especially during GA induction or spinal anesthesia. Turning supine to prone, consider a slight table tilt to diminish weight distribution over the IVC. To effectively administer IV fluids, do not depend on lower extremity IV access.



    For patients with RSD (or now called Complex Regional Pain Syndrome) of the lower extremity, if multiple blocks are planned, would it be better to just place an epidural catheter and reinject every other day on an out-patient basis, or to do multiple sympathetic lumbar blocks? Would the epidural approach be more comfortable for the patient, easier to place and less possible complications? Is it necessary to use fluroscopy it for the sympathetic lumbar block approach? How often should injections occur and for how long? Bottom line, IF the epidural approach works OK for a sympathetic block, why do a more complicated lumbar sympathetic block?   —Gary D Brown

    Dr. Rosenquist Responds:
    There are no perfect answers regarding the performance of epidural versus lumbar sympathetic blocks. I tend to favor the performance of lumbar sympathetic blocks as they allow the patient to use the extremity without weakness after completion of the block, and facilitates physical therapy. The recovery period after a lumbar sympathetic block is shorter as I do not worry about lower extremity weakness or urinary retention. In addition, the duration of the sympathetic block will be longer with bupivacaine delivered to the sympathetic ganglia than it would be with a short acting local anesthetic delivered into the epidural space. Lumbar sympathetic blocks may be successfully performed without the use of fluoroscopy if bony landmarks are used. Injection of a rapid onset local anesthetic and waiting for the affected foot to warm offers an additional endpoint before injecting a large volume (20 cc) of 0.25% bupivacaine. Epidural anesthesia is certainly capable of providing sympathetic block. I am unaware of any side by side comparisons of the two techniques with respect to treatment outcome to favor one over the other.



    Do you have any experience using Bretylium IV Bier block for RSD? What is the dose? What is the frequency of the blocks?   —Michael Cohen

    Dr. Rosenquist Responds:
    IV Regional Bretylium has been used for RSD for some time. It was first reported in the late 80's and early 90's. As with so many other treatments for RSD, it is successful in some patients and unsuccessful in others. The dose ranges from 100 mg to 500 mg along with lidocaine 0.5%. The frequency of the blocks is initially 1-2 weeks apart and then gets longer depending on the patient's response. If they have had no response after 3-4 blocks, it is unlikely that it will provide them with much benefit. If they are responding, the blocks should be continued until a treatment plateau is reached. As with other types of treatments, the psychological and physical aspects of the disease process should be treated as well.



    I have been reading some articles recently about the use of intrathecal ropivacaine. Do you know if studies are being conducted on the use of spinal ropivacaine, and if FDA approval is expected soon?   —Kary L. VanAllen, M.D.

    Dr. D'Ercole responds:
    In a recent article by Spencer Liu and D. Kopacz, hyperbaric spinal ropivacaine was studied to determine its relative potency to bupivacaine since its dose-response characteristics had not been previously described. They noted spinal anesthesia with ropivacaine was indeed significantly different from bupivacaine. When the duration of block was measured by pinprick, tourniquet tolerance, transcut-electrical stimulation, EMG, and achievement to discharge criteria, ropivacaine was approximately half as potent. Noteworthy, there was a 28% higher incidence of back pain associated with intrathecal ropivacaine.

    Liu and Kopacz concluded that, in equipotent doses, ropivacaine is half as potent as bupivacaine, with a higher incidence of side effects. Low-dose hyperbaric spinal ropivacaine does not appear to have to offer any advantage over bupivacaine for outpatient anesthesia.

    Regarding FDA approval, we do not expect the FDA to rush approval for any single intrathecal agent, as long as there exists another agent on formulary with proven efficacy (i.e. currently, spinal bupivacaine and lidocaine may be the most commonly used intrathecal agents).

    Reference:

    Liu SS, Kopacz D. Hyperbaric spinal ropivacaine: a comparison to bupivacaine in volunteers, Anesthesiology 90 (4): 971-7, 1999 APR.

    Editors Note: Please also see Dr. McGoldrick's commentary in this month's edition of AnesthesiaWeb:

    Intrathecal Ropivacaine for Ambulatory Surgery: A Comparison Between Intrathecal Bupivacaine and Intrathecal Ropivacaine for Knee Arthroscopy

    And the following additional references:
  • Gautier PE; De Kock M; Van Steenberge A; Poth N; Lahaye-Goffart B; Fanard L; Hody JL. Intrathecal ropivacaine for ambulatory surgery. Anesthesiology. 1999 Nov;91(5):1239-45.
  • Zaric D, Nydahl PA, Philipson L, Heierson A, Axelson K. The effect of continuous lumbar epidural infusion of ropivacaine (0.1%, 0.2% and 0.3%) and 0.25% of bupivacaine on sensory and motor blockade in volunteers: A double-blind study. Reg Anesth. 1996; 21:4-25.
  • Scott, DB, Chamley D, Mooney P, Deam RK, Mark AH, Haggloff B. Epidural ropivacaine infusion for postoperative analgesia after major abdominal surgery: A dose-finding study. Anesth Analg. 1995; 81:82-6.
  • Capogna G, Cellano D, Lyons G, Columb M. Determination of the minimum local analgesic concentration of epidural ropivacaine in labour (abstract). Br J Anaesth. 1998; 80(suppl):A506.
  • Polley LS, Columb MO, Naughton NN, Wagner DS, van de Ven CJM. Relative analgesic potencies of ropivacaine and bupivacaine for epidural analgesia in labor. Implications for therapeutic indexes. Anesthesiology. 1999; 90:944-50.
  • Hampl KL, Schneider MC, Ummenhoffer W, Dreive J. Transient neurologic symptoms after spinal anesthesia. Anesth Analg. 1995: 81:1148-53.
  • Freedman JM, Li D-K, Drasner K et al. Transient neurologic symptoms after spinal anesthesia: an epidemiologic study of 1,863 patients. Anesthesiology. 1998; 89:633-41.
  • Ben-David B, Solomon E, Levin H, Admoni H, Goldik Z. Intrathecal fentanyl with small-dose dilute bupivacaine: Better anesthesia without prolonging recovery. Anesth Analg. 1997; 85:560-5.



    We are in discussion with the ENT in our hospital about the utility of coagulation testing before surgery (e.g. amygdalectomy). I and most of my colleagues are quite sure that these tests are not useful if there is no sign of coagulation trouble at the preoperative consultation. The opinion of the ENT is different and they are alarmed if these tests are not performed; for them a coagulopathy, mainly a VW disease, may cause abnormal bleeding even if there is no problem for the daily life. Could you give me your recommendations and some references?   —Dr. Ives Michel M.D.

    Dr. Iain Sanderson responds:
    Roizen has stated that if you do a PT/PTT on everybody coming to surgery you could spend a million dollars before a single truly new and significant coagulopathy is picked up preop. The test has a low specificity (is poorly related to the pathology) and a high false positive rate, together with an extremely low incidence of pathology in the community - all of which make it a poor screening test.

    Our policy is as follows:
  • a history of significant bleeding with prior surgery or procedures.
  • a history of spontaneous bruising, silver dollar size.
  • a known history associated with coagulopathy or platelet disorder (e.g. alcoholism)
  • a history of taking coumadin, etc., i.e. hard indicators of pathological bleeding.

    There are 2 other factors which influence us:

  • the nature of the surgery - we have lower threshold for operations where a small amount of bleeding is likely to be catastrophic, e.g. neurosurgery
  • the nature of the surgeon - with some of them it is just too much fuss to argue rationally.

