An 85-year-old female with a history of diabetes was hospitalized for dizziness. She was bradycardic; otherwise, her vital signs were normal. An ECG (Fig. 1) was recorded by a Schiller system, an electrocardiograph commonly used in Europe. The interpretation software indicated a heart rate of 71/min, twice the true heart rate of 35/min. Computer diagnosis was atrial fibrillation, ventricular premature complexes, and bigeminy. The true rhythm, however, was a slightly irregular junctional bradycardia. On laboratory testing, the patient’s serum potassium level was found to be 9.2 mmol/L. After correcting the drug-induced hyperkalemia elicited by the coadministration of an angiotensin-converting enzyme- inhibitor and a potassium-sparing diuretic, the patient became asymptomatic, and the ECG returned to normal.

Our case supports the findings by Littmann et al that double counting of heart rate by ECG interpretation software may be a sign of Severe hyperkalemia. Moreover, it also proves that this ECG sign is not specific to the GE-Marquette electrocardiographs and interpretation softwares. In our case with the Schiller system and in several of Dr Littmann’s cases with the GE-Marquette system, the interpretation software mistakenly read the tall and peaked T waves as ventricular bigeminy. Clinicians treating critically ill patients need to be educated that whenever the ECG interpretation software double counts the heart rate and falsely diagnoses bigeminy, severe hyperkalemia should be suspected.

Janos Tomcsanyi PhD Vince Wagner MD Bela Bozsik MD

Department of Cardiology Hospitaller Brothers of St John of God, Budapest 1023 Arpad fejedelem u.7, Hungary

E-mail address: [email protected] doi:10.1016/j.ajem.2007.06.009

Reference

[1] Littmann L, Brearley WD, Taylor L, Monroe MH. Double counting of heart rate by interpretation software: a new electrocardiographic sign of severe hyperkalemia. Am J Emerg Med 2007;25:584-90.

Hypothermia for out-of-hospital cardiac arrest survivors: a single-center experience

To the Editor,

Out of hospital cardiac arrest (OHCA) patients have a poor prognosis, with only 10% of patients surviving. Recent randomized trials have shown that moderate therapeutic hypothermia improves neurologic outcome and survival in selected patients after cardiac arrest [1,2]. Therapeutic

hypothermia is now recommended by the Advanced Life Support Task Force of the International Liaisons Committee on Resuscitation and incorporated in the American and European Resuscitation guidelines as part of post resuscita- tion care [3].

We undertook this study to investigate the mortality and neurologic outcome of mild therapeutic hypothermia in surviving OHCA patients in a single university hospital in the southern part of the Netherlands with a catchments area of approximately 200 000 inhabitants, with a yearly incidence of sudden cardiac arrest of approximately 10 per 10000 inhabitants [4].

Medical charts of 101 consecutive OHCA patients admitted alive to our intensive coronary care unit were retrospectively analyzed. Forty-three patients receiving hypothermic treatment in 2004 and 2005 (hypothermia group) were compared to 58 historical control patients from 2001 to 2003 not treated with hypothermia (normothermia group). Data on cardiac arrest were recorded and analyzed according to the “Utstein style” recommended guidelines [5]. Differences between groups were analyzed using ?2, Mann- Whitney U, or Students t test. Our hypothermia protocol is primarily based upon the inclusion and exclusion criteria from 2 recent randomized controlled clinical trials; how- ever, the actual decision of initiation and duration of Mild hypothermia was left to the discretion of the treat- ing cardiologist [1,2]. All patients received current Standard care including percutaneous coronary intervention; were mechanically ventilated; and received intravenous midazo- lam and piritramide for sedation and analgesia, respectively, and intravenous pancuronium to prevent shivering. Mild hypothermia was initiated as soon as possible after admission and was induced and maintained at a target temperature of 33?C using a closed-loop endovascular system (Alsius CoolGard, Irvine, Calif). Patients were allowed to passively rewarm. The mean arterial pressure was maintained at z90 mmHg with inotropic support when necessary. The institu- tion’s ethics committee approved the study. Neurologic death was regarded when patients had absent somatosensory evoked potentials after 72 hours and died after active care was withdrawn. Cardiac death was regarded as death due to persistent cardiogenic shock despite (non)invasive measures. Discharged survivors or one of their relatives were contacted by telephone at least 6 months after discharge, and neurologic outcome was evaluated using predefined questionnaires (Glasgow Outcome Score [GOS] [6]). unfavorable outcome was defined as death, severe disability, or vegetative state (GOS 1-3). Discharge to home or a rehabilitation facility with GOS z4 was defined as Favorable neurologic outcome.

