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re. Fatal thyrotoxic cardiomyopathy in a young man
- Adam P Morton (20 February 2009)
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This death might have been avoided had metabolic meme complexes guided management.
- Richard G Fiddian-Green (21 February 2009)
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Beta-blockers and decompensated heart failure: never the twain shall meet.
- Jonathan R Dalzell (21 February 2009)
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Fatal thyrotoxic cardiomyopathy in a young man - the authors' response
- Michael Croxson, May Ching Soh (23 March 2009)
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Intravenous beta-blockade in the pulmonary oedema of thyroid storm
- Michael J Daly, David R. McCance (7 May 2009)
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Re: Intravenous beta-blockade in the pulmonary oedema of thyroid storm
- Michael S Croxson, Soh, May Ching (26 May 2009)
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Adam P Morton, Endocrinologist Mater Hospital, Raymond Tce, South Brisbane, Australia 4101
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I wish to thank Drs Soh and Croxson for their informative and fascinating lesson on fatal thyrotoxic cardiomyopathy in a young man. I would be interested to know if the right ventricular systolic pressure was able to be measured on echocardiogram. The young man had significant signs of right heart failure with ascites and abnormal liver function tests. Pulmonary arterial hypertension has been reported in 44-65 % patients presenting with hyperthyroidism, and beta-blockers have a deleterious effect on haemodynamics in the setting of pulmonary hypertension. This may account for his sudden deterioration following the second dose of intravenous propranolol. I would also be interested in the ethnicity of the young man. Thyrotoxic periodic paralysis is most commonly reported in young Asian men. A study in New Zealand also reported a 37 fold overrepresentation for Polynesian (Maori and Pacific Islander) ethnicity compared with New Zealand Europeans for thyrotoxic periodic paralysis. It would be interesting to know if Asian and Polynesian ethnic groups were also more at risk of developing cardiac muscle weakness with thyrotoxicosis. I have seen a case in a Maori patient with biventricular failure, pulmonary hypertension and atrial fibrillation in the setting of thyrotoxicosis due to Grave's disease. Atrial fibrillation, pulmonary hypertension and left ventricular dysfunction all resolved rapidly with gaining of the euthyroid state. Competing interests: None declared |
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Richard G Fiddian-Green, FRCS, FACS None
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This case is an excellent example of the perils imposed by haemodynamic meme complexes and the potential benefits of replacing them with metabolic meme complexes(1). This case also draws attention to an urgent need for a moratorium on the use of beta blockers (2). This young man had multiple organ dysfunction. He almost certainly had a systemic tissue acidosis caused by an impairment of ATP resynthesis due to excessive uncoupling by the abnormal exposure to circulating thyroid hormones. In the myocardium the K+atp channels would have been opened setting the stage for arrhythmias. Moreover a fall in intramycardial pH as little as 0.1 is said to be sufficient to reduce myocardial contractility by 50%. A fall in pH also inhibits phosphofructokinase and shifts substrate utilization by mitochondria from glucose to fatty acids. This should reduce myocardial workload if, as previously proposed, the added yield of ATP/mole fatty acids utilized decreases the need for blood flow relative to that with glucose. Given this scenario this young man was metabolically primed to the nth degree to protect his myocardium. By giving propranalol the ability to utilize fatty acids for oxidative phosphorylation was suddenly inhibited. The net effect might, therefore, have been an acute increase myocardial workload that precipitated his demise. Placing him on a ventilator might have helped by reducing ATP utilization. Giving him an inotrope would have subverted his heart's efforts to accommodate the impaired efficiency of ATP resynthesis by increasing his myocardial workload. A more rational appoach might have been to give cylosporin, which reduces mitochondrial permeability, in addition to the efforts made to treat his thyrotoxicosis. I know of no case in which this has been done. Giving magnesium to counter the effects of the rise in [Ca++] likely to have accompanied a tissue acidosis might possibly have been of additional benefit but I know of no clinical evidence to support the suggestion. Switching from haemodynamic to metabolic meme complexes goes against the grain for the clinical decisions being made are likely to be so very different. I believe it is a necessity if we are to make major inroads into the management of the acutely ill many of whom continue to die unpredictively and unexpectedly. Had metabolic meme complexes guided management in this case beta blockers would never have been given, certainly not without appropriate metabolic monitoring. 