    Suffice is to say, we spend a great deal of time in our clinic canceling tests ordered by the surgeon, which regularly causes conflict. No test is more controversial than the PT/PTT, despite all the evidence to the contrary. (except perhaps the routine ABGs regularly ordered on all gynecological cases by that group of surgeons!).

    The best reference I have found on this is:

    Anthony L. Suchman, Alvin I. Mushin. How well does the activated partial thromboplastin time predict postoperative hemorrhage? JAMA. 1986;256:750-753.

    It is a retrospective study of all 12, 338 adult patients undergoing invasive diagnostic or therapeutic procedures at a university hospital in Rochester, NY, during 1981. Patients were divided into two risk groups, one composed of patients with any condition which might indicate bleeding problems—i.e. known coagulopathy, anticoagulant use, liver disease, malnutrition, hemorrhage or trauma the other composed of the rest with no risk factors for hemorrhage. This study analyzed the outcomes of all the patients and determined that the incidence of perioperative hemorrhage was between 0.003% and 0.06%, depending on whether one used a "strict" definition of hemorrhage or a "broad" definition of hemorrhage. These figures allowed the calculation of positive predictive values. Because a moderately specific test (such as PTT at 86%) applied to a low risk population yields so many false positives, over 99% of the low risk patients who had a positive PTT, had no actual disease. This means that either one ignores abnormal results, or holds up surgery needlessly in 99 cases out of a 100.

    At our institution, we order coagulation studies only when there is a clear indication based on history or physical examination. Therefore, healthy children having a tonsillectomy, for example, no longer have routine PT and PTT evaluations. I believe this approach is common at many other university hospitals also.



    What are the anesthestic implications for a 47 y.o. healthy white female scheduled to have a facelift as an outpatient in office taking the following drugs for psychiatric history? What drugs should we avoid with patient taking Seroquel, Lithobid, Celexa, and Lamictal? What drugs are safe to use as vasopressors? Do any of these increase the risk of aspiration? Do any of these involve neuroleptic malignant syndrome?   —DL Hilt

    Dr. McGoldrick responds:
    I will attempt to answer this difficult question as best I can because many of these drugs are relatively new and, therefore, our current understanding of their implications is probably incomplete. Seroquel is an antipsychotic drug of the new dibenzothiazepine class. It antagonizes multiple neurotransmitters in the brain, including serotonin, dopamine, histamine, and alpha-1 and alpha-2 receptors. Orthostatic hypotension is not uncommon . Moreover, the drug has been implicated in the possible development of neurolept malignant syndrome (NMS). Seroquel's drug interactions have not been extensively evaluated but, clearly, caution should be used when given in combination with other centrally acting drugs. I would expect, for example, that this drug may potentiate the effects of inhaled and intravenous anesthetic agents. ECG effects have been reported and these include a prolonged QT interval and T wave abnormalities.

    Lithium has been associated with a prolonged response to depolarizing and nondepolarizing muscle relaxants. Assorted cardiovascular effects have been reported including, dysrhythmias, AV block, hypotension, and benign ST/T wave changes. One should anticipate a reduced requirement for injected and inhaled anesthetic agents in a patient on lithium. Moreover, one may see a reduced pressor effect of norepinephrine, nephrogenic diabetes insipidus, and electrolyte abnormalities . Lithium should not be used in combination with haldol because an encephalopathic syndrome may occur.

    Lamictal is an antiepileptic drug of the phenyltriazine class that has a weak 5HT3 antagonist action and weak effects at sigma opioid receptors. It does NOT inhibit uptake of norepinephrine or dopamine. Severe, potentially life-threatening rashes, including cases of Stevens-Johnson syndrome and toxic epidermal necrolysis have been reported with this drug.

    Celexa is a serotonin reuptake inhibitor with a chemical structure unrelated to that of other SSRIs or any other antidepressant. Celexa is highly selective and has minimal effect on norepinephrine and dopamine neuronal reuptake. It is not typically associated with orthostatic changes. However, although no causal relationship to Celexa therapy has been established, at least 3 patients (of approximately 8 million) have developed neurolept malignant syndrome.



    A 24 y.o. male on methadone for addict recovery presented to surgicenter for pin removal from the metacarpal. Versed, 2 mg., was used to sedate and an additional 4 given to facilitate Ax block administration. Ax block was successfully placed and the patient became adamant about having some water. When his request was denied, he tore out his IV, hit a nurse and ran from the facility. The police picked up the patient several blocks away, and took him to an ER where the pin was removed. The ER doc commented that the patient should not have been given versed due to "Versed rage". We had not heard of this. Is there any literature on it and the use of versed with methadone?   —Elizabeth Binnings CRNA

    Dr. Grichnik responds:
    Three of the editors in anesthesia are not familiar with "Versed rage". A literature search turned up no articles on the subject. In contradistinction, there is much literature on treatment of methadone addicts with midazolam when transitioning the methadone-treated addict to another drug such as naltrexone. (Lancet 1989;16:684-4, Am J Psychiatry 1991;148:933-5, Drug and Alcohol Dependence 1998;52:243-50). It is known that idiosyncratic reactions to midazolam are common. The literature supports the treatment of a paradoxical reaction to midazolam with haloperidol. (Anesthesia and Analgesia 1997;85:213-5). We would speculate that a somewhat difficult patient with perhaps pre-existing personal problems may become disinhibited. This could have happened with virtually any similar agent and is probably not unique to the midazolam/methadone combination.



    I have a patient with post-traumatic left elbow pain which is persisting for a very long time. The patient is 40 years of age, female, and obese. The working diagnosis is post-traumatic causalgia. How many Stellate ganglion blocks must I do before accepting treatment failure? The patient already had initially 12 stellate ganglion blocks, 4 Bier blocks including bretylium, 3 axillary blocks followed by another set (10) stellate ganglion blocks.   —Istrati Kupeli

    Dr. Rosenquist Responds:
    If this patient has had as many blocks as you listed, and she has still not received significant benefit in terms of pain control and improved function at this time, I think that more than enough has been done, and treatment with blocks may be declared a failure.



    Does anyone have any information on renal effects of clonidine? I have in the mists of my mind some reference to improved postop renal function in cardiac surgery. I have also noticed that ICU patients on clonidine for sedation seem to produce more urine.   —Joe Jaidev

    Dr. Grichnik responds:
    Clonidine is an alpha-2 adrenergic agonist, which has specific effects on reduction of central sympathetic tone. Clonidine is known to have natriuresis and diuresis properties. This may be due to decreased renal sympathetic nerve activity (Feng, 1992). In humans, clonidine, given as an oral premedicant, caused a significant diuretic effect during surgery under GA, however, apparently not related to an arginine vasopressin (AVP) effect (Hamaya 1994). In these patients, urine output was increased, urine osmolality was reduced but plasma AVP and atrial natriuretic peptide levels were not different than control. In dogs, clonidine is thought to decrease sympathetic outflow to the kidney and increase renal medullary blood flow. It was also suggested that urine flow increases may also be mediated by an indirect pathway such as the renin-angiotensin system (Kover 1989). In rats with CHF, the effects of clonidine are less pronounced, suggesting down-regulation of the vascular appha-2 receptor in CHF, experimentally (Feng 1992). There were no specific articles on clonidine and urine output in the ICU setting found.

