Article, Cardiology

The authors respond: methadone overdose

The interventricular septum has a double supply, by septal perforator branches of the LAD and by the right conal artery, which most frequently originates from the RCA or, in 36% of cases, has an independent origin from the right coronary sinus [15]. In addition, the right conal artery often communicates with the left conal artery from the LAD, forming the Vieussens arterial ring [15].

For these reasons, transmural ischemia of the basal part of the septum and ST-segment elevation in Lead aVR can be sporadically absent although the LMCA is totally obstructed. According to literature data, these conditions are usually asso- ciated with the presence of well-developed collateral circula- tion from the RCA or directly from the right conal artery [3,4]. In support of these anatomical-clinical observations, we present interesting ECGs of a 53-year-old white man with acute anterolateral myocardial infarction, complicated by cardiogenic shock and pulmonary edema, due to acute isolated LMCA occlusion (Fig. 1A and B). Twelve-lead ECG recorded on admission (Fig. 2A) revealed a regular, accelerated junctional rhythm of 67 beats per minute, left axis deviation, and ST-segment elevation (Pardee wave) in leads I, aVL, and V1 through V6, with reciprocal ST-segment depression in leads II, III, and aVF. However, no ST-segment changes in lead aVR were present. Immediately after LMCA stenting, the ECG showed sinus tachycardia of 116 beats per minute; Right axis deviation; pathologic Q waves in leads I and aVL, with concomitant persistent ST-segment elevation and Negative T waves in these leads; and ST-segment

depression in inferior leads (Fig. 2B).

Importantly, in this case, collateral circulation to the LAD was not observed, but the well-developed right conal artery was present (Fig. 1B).

On the basis of literature review and our own experience, we conclude that ST-segment elevation in lead aVR is a reliable predictor of acute occlusion of the LMCA in ACS.

Pawel Rostoff MD Wieslawa Piwowarska MD, PhD Andrzej Gackowski MD, PhD Ewa Konduracka MD, PhD Nader El Massri MD, PhD

Pawel Latacz MD Department of Coronary Disease, Institute of Cardiology Jagiellonian University Medical College

John Paul II Hospital, 31-202 Krakow, Poland E-mail addresses: [email protected] [email protected]

Tomasz Pawelec MD Krzysztof Zmudka MD, PhD

Department of Hemodynamics and Angiocardiography

Institute of Cardiology Jagiellonian University Medical College

John Paul II Hospital, 31-202 Krakow, Poland

doi:10.1016/j.ajem.2007.01.025

References

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  2. Shahian DM, Butterly JR, Malacoff RF. Total obstruction of the left main coronary artery. Ann Thorac Surg 1988;46:317 – 20.
  3. Yip HK, Wu CJ, Chen MC, et al. Effect of primary angioplasty on total or subtotal Left main occlusion. Analysis of incidence, clinical features, outcomes, and prognostic determinants. Chest 2001;120:1212 – 7.
  4. Yamaji H, Iwasaki K, Kusachi S, et al. Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography: ST segment elevation in lead aVR with less ST segment elevation in lead V1. J Am Coll Cardiol 2001;38:1348 – 54.
  5. Kurisu S, Inoue I, Kawagoe T, et al. Electrocardiographic features in patients with acute myocardial infarction associated with left main coronary artery occlusion. Heart 2004;90:1059 – 60.
  6. Hirano T, Tsuchiya K, Nishigaki K, et al. Clinical features of emergency electrocardiography in patients with acute myocardial infarction caused by left main trunk obstruction. Circ J 2006;70:525 – 9.
  7. Rostoff P, Piwowarska W, Konduracka E, et al. Value of lead aVR in the detection of significant left main coronary artery stenosis in acute coronary syndrome. Kardiol Pol 2005;62:128 – 31.
  8. Rostoff P, Piwowarska W. ST segment elevation in lead aVR and coronary artery lesions in patients with acute coronary syndrome. Kardiol Pol 2006;64:8 – 14.
  9. Engelen DJ, Gorgels AP, Cheriex EC, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 1999;34:389 – 95.
  10. Gorgels AP, Engelen DJ, Wellens HJ. Lead aVR, a mostly ignored but very valuable lead in clinical electrocardiography. J Am Coll Cardiol 2001;38:1355 – 6.
  11. Makaryus AN. Global electrocardiographic changes accompanying acute presentation of 3-vessel coronary disease. Am J Emerg Med 2006;24:355 – 6.
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[accessed January 21, 2007].

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The authors respond: methadone overdose

One of the greatest satisfactions of research is having other colleagues comment on your work. Research almost always leads to more questions, more research, and occasionally a step backward that is associated with controversy. Questioning dogma of routine practice almost always leads to the latter.