1. Defining existing medical memes, meme complexes, eradicating mutations and evolving new ones. Richard G Fiddian-Green (29 October 2004) eLetter re: John Gabbay and Andrée le May Evidence based guidelines or collectively constructed "mindlines?" Ethnographic study of knowledge management in primary care BMJ 2004; 329: 1013 The need for a moratorium on use of beta blockers? Richard G Fiddian-Green (7 September 2004) eLetter re: P.J. Devereaux, Salim Yusuf, Homer Yang, Peter T.-L. Choi, and Gordon H. Guyatt Are the recommendations to use perioperative ß-blocker therapy in patients undergoing noncardiac surgery based on reliable evidence? CMAJ 2004; 171: 245-247. Competing interests: None declared |
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Jonathan R Dalzell, Clinical Research Fellow in Cardiology Department of Cardiology, Western Infirmary, Glasgow, G11 6NT, UK
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Soh and Croxon report a fatality following multiple intra-venous doses of beta-blockade in a hyperthyroid patient presenting with overt decompensated heart failure, pneumonia and fast atrial fibrillation[1]. The subsequent lesson is that beta-blockers may precipitate circulatory collapse in thyrotoxic patients with low output heart failure. This lesson should be extended to state that there is no role for beta-blockade (especially intra-venous) in acute heart failure no matter what the underlying cause. The American College of Cardiology/American Heart Association guidelines referenced by the authors as evidence for the established role of beta- blockers in controlling arrhythmias in HF are guidelines for patients with chronic stable heart failure[2]. Oral beta-blockade is known to improve survival in patients with chronic stable heart failure[3,4] but beta- blockade is to be avoided in decompensated patients[5]. As pointed out by the authors, left ventricular systolic dysfunction associated with thyrotoxic cardiomyopathy frequently improves when the patient becomes euthyroid making appropriate management of these patients all the more important. Early involvement of all appropriate specialties is to be encouraged in such complex cases. References 1. Soh MC, Croxson M. Fatal thyrotoxic cardiomyopathy in a young man. BMJ. 2008 Nov 28;337:a531. 2. Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG et al. American College of Cardiology; American Heart Association Task Force on Practice Guidelines; American College of Chest Physicians; International Society for Heart and Lung Transplantation; Heart Rhythm Society.ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation. 2005;112(12):e154-235. 3. The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial. Lancet. 1999;353(9146):9-13. 4. Hjalmarson A, Goldstein S, Fagerberg B, Wedel H, Waagstein F, Kjekshus J et al. Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group. JAMA. 2000;283(10):1295- 302. 5. Task Force for Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of European Society of Cardiology, Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ, Ponikowski P, Poole-Wilson PA, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur Heart J. 2008;29(19):2388-442.3. Competing interests: None declared |
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Michael Croxson, Endocrinologist Thyroid Clinic, Greenlane Clinical Centre, PO Box 92-189, Auckland, New Zealand, May Ching Soh
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We thank respondents and emphasise that this was case of a young man who had presented with acute systolic heart failure and hypotension to an emergency department who rapidly decompensated further after use of a beta -blocker and died shortly afterwards. In reply to Dr Morton, pulmonary arterial pressures were not measured or not recorded during the rapid echocardiogram. His ethnicity remains confidential. In contrast to the ethnic association with periodic paralysis, we are not aware of any similar ethnic association with thyrotoxic cardiomyopathy. Dr. Dalzell pinpoints the crux of the lesson: beta-blockers are contraindicated in acute unstable heart failure whatever the cause, especially in the presence of hypotension. In addition to the useful reference he cites from the European Society of Cardiology, the management of heart failure has been reviewed in a recent Lancet seminar(1). Ventilation, inotropes such as dopamine or dobutamine, digoxin, loop diuretics, and possibly an assisted device in a coordinated intensive care unit may have led to a better outcome in this case. Reference 1 Krum H, Abraham, WT. Heart failure. Lancet 2009: 373: 941-55 Competing interests: None declared |
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Michael J Daly, Cardiology Research Fellow Royal Victoria Hospital, Belfast, UK BT12 6BA, David R. McCance