    References:
  • Feng Q, Carlsson S, Thoren P, Hedner T. Effects of Clonidine on renal sympathetic activity, natriuresis and diuresis in chronic congestive heart failure in rats. J Pharm Exper Ther. 1992;261:1129.
  • Hamaya Y, Nishikawa T, Dohi S Diuretic effect of clonidine during isoflurane, nitrous oxide and oxygen anesthesia. Anesthesiology. 1994;81:811.
  • Kover G, Tost H., Darvasi A. The effects of clonidine on the kidney function in the anesthetized dog. Acta Physiologica Hungarica. 1989;74:229.



    There was recently some discussion in our hospital about the high costs of using sevoflurane. I currently use isoflurane and I'm completely happy with this anaesthetic. The main advantage is induction, which is fantastic with sevoflurane. On the other hand while using sevoflurane on minimal flow, the difference in costs is not so big, as isoflurane can also be used in this way. Are there big advantages in recovery time/nausea & vomiting/shivering/hangover effect/time to discharge between sevoflurane and isoflurane? Where can I find evidence-based researches on this subject?   —Piotr Konopka

    Dr. McGoldrick responds:
    Your points about isoflurane vs sevoflurane are well taken. If you are using low flow sevoflurane to save money, however, it is important to be aware (for medicolegal reasons) that sevoflurane has not been approved for use in the USA at lower flows than 2L/min owing to fear of high levels of Compound A leading to nephrotoxicity. Sevoflurane will indeed give a faster induction and a faster emergence than isoflurane, however, time to discharge does not seem to differ between the two agents. Incidence of PONV seems to be similar; emergence excitement is more common with both sevoflurane and desflurane versus isoflurane.

    Two relevant articles are:

  • Frink EJ et al. Clinical comparison of sevoflurane and isoflurane in healthy patients. Anesth Analg 1992; 74:241-5.
  • Philip BK et al. A multicenter comparison of maintenance and recovery with sevoflurane or isoflurane for adult ambulatory anesthesia. Anesth Analg 1996;83:314-9.



    To your knowledge, is there anything one can do before an amputation to prevent phamtom limb syndrome?   —Dr. Ives Michel

    Dr. Grichnik responds:
    Phantom limb pain is a very difficult problem to deal with. It has been shown that the amount of pain experienced preoperatively correlates with the amount of pain postoperatively. Phantom limb pain is a significant problem, as more than >70% of amputees experience phantom limb pain years after amputation. An approach to the problem has postulated that preoperative ablation of pain may decrease the incidence of phantom limb pain. The idea behind preemptive analgesia is that analgesics or local anesthetics given prior to surgery can reduce postoperative pain (Lancet 1997;350:1338-1339). The hypothesis is that the transmission of noxious input from the periphery to the spinal cord produces a prolonged state of central neural sensitization or hyperexcitability that amplifies subsequent input from the wound and leads to increased postoperative pain (Lancet 1997;350:1338-1339). Interruption of the transmission of noxious stimulation in a pre-emptive manner, may result in reduced pain and analgesic requirements after surgery even after the pre-emptive agents have worn off. Some studies have shown that preoperative use of epidural analgesia may decrease phantom-limb pain (Pain1988;33:297-301; Reg Anesth1995;20:256). Other studies don't show a difference with the use of preoperative epidural analgesia (Lancet 1997;350:1353-57). Clearly this issue is still unresolved. Preoperative and intraoperative analgesic techniques include epidural analgesia and anesthesia, spinal anesthesia, and catheters inserted into the amputated nerve sheath to be infused with local anesthetics.



    I have a 20 year old man undergoing oral dental rehabilitation who has metachromatic leukodystrophy. Is this patient at risk for malignant hyperthermia (MH)? I suspect not, due to the demylinating nature of the disease.   —Kevin Przybyla

    Dr. McGoldrick responds:
    Metachromatic leukodystrophy (MLD) is a disorder of the white matter of the brain. MLD may present at any age and has been divided into late infantile, juvenile, and adult forms. The disease results from the deficient activity of arylsulfatase A and the accumulation of galactosyl sulfatide in the white matter of the CNS and the peripheral nervous system. The infantile form is typically fatal, whereas the juvenile and adult forms are more variable and include gait disturbances, mental regression, peripheral neuropathy, seizures, and (in adults) behavioral disturbances and dementia. I am unaware of any association with malignant hyperthermia. However, I do not claim to be an expert on this disease.



    I administered a general anesthetic to a 16 year old at 32 weeks gestation who was on terbutaline who had refused regional anesthesia. Fetal heart rate monitoring was used. Maternal heart rate rose from 120 pre-induction to 180 post-induction and inderal was administered. Fetal heart rate fell from 120 to 60 with no evidence of hypotension or hypoxemia and concomitant with inderal administration. It returned to 120 over a period of 10 minutes. Surgery for ureteroscopy and stent had not commenced. The obstetric nurse monitoring fetal tones requested immediate c-section while I insisted that fetal distress was not present, but that rather a pharmacologic effect on fetal heart rate by inderal was of no harm to the fetus. Is there any evidence that pharmacologic slowing of fetal heart tones is harmful?   —VLMR1228

    Dr. Dwane Responds:
    To begin with, the main benefit of intraoperative fetal monitoring is as an additional monitor which aids in optimizing the maternal environment: position, surgical retraction, oxygenation, cardiac output, oxygen content, and maternal blood pressure. Also, when intraoperative fetal monitoring is planned for a patient there should be an obstetric consult, and one question that should be asked is what the planned response to prolonged fetal bradycardia will be.

    Specifically for this incident, certainly propranolol has been shown to cross the placenta and cause fetal bradycardia by its direct action. Although you couldn't be absolutely sure, at the time the bradycardia occurred, that it was not caused by fetal distress, certainly a period of observation in the operative setting is in order. The exact length of that period of "observation" is not clearly defined, and this is where the preoperative obstetric consult may have been of some help.

    Certainly if the maternal parameters were normal, and patient position and surgical traction were not felt to be factors, the presence of fetal bradycardia intraoperatively in the short term (less than 10 minutes) does not carry the same weight as sustained fetal bradycardia or late decelerations during labor.

    The bradycardia as you present it in this case was most likely not the result of fetal asphyxia but rather a result of the pharmacological effect of the drug. However, a confounding effect of beta blockers might be the increased uterine tone, which may have subsequently contributed to the bradycardia.

    In retrospect it was reasonable not to have performed a cesarean section. However, at the time and without prior obstetric consideration, after the 10 minute period of bradycardia I would have found it progressively more difficult not to have agreed that a cesarean section was perhaps appropriate. An early attempt to confer with your obstetric colleague might have been of help, especially if the bradycardia had persisted.

    In answer to your direct question, if the fetal bradycardia is prolonged and severe, even if it is only a pharmacological effect, it could be harmful to the fetus because it will reduce the fetal cardiac output to a point where fetal metabolic needs would not be met, and metabolic acidosis and ultimately death would occur.

    With higher dose, chronic use of propranalol, intrauterine growth retardation is sometimes seen, and the likely cause is the reduced maternal/fetal perfusion.