Baseline characteristics were comparable between both

groups; however, patients in the normothermia group tended to be older, were more likely to have bystander cardiopul- monary resuscitation (CPR), and had shorter arrival of paramedics and return of spontaneous circulation (ROSC) times (Table 1). Hypothermia was initiated at a median of 4 hours (1.8-6.4 hours) after ROSC. The target temperature

Hypothermia (n = 43)		Normothermia (n = 58)	P
Baseline characteristics
Age (y)
Mean +- SD	56.2 (12.8)	63 (10.9)	.12
Female sex (%)	14 (33)	18 (31)	.87
Initial rhythm
VT/VF (%)	37 (86)	54 (93)	.24
Asystole (%)	3 (7)	4 (7)
PEA (%)	3 (7)	0
Bystander-performed CPR	22 (51)	42 (72)	.05
(%)
Time collapse-arrival of	10 (2-25)	8 (1-30)	.6
paramedics (min)
(median [range])
Time to ROSC (min)	27 (11-75)	22 (8-60)	.50
(median, [range])
Outcome
Unfavorable outcome (%)	22 (51)	28 (48)	.56
GOS (%)
1	22 (51)	27 (47)
2	0	0
3	0	1
4	11	12
5	9	17
Lost to follow-up	1	1
PEA indicates pulseless electrical activity; GOS 1, dead; GOS 2, vege- tative state; GOS 3, severe disability; GOS 4, moderate disability; GOS 5, good recovery; VT/VF, ventricular tachycardia and ventricular fibrillation.

was reached in all patients at a median of 3 hours (0.1- 7 hours) and was maintained for 16.2 +- 6.3 hours. Two patients were lost to follow-up.

Table 1 Baseline characteristics and outcome

Twenty-two (51%) of 43 patients treated with hypothermia vs 28 (48%) of 58 normothermic patients had an unfavorable outcome. Mortality was 51% in the hypothermia group vs 47% in the normothermia group. The cause of death was not significantly different between both groups with all deaths occurring in hospital. Uncomplicated hyperglycemia, which was controllable with insulin, and the need for inotropic support were significantly more prevalent in the hypothermia group. Only 9 (21%) of 43 hypothermic patients completely fulfilled our protocol criteria. These patients were compared with 8 (14%) of 58 patients from the normothermia group who would have been eligible for hypothermia when available at that time. Again, no significant difference in mortality was found (66.7% vs. 62.5%).

Thus, we were unable to demonstrate a significant benefit of moderate hypothermia for OHCA patients in our hospital. Physicians should all be aware that the available evidence is based on randomized clinical trials with strict inclusion and exclusion criteria, excluding approximately 92% of patients initially screened. In addition, the variation in survival rates among communities can be attributed to

differences in the Chain of survival concept. Relatively high bystander CPR rates have previously been reported in the Netherlands and may make it more difficult to demonstrate additional improvement in outcome after mild hypothermia [7]. Our protocol was frequently violated, and patients were cooled more liberally but, on the other hand, more closely followed the recommended International Liaisons Committee on Resuscitation guideline indications [3]. Our study partly demonstrates the difficulty in generalizing randomized trial results to everyday practice. Further research is therefore needed, and prospective randomized trials should be done to determine the broadest application of moderate therapeutic hypothermia.

