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.

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.

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.

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.

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.

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.

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.

Dr. Katherine Grichnik responds:

Dr. David Lubarsky responds:

Dr. Katherine Grichnik responds:

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.
    
    

Dr. Katherine Grichnik responds:

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
    
    

Dr. Beverly Philip responds:

Dr. David Lubarsky responds:

Dr. Douglas Coursin responds:

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.

Dr. Katherine Grichnik responds:

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
   
Click here for abstract
3. 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
   
Click here for abstract

Dr. Francine D’Ercole responds:

• 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.

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.

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

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.

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

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.

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.

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.

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.

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.

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.

—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.

Dr. David Lubarsky responds:

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.

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
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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
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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
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12. Rosenfeldt, et al. Pharmacology of coronary artery bypass grafts. Annals of Thoracic Surgery. 1999;67:878-88
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13. Mills NL, Everson CT Current Opinion in Cardiology. 1995:10:562-8

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.

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.

• anesthesia and acute alcoholism
  
  
• anesthesia and chronic alcoholism

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
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