    I am writing to request information on anesthesia and emphysema. I have emphysema and I currently require obstetrical surgery so I wish to learn more about it at the level of taking medication.   —AT6262

    Dr. Grichnik responds:
    There are no specific answers in the literature about emphysema and surgery during pregnancy. Therefore one must be guided by the usual perioperative considerations for surgery in patients with severe chronic obstructive pulmonary disease. This includes preoperative optimization of pulmonary function, especially with respect to control of secretions, treatment of infection and use of bronchodilators. Preoperative tests should include a chest x-ray, a room air blood gas and standard PFTs with and without bronchodilators. One can consider using an arterial line for monitoring during surgery to be able to analyze blood gases and to adequately assess hemodynamic instability should it occur due to breath stacking or tension pneumothorax. Other intraoperative considerations include limiting overzealous ventilation with induction of anesthesia, limitation of peak inspiratory pressures, possible use of a pressure limited ventilator, vigilance for the possibility of breath stacking, use of a regional anesthetic technique if indicated by the type of surgery considered, and intraoperative use of bronchodilators if not contraindicated by the pregnancy.

    Postoperative analgesia should not cause excessive sedation with the risk of an elevated carbon dioxide tension. Postoperative care may be considered in a more monitored setting than a standard postoperative ward bed.



    It is my understanding that it is not recommended to place an epidural catheter while the patient is under general anesthesia due to possible nerve damage. Is this also the case for other nerve blocks? For example, could you do a femoral nerve block for post op analgesia before the patient wakes up or while a spinal is still in effect? Bottom line: does the patient need to be awake (and able to tell you they're having pain on injection) in order to respond to direct neural injection before doing any blocks?   —Gary Brown, CRNA

    Dr. D'Ercole responds:
    Avoid placing epidurals in the sleeping patient !!! This is very wise, as you stated. The distinct difference between placing epidurals while the patient is asleep and performing peripheral nerve blockade (PNB) while the patient is asleep is that an awake patient gives you have the opportunity to utilize a nerve stimulator to perform the nerve block. (The author uses a Braun stimulator with insulated stimuplex needles). In my opinion, peripheral nerve blockade placement should be avoided during general anesthesia (GA) unless you have a nerve stimulator. Stated another way, how can you receive feedback from a sleeping patient if you are using the 'parathesia technique' which does not employ a nerve stimulator??

    Additionally, I strongly recommend being proficient at using a peripheral nerve stimulator in the awake (but sedated) patient prior to performing peripheral blocks during GA. At our institution, most PNB is performed in a sedated patient. However, there may be the patient who requests a block but may not tolerate the procedure, for example, pediatrics or anxious children. If this is the case, the block should be performed by 'experienced' hands. Pitfalls to watch for (and some remedies) may include:
  • Always be sure that no residual IV muscle relaxants are on-board or you may miss a peripheral nerve stimulation and, worse yet, traumatize the nerve by multiple blinded passes.
  • Never force the injection.
  • Use epinephrine as a tracer for potential intravascular injections with continuous EKG monitoring during intermittent injection/aspiration.
  • Be sure to perform meticulous calculation of dosage in pediatrics.

    For those cases in which the patient may benefit from PNB after an extensive (e.g. knee) procedure a femoral nerve block or femoral 3:1 block is a simply elegant opportunity to provide your patient with outstanding pain control placed (preferably) preoperatively; after induction with return of full train-of-four; prior to emergence; after spinal anesthesia and ALL performed with a peripheral nerve stimulator. One of the most significant references advocating PNB (when compared to central blockade) performed during anesthesia is the publication by Giaufre et al. evaluating regional anesthesia in children.

    Reference:

    Giaufre E, Dalens B, et al. Anesth and Analg 1996;83:904-912.




    I need some information or references on anesthesia for pulmonary lavage in alveolar pulmonary proteinosis. I am particularly worried about a patient because he is already dependent on oxygen for his baseline activities. What techniques for improving oxygenation in this lung scenario can be used? Because the lung being lavaged is usually subjected to 30 cm of H20 pressure, could this help divert the pulmonary blood flow to the ventilated lung.? What pulmonary preoperative tests would be advisable? This is a very rare condition and procedure, and I certainly need your help.   —E. Carrero MD, San Juan, PR

    Dr. Richard Moon, Director of the SW Hall Hyperbaric Center, Duke University Medical Center, Responds:
    Lung lavage can be associated with significant hypoxemia, for obvious reasons. The increase in alveolar pressure on the lavaged side does help to reduce blood flow during the "filling phase", but does not help during the emptying cycle. We do ours in the hyperbaric chamber, and about half of our patients require an increase in ambient pressure in order to maintain an acceptable SpO2. Our preliminary experience was written up in a Workshop Proceedings, which may be relatively inaccessible, but there is an article in Chest from the Amsterdam group reporting the use of hyperbaric oxygenation (HBO) for this procedure.

    Other solutions include veno-venous bypass or manipulating a PA catheter into the side to be lavaged and overinflating the balloon with saline to reduce blood flow to that lung (it is in the literature but I don't have the reference at hand).

    Jansen HM; Zuurmond WW; Roos CM; Schreuder JJ; Bakker DJ. Whole-lung lavage under hyperbaric oxygen conditions for alveolar proteinosis with respiratory failure. Chest. 1987 Jun;91(6):829-32.

    Biervliet JD; Peper JA; Roos CM; v.d. leij AJ; Bakker DJ; Hansen HM. Whole lung lavage under hyperbaric conditions: 1. The monitoring. Adv Exp Med Biol. 1992;317:115-20.

    van der Kleij AJ; Peper JA; Biervliet JD; Bakker DJ; Roos CM; Jansen HM. Whole lung lavage under hyperbaric conditions: 2. Monitoring tissue oxygenation. Adv Exp Med Biol. 1992;317:121-4.



    Could you refer me to an article that discusses operative length and its risks. For example, do you believe that increased surgical length is a risk factor for some patients?   —AGeer

    Dr. Lubarsky Responds:
    Length of surgery is not an independent risk factor. Length of clamp times when blood flow to critical organs is stopped (CPB, suprarenal arterial clamps, carotid clamp, etc.) is a predictor of risk.



    Is regional anesthesia (spinal or epidural) contraindicated in sickle cell disease?   —zahra

    Dr. Lubarsky Responds:
    No it is not. The key is to maintain blood flow, oxygen saturation, and warmth. Theoretically, regional anesthesia increases blood flow to the lower extremities (that's why there is a lower DVT rate with regional anesthesia).



    Which regimen do you recommend for management of insulin dependent diabetes mellitus? Is it enough to give 66-100g of glucose/24h in combination with insulin. How do you give insulin: sc or continuously IV?   —Rolf Ensner

    Dr. Lubarsky Responds:
    It's not what you do, it's how you monitor it. Both approaches are perfectly acceptable. My own regimen is D5W at 75cc/hr, 1/2 the usual NPH does in the AM. I check glucose (Accucheck) qhr in the OR and upon arrival to the PACU, then q2h in the PACU, and q4h once stable and sent to the floor with a sliding scale. Obviously, if there is either a low value, or a tend towards a low value, I reevaluate more frequently and give more glucose. If there is any question of symptoms, I do both an Accucheck and a lab confirmation. There are many recipes for insulin/glucose infusions. Any text will outline these for you. The key is still to check carefully the effect of your therapy.



    A short time ago that I was performing a pre-anesthesia interview on a patient having a right knee arthroscopy. This patient was healthy in every respect, with the exception of his airway. I rated it as a Malmpatti III (just soft palate visible). The patient had full range of motion in the neck and all 32 teeth were intact. The mouth opening was 3 finger breaths and the thyro-mental distance was greater than 6.5 cm. I obtained consent from the patient for an epidural. I was later ridiculed by my colleagues for "not securing the airway" and not obtaining consent for general anesthesia. Any comments or ideas would be helpful.   —En Defiant

    Dr. Lubarsky Responds:
    There is no "right" way to do something. It is the attention to detail, the understanding of the potential complications involving a lost airway, preparation for that eventuality, etc. that are important. As for losing the airway, it is my anecdotal experience (at an academic medical center doing 30,000 cases per year), that lost airways occur just as frequently while sedating patients for awake intubations as they do with regional anesthesia. Accept no ridicule. Personally, I would have done the case that same way.