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We read Drs Soh and Croxon's 'Lesson of the Week' (1) with great interest, having recently described a similar case of non-fatal dilated cardiomyopathy complicated by acute pulmonary oedema and ventricular fibrillation associated with thyrotoxic storm (2). The diagnostic criteria for thyrotoxic storm are well described in the literature (3). In the case of this young man, the absence of both thermoregulatory dysfunction and central nervous system effects does not exclude the diagnosis. Indeed, the presence of abdominal pain, hyperbilirubinaemia, atrial fibrillation with a ventricular rate greater than 140bpm and severe pulmonary oedema give this case a cumulative score of 70, with a score greater than 45 being highly suggestive of thyroid storm. The medical management of thyroid storm consists of an array of medications administered early that act to halt the synthesis, release and peripheral effects of thyroid hormone. Generally this would include larger doses of antithyroid drugs than described by the authors and early recourse to diuretics. Beta-blockade is essential in controlling the peripheral actions of thyroid hormone, with propranolol having a well established role in both reducing peripheral T4 to T3 conversion and beta- adrenergic receptor antagonism. The use of intravenous propranolol has been shown to result in a significant decrease in both cardiac output and stroke volume with the administration of a second 1mg bolus (4) as in this case; other reports of cardiovascular collapse after the administration of oral propranolol in the context of thyroid storm have also been described (5). As a consequence, beta-blockade is not surprisingly contraindicated in acute decompensated heart failure (6), however because the use of beta- adrenergic receptor antagonists can be beneficial in the treatment of thyrotoxicosis, careful individual consideration is required. If the cause of the heart failure is felt likely to be due to the underlying tachycardia, beta-blockade may be particularly useful. However, in situations similar to this case, in which the cause of the left ventricular dysfunction was uncertain, and when severe pulmonary oedema ensues, short-acting beta-blockade, e.g. intravenous esmolol 50-100 mcg/kg/min is worthy of consideration, administered under close haemodynamic monitoring (7). 1. Soh MC, Croxon M. Fatal thyrotoxic cardiomyopathy in a young man BMJ 2008;337:a531 2. Daly MJ, Wilson CM, Dolan SJ, Kennedy A, McCance DR. Reversible dilated cardiomyopathy associated with post-partum thyrotoxic storm. Q J Med 2009;102:217-9 3. Burch HB, Wartofsky L. Life threatening thyrotoxicosis - Thyroid Storm. Endocrinol Metab Clin North Am 1993;22(2):263-77 4. Letac B, Letournel J. Evaluation of haemodynamic effects of intravenous propranolol at low dosage (1 and 2mg) in acute myocardial infarction. British Heart Journal 1975;37:624-628 5. Dalan R, Leow MK. Cardiovascular collapse associated with beta blockade in thyroid storm. Exp Clin Endocrinol Diabetes 2007;115(6):392-6 6. Krum H, Abraham WT. Heart Failure. Lancet 2009;373:941-55 7. Nayak B, Burman K. Thyrotoxicosis and Thyroid Storm. Endocrinol Metab Clin N Am 2006;35:663-686 Competing interests: None declared |
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Michael S Croxson, Endocrinologist Greenlane Clinical Centre, Auckland, New Zealand, Soh, May Ching
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We are not sure why Daly et al wish to describe the present case or their own as examples of ‘thyroid storm’. The diagnostic criteria suggested by Burch and Wartofsky (1) and reprised by Ross (2) were based on 61 published cases of thyroid storm and therefore had a sensitivity approaching 100%. The specificity and utility of the index remain untested. We suspect that the specificity of the index may be nearer 50% and therefore a doubtful guide to diagnosis and management. We prefer to keep the epithet for the combination of severe hyperthyroidism with fever, tachycardia and confusion without an alternative explanation. The term is also used to describe the hypermetabolic state associated with fever and tachycardia in hyperthyroid patients during anaesthesia. Whatever the semantics the practical treatment issues are the same in any given case of severe hyperthyroidism (3). In our patient with severe hyperthyroidism, pneumonia and decompensated low output heart failure, beta-blockers including the short- acting esmolol are better avoided for reasons already outlined both in the paper and subsequent online discussion. We agree with the recommendation to use a cocktail of antithyroid drug treatment to lower the circulating hormones as quickly as possible, as initially described (4). References 1 Burch HB, and Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin N America 1993; 22 (2): 263-77. 2 Ross DS. Thyroid storm. In: UpToDate, Basow, DS. (Ed) 2009; UpToDate, Waltham, MA 3 Davies TF, and Larsen PR. Thyroid storm. In Chapter 11. Thyrotoxicosis. Williams Textbook of Endocrinology. Ed Kronenberg HM, Melmed S, Polonsky KS, Larsen PR. (Saunders), 11th Edition. 2009, 357-8. 4 Croxson MS, Hall TD, Nicoloff JT. Combination drug therapy for treatment of hyperthyroid Graves’ disease. Journal of Clinical Endocrinology & Metabolism 1977; 45 (4): 623-30 Competing interests: None declared |
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