In reviewing the comments about our article, we agree that many shortcomings were present in this study as well as in almost all studies [1]. We further agree that some clarification is needed.

We understand there is a curiosity in knowing if a supra- therapeutic ingestion is bintentional,Q baccidental,Q or bsuicidal.Q However, in toxicology patients these designa- tions are frequently misrepresented by the patient, and the patient’s intent should never alter management. The authors rarely find these categories helpful in clinical practice. On the other hand, we agree that ingested dose is

an important fact that was only briefly discussed in the article. However, these were reported doses in a retrospec- tive study that are known to be unreliable. The exact dose is less important than knowing a supratherapeutic ingestion occurred. Again, the authors rarely find the precise dose (as reported by the patient) helpful because of the reliability of the history.

When patients ingested methadone in an acute overdose, if they developed symptoms, they did so within 9 hours of ingestion. We had recommendations of observing patients for as long as 24 to 36 hours after methadone overdoses. All of our patients were observed for at least 24 hours. Most patients (32/44, 72%) developed symptoms early, namely, within 3.2 hours. One patient developed symptoms (lethargy) 8.2 hours after ingestion. The latter has lead to our statement of bAcute isolated methadone toxicity typically results in symptom presentation within 9 hours of ingestion.Q

We are not attempting to change the standard of care but only to question it. The goal of our article is to question the dogma of watching all methadone patients for up to 72 hours as some sources have recommended [2,3]. There is a scarcity of literature regarding acute methadone ingestions. We agree that a negative study (no deaths) in 44 patents is not enough evidence to say there will bneverQ be a death. We treat many of these patients and other overdose patients in our inpatient service and would never accept a Death rate of b0% to 9%Q or consider this binsignificant.Q Further study needs to be done in this field and many others.

Frank LoVecchio DO, MPH Banner Poison Control Center Maricopa Medical Center Phoenix, AZ, USA

Anthony F. Pizon MD University of Pittsburgh School of Medicine Division of Medical Toxicology

Pittsburgh, PA, USA E-mail address: [email protected]

Bradley Riley MD Helen DeVos Children’s Hospital Regional Poison Center

Grand Rapids, MI, USA

doi:10.1016/j.ajem.2007.06.004

References

  1. LoVecchio F, Pizon A, Riley B, et al. Onset of symptoms after methadone overdose. Am J Emerg Med 2007;25(1):57 – 9.
  2. Wolff K. Characterization of methadone overdose: clinical con- siderations and the scientific evidence. Ther Drug Monit 2002;24(4): 457 – 70.
  3. Marx JA, Hockberger RS, Walls RM, et al, editors. Hanster CE, Chapter 160, in Opioids. 6th ed. Philadelphia7 Mosby; 2006.

Letter to the editor

To the Editor,

We read the article by Dr Nouira et al titled bA Clinical score predicting the Need for hospitalization in scorpion envenomationQ in the May 2007 issue with great interest. However, we would like to remind readers that the clinical score developed for the Androctonus australis Hector scorpion found in Northern Africa is not applicable to North American scorpion envenomations.

The most commonly encountered venomous scorpion in North America is the Centuroides exilicauda or bark scorpion located in southwest United States and northern Mexico. Symptoms are most pronounced in infants, young children, and the elderly. The neurotoxic effects of this scorpion envenomation range from Local pain and paresthe- sia to the sting area to systemic symptoms including skeletal muscle jerking, Blurred vision, wandering eye movements, hypersalivation, tongue fasciculation, and upper airway dysfunction [1,2]. infants and children are at particular risk due to airway compromise secondary to the inability to control oral secretions and airway dysfunction. In most children, symptoms develop typically within 14 minutes. If the victim is not being treated with antivenom, symptoms may last up to 24 hours. In fact, if patients are asymptomatic beyond 140 minutes, they will not develop clinically relevant symptoms [3]. In Dr Nouira’s study, priapism was seen in 82.6% of his patients. This has not been observed in Centuroides scorpion envenomations.

Dan Quan DO Frank LoVecchio DO

Banner Good Samaritan Medical Center Department of Medical Toxicology

Phoenix, AZ, USA E-mail address: [email protected]

doi:10.1016/j.ajem.2007.06.005

References

  1. Curry SC, Vance MV, Ryan PJ, et al. Envenomation by the scorpion

Centruroides sculpturartus. J Toxicol Clin Toxicol 1983;21:417 – 49.

  1. Gateau T, Bloom M, Clark R. Response to specific Centruroides sculpturatus antivenom in 151 cases of scorpion stings. J Toxicol Clin Toxicol 1994;32(2):165 – 71.
  2. LoVecchio F, McBride C. Scorpion envenomations in young children in central Arizona. J Toxicol Clin Toxicol 2003;41(7):937 – 40.

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