    What would you do for a patient with persistent, severe, scintigraphy-confirmed coronary artery disease who continues to be symptomatic even at rest (despite several angioplasties), when there is no way to improve myocardial vascularization, and the patient has malignant pathology with adenopathies?

    The surgeon intends to operate in order to remove the adenopathies, although we don't know where the original cancer is. We are certain that the patient's prognosis is very bad with regard to both the malignant disease and the CAD. Can we take the risk of operating on such patient?   —Dr. PM

    Dr. Lubarsky Responds:
    We often see such dilemmas at Duke. Our job is to get the patient in optimal shape for surgery. After that, it is the surgeon's and patient's decision to decide whether to proceed. Given that this man will die from his cancer, one can only ask: will he be better off with or without surgery? If the patient and medical team decides it is worth the risk of shortening whatever life span this gentleman still has, and if his ischemia and myocardial function are maximally treated with drugs, and beta blockers are employed perioperatively, that is all you can do.



    I was recently frustrated when a nondependent lung failed to collapse all the way (there was only 30% collapse) despite a perfectly placed endobronchial tube that was repeatedly verified fiberoptically. The lung never moved with respiration, and simply failed to collapse. The procedure was for a thorocoscopic lung biopsy required for the diagnosis of interstitial fibrosis in a 1/2 pack-per-day smoker in her 40s. Even suctioning through the fiberoptic scope would not help, and the surgeon ended up performing an open lung biopsy. He does not agree with my explanation of a stiff lung since the same thing happened with another anesthesiologist some time ago. Do you have any references or explanations to hand over this surgeon?   —Abdulkader M. Kulam MD

    Dr. Lubarsky Responds:
    As Chief of Vascular and Thoracic Anesthesia for many years at Duke University, I have only occasionally encountered this type of problem. To my knowledge, nothing exists in the literature regarding this problem. Basically, there are two main reasons why a lung will not collapse: (1) airways are obstructed at lower lung volumes, thereby trapping air in the post-collapse alveoli, or (2) the visceral pleura is adhering to the chest wall. Two options exist: put a suction catheter down and apply suction, or have the surgeon manually squeeze the lung. In a throracoscopic procedure, careful application of a little positive pressure in the thoracic cavity may help (or may drop the blood pressure). If that doesn't work, it doesn't work. Not all physiologic problems are the anesthesiologist's fault, but its easier for some of our surgical colleagues to blame someone than to accept life as it is.



    Under what conditions is it acceptable to use a ventilator with a laryngeal-mask-airway in place?   —MajorCarl

    Dr. Karl Responds:
    Several people have written about using a ventilator with low inspiratory pressures; I wouldn't do it.



    Would you perform local anaesthesia with bupivacain for a patient with acute intermittent porphyria scheduled for eye surgery?   —Jacques E. Moerlen, Anesthesiologist, Basel

    Dr. Karl Responds:
    The short answer to your question is yes: bupivacaine is listed among the drugs that are safe or likely to be safe in acute intermittent porphyria (AIP). Safe anesthetic management of a patient scheduled for eye surgery, however, requires special preparation and thought. (See Jensen, NF et. al. Anesthetic considerations in porphyrias. Anesth Analg. 1995; 80:591-599 for a complete discussion):

    1) Preoperative preparation
  • because of the neuropathies frequently present in patients with AIP, carefully examine the area of the block and document pre-operative function
  • confirm that the patient is not in acute crisis prior to elective surgery
  • evaluate cardiac status: acute attacks of AIP commonly include hypertension and tachycardia
  • because dehydration is a trigger for acute attacks, IV infusions should be started early
  • anxiety is also a trigger for acute attacks: lorazepam and midazolam are on the list of "safe or likely safe" drugs

    2) Intraoperative management

  • assure sufficient sedation/analgesia for block placement: propofol, morphine and fentanyl also are "safe or likely safe"
  • Tachycardia, changes in mental status, vomiting and abdominal pain are among the symptoms of acute crisis
  • Keep a photocopy of a list of "safe" and "unsafe" drugs (e.g. the one from the above article) in case you need to treat vomiting, seizures, etc.

    3) Postoperative management

  • Instruct the patient to avoid stress and dehydration and to monitor for potential onset of porphyric crisis for up to 5 days post op (most are probably more aware of this than we are)
  • Document return of neurologic function after the block has worn off

    Good luck!




    In a patient with radiological evidence of a pneumothorax (say about 10% after CVC insertion and/or in the presence of a single rib fracture) who is mechanically ventilated, would you drain it immediately, monitor it with another CXR a few hours down the line, or wait until there is evidence of deterioration before inserting a chest tube? I presume it will be worth inserting a chest tube if the patient is undergoing GA plus a relaxant for surgery. However, in the ICU (in the absence of infection), it has been argued that a small pneumothorax may seal off, and therefore should be treated with a chest tube only when it produces problems.   —Jeff

    Dr. Sladen Responds:
    The general rule is: always place a chest tube for pneumothorax in a patient on mechanical ventilation. Exceptions could be made in a patient on low levels of mechanical ventilation (e.g. CPAP with low pressure support), or in someone who will be extubated soon. In any patient requiring high levels of airway pressure therapy and PEEP, it would be safer to place a chest tube immediately, especially if there are other signs of barotrauma (e.g. interstitial pulmonary emphysema, pneumomediastinum). In some patients with severe ARDS and barotrauma, we may have to accept 10% residual pneumothoraces despite multiple chest tube placement.

    In a spontaneously breathing patient with a 10% pneumothorax, I would certainly follow the patient closely with serial radiographs. If there was any evidence that the pneuomothorax was increasing in size, I would place a chest tube - preferably before any signs of hemodynamic compromise occur. An alternative to a standard chest tube is a slim, "S" shaped metal device which can decompress a small pneumothorax with less risk of infection. Keep in mind, however, that the initial x-ray after line placement may miss or underestimate the ultimate size of a pneumothorax, which can take 1-2 hours to fully develop in some patients. Also, the large transpulmonary pressure gradient created just before a cough in an extubated patient can itself generate a pneumothorax, or worsen an existing one.

    Hope this is of help.


    A 30 y.o. man with post-traumatic infarction of the anteriol wall of the heart had a coronary angiography which showed a pseudoaneurysm on the first part of the left anterior descending coronary artery without stenosis. He also suffered from fractures of the face (Le Fort III on the right side and Le Fort II on the left side) with double vision. The exercise ECG was not made for orthopedic problems and pharmacologic stress testings were not made after 15 days from myocardial infarction. The patient had an absence of anginal symtoms. This patient should undergo an surgical operation for the fractures of the face 15 days after myocardial infarction.

    Do you know if, in the evaluation of incidence of reinfarction, I can use the studies of Rao (Anesthesiology 1983; 59:499-505) and Shah (Anesth.Analg. 1990; 71:231-235)? Is the cardiac risk of this patient the same as the patients whom have had a myocardial infarction 15 days previously? Is it possible in treating this patient to use the following guidelines:
    "The American College of Cardiology/American Heart Association Task Force, in its recently published Guidelines on Perioperative Evaluation of the Cardiac Patient Undergoing Noncardiac Surgery, has advocated using the occurence of MI less than 30 days before surgery as an identifier for the group at highest risk and , after that period, basing risk stratification based on the presence of disease and exercise tollerance." (Lippincott-Raven; Problems in Anesthesia 1997; 9:146.)

      —Dr. Umberto Marzi

    Dr. Sladen Responds:
    I don't think that this patient fits into any usual category of postmyocardial infarction risk. He has suffered an acute MI in the absence of coronary artery disease. What was the etiology? Severe sympathetic stress during his trauma or severe hypoxia? In any event, the statistical data accumulated by Rao, Shah or anyone else do not include such a patient - he must be considered a unique case!

    The main issue is whether he has myocardium still at risk of ischemia. The simplest way to evaluate this would be to perform a dobutamine stress echo. If it is negative (i.e. no inducible ischemia) then in the absence of underlying coronary artery disease, his risk could be considered relatively low for reinfarction. If it is positive, then you must consider the urgency of repair of the Le Forte fracture (optic displacement, nerve injury, ischemic injury, infection) vs. the risk of myocardial ischemia. Obviously there is no coronary artery disease to revascularize so that is not a consideration. If you have to go ahead in the face of a positive stress echo, precautions such as pulmonary artery catheterization, esmolol infusion, etc. are warranted.

    If a dobutamine stress echo is not possible, a simple bedside transthoracic echo or, if safely feasible, a transesophageal echo could define his present myocardial contractility and ejection fraction, and the presence or absence of regional wall abnormalities suggestive of possible ischemia.



    When the bacterial filter of an epidural catheter (filled with Bupicaine 0.25%) is gone, what do you propose as a course of action?
    1) Remove the whole catheter?
    2) Install a new filter and continue with same concentration?
    3) Fill the catheter with some milliters Bupivacaine 0.75% for the antimicrobiotic properties?   —Dietrich Wolf

    Dr. Lubarsky Responds:
    The most conservative approach would be to discontinue the catheter. However, patient priorities and co-morbidities might make that decision unwise in some instances. If you decide the risk of infection is outweighed by the continued use of the catheter, you may consider sterilizing the last few cm's of the catheter (betadine), using a sterile scissors to snip off the end, and re-attaching a new sterile bacterial filter. While I have personally never read about using a different solution, that is more likely to be bacteriocidal, that makes sense.



    Which coduction blocks (First degree, Type 1 and 2 second degree, third degree, hemiblocks, and any combination of these) call for either cancellation of a case, preoperative IV pacers, or external pacer availability? Thanks, references would be appreciated.   —Gator92

    Dr. Sladen Responds:
    Here's a quick response. Actually I have not yet found a succinct reference on indications for perioperative pacing - the standard textbooks handle this area poorly, and one has to put it together based on discussion of the individual conduction disorders. But here goes...

    Indications for perioperative pacing:
  • Third degree heart block
  • Mobitz type II second degree heart block (regular rhythm, usually LBBB or intraventricular conduction defect in QRS)
  • Trifascicular block (RBBB, left anterior hemiblock + 1st degree heart block)
  • Documented sick sinus syndrome (tachycardia-bradycardia syndrome)
  • Severe sinus bradycardia (e.g. induced by amiodarone therapy)

    Note: First degree heart block, Mobitz type I second degree heart block (Wenckebach, normal QRS conduction), bifascicular block (RBBB + LAHB) are not indications for preoperative pacing.

    A Special Case: LBBB + pulmonary artery catheter insertion

    There is a low risk (probably around 15%) of transient or not so transient complete heart block in this situation, because of PAC-induced RBBB. The approaches that I have used include:

  • Carefully evaluate the risk-benefit of using a PAC in this case.
  • External (Zoll) pacer attached at start of case (it's important to have it in place before beginning!). This is reasonably reliable but is not tolerated for long by an awake patient.
  • For cardiac anesthesia: Float PAC to 25 cm at start of case. Wait until aortic and venous cannulas are in place before floating PAC into pulmonary artery. Then, if CHB occurs, you can immediately go onto CPB

    I don't think that either a multipurpose PAC (too unreliable) or a Paceport PAC (too slow - you may induce CHB while floating the catheter!) are appropriate, and in my opinion floating a ventricular pacing wire prior to floating the PAC is unnecessary except in rare circumstances.



    We have various thresholds for doing epidurals/spinals in the presence of coagulopathies. For now, I have seen guidelines for Low Molecular Weight Heparins, but what about the values for INR and platelets for which regionals would be consider safe. Bleeding time...I guess that's a thing of the past and I know there's always this caveat of "weighing the risks and benefits". Please advise.   —Jeffrey Kua Seng Wee

    Dr. Lubarsky Responds:
    There are no specific guidelines. Basically, INR's are only useful when a patient is on coumadin. Otherwise we ignore them. Most people consider a PT or PTT ratio less than 1.2 safe (anecdotal evidence). Some people will place blocks outside the epidural area with a ratio up to 1.5. Given the lack of any evidence that regional anesthesia contributes to a better outcome, I personally do not support it and err on the side of much greater caution given the relative safety of general anesthesia for most patients.



    In the event of an inadvertent dural puncture by a Tuohy needle, would the placement of an intrathecal catheter for 24 hours lessen the likelihood of post dural puncture headache?   —Jeffrey Kua Seng Wee

    Dr. Lubarsky Responds:

    No. At least this has never been published to my knowledge.



    Blended anesthesia can be performed using a thoracic epidural catheter. If the catheter is a medium thoracic (T7-8) the cardio-sympathetic system (T1-5) is almost always blocked. As consequence of this, the negative inotropism and vasodilation can blunt arterial pressure; if TIVA is associated, further negative inotropic effects can be added (for example: from propofol use).

    The questions are:

    1) What is the best drug of choice to treat hypotension during TIVA plus epidural anesthesia?

    2) Would you recommend this kind of anesthesia in cardiac patients?   —Alessandro Albani MD

    Dr. Sladen Responds:

    1) Phenylephrine for elderly patients with coronary artery disease or hypotension associated with faster heart rates, ephedrine for hypotension associated with bradycardia.

    There is some evidence (notably from the ASA Closed Claims Study) that patients with a high spinal who develop hypotension or cardiac arrest are relatively resistant to phenylephrine and ephedrine, and respond predictably only to epinephrine. I would therefore have low dose epinephrine (5 mcgs/mL) available in a syringe for bolus doing in such a circumstance.

    2) This has advocates for and against. Those for contend that there is earlier weaning and extubation and better myocardial stress protection. Those against contend that there is always a concern regarding epidural hematoma - even if it is a rare phenomenon - and that patients undergoing sternotomy have considerably less pain, discomfort and respiratory restriction than those undergoing thoracotomy (i.e. epidural anesthesia for sternotomy is not worth the increased complexity or risk). My own bias is toward the latter.



    I was asked about a 30-year-old man who received lacerating wounds on the leg 10 days previously and right then came for debridement. He was well conscious but had locked jaw. He was already given tetanus toxoid and immune globulin. What should be the anesthetic technique of choice?   —Kamthorn Tantivitayatan

    Dr. Sladen Responds:

    I assume the patient is either intubated or has a tracheostomy in place.

    If he is not intubated, avoid succinylcholine - it can induce ventricular arrhythmias through potassium release.

    Tetanus is associated with considerable autonomic dysfunction and a hyperadrenergic state. Therefore I would choose anesthetic agents that are generally sympatholytic or neutral (fentanyl, remifentanil, midazolam, barbiturates, vecuronium, cisatracurium), volatile agents that have a high threshold of ventricular irritability (enflurane, sevoflurane) and be prepared to use beta-blockers such as esmolol and/or metorprolol to deal with tachycardia and hypertension.

    Avoid agents that directly or indirectly increase sympathetic tone or release catecholamines (pancuronium, morphine, ephedrine, desflurane) or volatile agents that may induce ventricular irritability (halothane).



    I have a man aged 74 with a tumor of the pancreas. His liver is damaged (was alcoholic) and biliar stasis is now. The choledochus is obstructed by tumor mass. He has a giant ascites, starting hepatal encephalopathy, contact is bad. His treating doctor wants to do external drainage of the biliar tract in analgosedation. Which drugs I can use safetily in this case?   —M.Svitek, MD

    Dr. Sladen Responds:

    Low dose propofol (5-10 mcgs/kg/min) + local infiltration of local anesthesia by the surgeon.



    What is the current opinion concerning the use of succinylcholine in patients with severe muscle contractures? A reference source would be helpful.   —Aljmel

    Dr. Coté Responds:

    There should not be any increased risk in pediatric patients with contractures due to cerebral palsy. If however the contractures are due to prolonged hospitalization and a patient being chronically bedridden, then there may be a risk for hyperkalemia. Also, if the contractures are due to a denervation injury this also may potentially present a risk. It should be noted that there is always a small rise in serum potassium with succinylcholine, but that this change is not generally clinically important.

    Reference: Dierdork SF, et al: Effect of succinylcholine on plasma potassium in children with cerebral palsy. Anesthesiology 1985;62:88-90.



    Do you have or know of literature for patients on the use of epidural analgesia in cancer pain? I have a patient in whom epidural analgesia would be the treatment of choice, but he would like more patient-friendly info before proceeding.   —BDymock281

    Dr. Watkins Responds:

    I did not have an answer directly, but I contacted a trusted colleague about this matter. James Alpers (MD) (Assistant Professor, Anesthesiology/CCM, Univers. of Pittsburgh Medical Center Health System), a consultant in our department for matters related to regional anesthesia and pain, offered the following advice:"Perhaps the most extensive resource in this regard devoted to the needs of the cancer patient is a book entitled You Don't Have To Suffer written by Richard B. Patt, MD from MD Anderson in Houston. This is a thorough reference, available through book stores, dealing with all modalities of cancer pain treatment strategies including such "high tech" options as epidural implantation. This is a book written by an expert in cancer pain specifically for patients with cancer pain. The table of contents of this accessible over the internet.

    Bard Access Systems publishes a "use and maintenance" brochure to accompany the commercial Du Pen Long-Term Epidural Catheter which is for both patients and physicians. It briefly addresses the reasons for epidural placement, logistics of placement and then care of the implanted catheter. It is not a highly detailed brochure.

    The National Cancer Institute (1-800-4-CANCER), American Cancer Society (800-ACS-2345), Wisconsin Cancer Pain Initiative (608-262-0978) and the American Academy of Pain Medicine (847-375-4731) all publish information for treatment of cancer pain which tend to be more general in nature and, while touching on epidural techniques, do not provide much detail."

    Hopefully, this information will assist you and your patient(s). My thanks to Dr. Alpers for his useful suggestions.



    I am reviewing a case of an epidural hematoma. There was some blood through the catheter which was removed and replaced at another interspace. The case then proceeded. He had several reasons such as a potentially difficult airway which made a regional desirable. I can find some reports of hematomas, but I don't know the per cent of anesthesiologists who would have canceled this case until another day due to the blood and how many would have gone to another space as was done. Can you help me with this? The heparin is usually not given until 1 - 2 hours after epidural placement.   —Debbie McClain, MD

    Dr. Lubarsky Responds:

    You ask a difficult question that has never been fully answered. What we do know is that if you get a bloody tap (defined as frank blood through the needle or catheter) and postpone the case, you will probably not increase the risk of getting an epidural hematoma following surgery the next day. If you proceed on the same day, no one knows how long the delay should be. Obviously, if you are getting frank blood through the catheter, you don't want to give heparin (which prevents clotting) until the bleeding has stopped. Similarly, you do not want to pull a catheter that passes through an epidural space that has had bleeding if the patient is on heparin. Finally, a heightened level of concern is appropriate - eg. neuro checks frequently after surgery to make sure an epidural hematoma doesn't develop, and avoiding local anesthetic in the epidural postoperatively so as not to mask the symptoms of an epidural hematoma.

    In our practice, given the lack of data, we wait a minimum of two hours before giving heparin to those with bloody taps. We might monitor the ACT more closely as well. Postoperatively, we are careful not to remove a catheter unless the heparin has been off for a few hours. From my experience travelling around the country as a visiting professor, I can report that this seems to be a common approach.

    As for benefitting from a regional, while I believe regional is a little better, the data still is not strong enough to make me do a regional if there is any type of potential problem that could otherwise be avoided with a general anesthetic.




    If there is blood return in either the needle or catheter do you continue by going to another interspace or postpone the case until the next day? Heparin is usually given 1 - 2 hours after placement in my hospital.   —Debbie McClain, MD

    Dr. Lubarsky Responds:

    Waiting a minimum of two hours before heparin administration is OUR practide. No hard data exists to suggest that is optimal. It just makes common sense.

    We may or may not go to a different interspace.




    A woman aged 75 suffering from total bowel obstruction was rushed to the OR with the surgeon barely notifying the anesthesiologist on duty. The patient was alcoholic with overt ascites and jaundice and known alcoholic cirrhosis. Also, the patent was anuric. A hepatorenal syndrome was suspected and the relatives were notified that the patient was dying. The question is: can the anesthesiologist say no to the surgeon? The patient died 7 hours later in the recovery room of overt pulmonary edema which was intractable to any therapy   —Perikles Yannakopoulos, Athens, Greece

    Dr. Lubarsky Responds:

    The issue you raise is an important one, and one that often appears on the board exam. The classification of the case is urgent, but not emergent. A true surgical emergency is a condition that:

    (1) will get better with surgery

    and

    (2) where vital signs are deteriorating despite adequate resucsitation.

    An emergency dictates proceeding immediately with the case despite suboptimal preparation. Urgent cases like this run the gamut from having to be done in a few minutes to a few days. Most everyone would agree that a total bowel obstruction that had not ruptured would allow a few hours to optimize the patinet's condition. In this case, if cariopulmonary or renal factors were deemed more of a threat than the bowel obstruction to the patient, some delay would have been merited. Invasivbe monitoring and fluid status optimization and renal perfusion optimization might have been a good idea.

    So, no, you can't say no. But you can dictate a more appropriate time course.




    I experienced a wet tap with an epidural for post thoracotomy analgesia. Five minutes after insertion of catheter at a higher interspace the patient complained of intense headache after sitting up to move to OR table. What should I have done?   —Larry R. Stevner

    Dr. Lubarsky Responds:

    The evidence is contradictory about what to do in this instance. If you give a prophylactic bloodpatch immediately, the success rate is not as great as if you waited 24 hours and did a blood patch, but greater than if you do nothing. However, you end up giving a blood patch in that instance to several people who might not need any invasive procedure (i.e. those whose headache resolves spontaneously). If you decide to give a prophylacitc blood patch, you limit the use of your new catheter as what you inject into it may not spread past the blood patch. If you use the epidural, it has been reported that an exaggerated effect may occur. Not only can CSF leak out, but injected local anesthetic can potentially leak into the CSF. It is not contraindicated to use the catheter, but greater care in dosing, perhaps using smaller increments than usual, would be appropriate.




    I was asked to intubate a patient in the intensive care unit who had failed extubation. He had been admitted to the hospital 3 weeks earlier for resp.failure and was intubated at that time. He was an ivda found to have botulism. It was felt that he would fly after extubation but didn't. I entered the scene with this history. He was breathing very shallow on 100% o2 with an abg showing a pc02 of 90. I intubated him using sux and amidate. After intubation he went into v-tach and eventually v-fib and torsades. I treated this with the usual defib. and drugs including magnesium and I treated him empiracally for hyperkalemia. My question: is there a correlation between sux and botulism cmbo. causing hyperkalemia as there is with burns?   —ZZMD

    Dr. Sladen Responds:

    I was unable to find a reference to an interaction between botulism and succinylcholine or hyperkalemia in a Medline search between 1975 to 1997.

    As far as I am aware, botulin toxin binds irreversibly with the presynaptic neuromuscular junction and cholinergic synapses, where it inhibits acetylcholine release. Thus, although the predominant clinical features include progressive cranial nerve and peripheral paralysis, features of sympathetic predominance also exist, e.g. dry mouth. It is conceivable that in this setting, when a profound respiratory acidosis is rapidly corrected by intubation and ventilation with an abrupt increase in pH, potassium could flux into the cell and precipitate ventricular arrhythmias. It would be helpful to know what his pH was with a PaCO2 of 90! Hope this is helpful.




    Since 4 days I have had some clinical problems with an ARDS patient regarding his Nitrogen balance: energy expenditure 1600 Kcal/day and energy intake 1600 Kcal/ die;pH 7.41, PaO2/FiO2 < 100 mmHg, PaCO2 80-90 mmHg; urine Nitrogen excretion 24 g/day, Nitrogen Intake 12 g/day, Nitrogen concentration in the blood 40 mg/dl, no fever, no sepsis, furosemide infusion (2mg/kg). What is the reason of such a difference between IN and OUT? Could it be caused, at least in part, by an extra-elimination of Nitrogen due to glutamine-urea tubular buffer system? Help! Thank you in advance.   —Massimo Girardis, UNIVERSITA' DEGLI STUDI DI UDINE, Policlinico Universitario a Gestione Diretta.

    Dr. Sladen Responds:

    I am afraid I do not have a ready answer for Dr. Giradis. There are a number of possibilities:

    1. Technical error of measurement - depending on technology of energy expenditure, the estimation of oxygen consumption could be incorrect because of air leaks (tracheostomy, pleural tubes), use of high FiO2 (> 0.6); there could be a technical error of urinary nitrogen estimation. I'm not aware that furosemide infusion promotes proteinuria.

    2. High catabolic rate despite the absence of obvious fever or sepsis - SIRS may exist without fever, ARDS is a highly catabolic process, hypercarbia may promote catabolism even if compensated (cf "pink puffer" with emphysema).

    At this point the patient sounds sick enough from his/her ARDS that I would not recommend increasing caloric intake to try to suppress proteolysis because of the risk of increased CO2 production (although some have advocated combining glucose and insulin to suppress catabolism in trauma). Protein intake could be carefully increased with reassessment of nitrogen balance. Good luck!




    Our group recently had a case where the patient had a Mi folowed by a CABG six weeks prior to presenting to our hospital with complaints of decreased appetite. Her surgeon wanted to performe an egd. The anesthesiologist informed the patient that any stessful procedure may result in a mortality risk of about 35%. The patient and surgeon decided to procede. The procedure was performed with light sedation with out complications. She died three days later from a Mi. Do you think the anesthesiologist should have refused to do this elective case?   —Adlak (adlak@aol.com)

    Dr. Lubarsky Responds:

    Once the CABG is performed, the risk is the same as if the patient did not have CAD or a recent MI. The anesthesiologist probably overstated the risk. That assumes that there was a successful operation and no post CABG angina was occurring. The loss of appetite may have been related to a cardiac cause, so that might have indicated a problem. It is impossible to give a definite answer as to who was right or wrong. It is most unfortunate that the patient did not do well.




    I recently had a patient whose diastolic BP was hovering around 120-130 and who had not taken his anti-hypertensive medications for approximately one week. Despite this, the orthopedic surgeons tried to persuade me to continue on with the procedure for an ORIF of an ITT Fx.

    Their arguments were that this particular patient had Multiple Myeloma with pathologic fx's and that his BP in ward was near normal levels. I gave this patient Versed & Fentanyl and despite this his blood pressure never lowered to acceptable levels. I postponed the case until adequate control of his BP. A polemic has ensued.  —Dr. Jose Santos

    Dr. Lubarsky Responds:

    The data demonstrating increased cardiopulmonary morbidity (Death. MI, CHF, V Tach) dates from a 1973 Prys-Roberts study in England. At that time no good IV agents were available to acutely control BP. Therefore, that data may not be applicable in toady's population. However, if postoperatively this patient were placed on the ward rather than the ICU, the data may indeed be directly extrapolatable to your patient.

    There are no studies that say it is safe to proceed with a diasotlic BP > 110, and medico-legally, delaying this elective case for appropriate BP control is the most prudent course of action. Markedly increased BP lability is expected under anesthesia with pre-existing uncontrolled hypertension, as is an increased incidence of preioperative myocardial ischemia. If the patient is prone to intracranial, renal, or cardiac problems, it is not only medico-legally but clinically imperative to delay the case with that level of BP.

    As to "normal" ward pressures, they may not have been measured accurately. I cannot count how may times I have seen 130/80 when the BP was nowhere near that figure. If sedation did not control your patient's BP, then it is likely that your elevated pressures were correct and representative of the patient's real BP.




    We have been having an increasing number of patients coming to our outpatient surgicenter stating they have latex allergy either the night before surgery when we call them or the day of surgery if we can't get a hold of them. Some describe what sounds like a contact dermatitis and others describe a questionable allergic reaction. I recently had a patient tell me when she blows up balloons, her mouth and face swell. What is your approach to this problem. Would you postpone surgery and have them skin tested (I know that the results are questionable).  —Dr. JL Topkis

    Dr. Philip Responds:

    If patients think that they may be allergic to latex, it is always safer to treat them as though they were allergic. Skin testing immediately pre-op is not neccessary, although you may recommend that the patient obtain testing after the procedure, to answer the question.

    It may be helpful if your facility has a planned protocol for the care of latex allergic patients, which includes pre-op and intra-op preventive measures, and what to do if the allergic reaction occurs. Some factilites keep this protocols and all the neccessary latex-free equipment together in a "latex allergy box".

    Read Dr. Karl's commentary on latex allergy

    Read Dr. Cote's analysis of an article on Latex-allergic children.




    A surgeon I work with asked if I knew of any research on anesthesia and its effect on dreams. I cannot find any references. Do you know of any research in this area?   —Teresa Gardner, CRNA

    Dr. Philip Responds:

    I do not know of research on dreams, but it is generally believed that the "dreams" patients report are while losing consciousness or awakening, and not at anesthetic depth. Anesthesia is not "sleep", but a chemically-depressed mental state.

    Dr. Lubarsky Adds:

    There are some associations of propofol and sexual dreams (but either under sedation or immediately postop). I'm not sure if that effect lasts more than a few hours.


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