Sebastiaan C.A.M. Bekkers MD Bob J.W. Eikemans MD Robert Tieleman MD, PhD Simon H.J.G. Braat MD, PhD

Willem Dassen PhD

Jean Partouns Chris de Zwaan MD, PhD Harry J.G.M. Crijns MD, PhD Department of Cardiology University Hospital Maastricht

P.O.Box 5800, 6202 AZ Maastricht

The Netherlands E-mail address: [email protected]

Marc C.T.F.M de Krom MD, PhD Department of Neurology University Hospital Maastricht

P.O. Box 5800, 6202 AZ Maastricht, The Netherlands

doi:10.1016/j.ajem.2007.06.008

References

1. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557-63.
2. The Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549-56.
3. Nolan JP, Morley PT, Hoek TL, et al. Therapeutic hypothermia after cardiac arrest. An advisory statement by the Advancement Life support Task Force of the International Liaison committee on Resuscitation. Resuscitation 2003;57:231-5.
4. de Vreede-Swagemakers JJ, Gorgels AP, Dubois-Arbouw WI, et al. Out-of-hospital cardiac arrest in the 1990’s: a population-based study in the Maastricht area on incidence, characteristics and survival. J Am Coll Cardiol 1997;30:1500-5.
5. Cummins RO, Chamberlain DA, Abramson NS, et al. Recommended guidelines for uniform reporting of data from out-of-hospital cardiac arrest: the Utstein Style. A statement for health professionals from a task force of the American Heart Association, the European Resuscitation Council, the Heart and Stroke Foundation of Canada, and the Australian Resuscitation Council. Circulation 1991;84:960-75.
6. Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet 1975;1:480-4.
7. Waalewijn RA, de Vos R, Koster RW. Out-of-hospital cardiac arrests in Amsterdam and its surrounding areas: results from the Amsterdam resuscitation study (ARREST) in “Utstein” style. Resuscitation 1998;38:157-67.

shaken baby syndrome vs inflicted brain injury

To the Editor,

I read with interest the article by Healey and Schrading [1], describing an alleged case of shaken baby syndrome (SBS) with unilateral Retinal hemorrhages and no associated Intracranial Hemorrhage . It is applaudable that the authors were alerted to the potential that the child was likely the victim of abuse. The authors’ conclusion that the child was a victim of SBS however is not supported by their findings and must be viewed cautiously. Although the issue I raise may be viewed as semantic, it is crucial that physicians be careful not to make assertions that cannot withstand scrutiny.

The term SBS is often erroneously used synonymously for inflicted traumatic brain injury (ITBI) in infants. One must remember however that shaking is only one of many mechanisms of injury that can lead to brain injury and retinal hemorrhages.

Although I agree that the reported case likely constitutes a case of ITBI, it is not necessarily a case of SBS. The authors seem to have fallen victim to the use of the term SBS as a synonym for child abuse in their efforts to convey that unilateral retinal hemorrhages may point to a diagnosis of SBS even in the absence of ICH. I find it important to point out that the simple presence of retinal hemorrhages in an infant with evidence of brain injury does not automatically imply a diagnosis of SBS, as seems to be suggested by the authors. The determination of the cause of injury should be based on a more thorough investigation including skeletal survey, nuclear bone scintigraphy, elimination of differential diagnostic possibilities, and interprofessional collaboration.

A number of features go against shaking alone as a mechanism of injury in the reported case. The presence of bruising on the head of the child represents definitive

evidence of an impact to the head, a feature not seen in shaking alone. The retinal hemorrhages, although concern- ing, are not sufficiently described to allow their attribution solely to shaking, stressing the need to consider other causes, such as an impact to the head, in the differential diagnosis. In addition, although the absence of ICHs in shaking injuries has been reported in the literature [2,3], such a presentation is unusual. Overall, the sum of all of these factors points to an impact to the head as a distinct possibility to account for this child’s findings; and although shaking could have occurred in addition to blunt trauma, the term SBS should not have been used in this case.

Inflicted traumatic brain injury is a more generic, less mechanism-specific term for cases of inflicted head injury. The use of this term reflects a broader, more inclusive approach to the diagnosis of abusive head injuries in children that acknowledges the fact that ITBI and its associated findings (retinal hemorrhages, fractures, bruising) may be the result of shaking, impact, or both.

Physicians who face suspected cases of abusive head injuries can best serve their patients by using the term ITBI instead of SBS. Discussions of specific mechanisms of injury are best addressed by physicians experienced in neurotrauma or child abuse pediatrics.

Steven Bellemare MD

Dalhousie University, Child Protection Team IWK Health Centre, PO Box 9700, Halifax, Nova Scotia

Canada B3K-6R8 E-mail address: [email protected]

doi:10.1016/j.ajem.2007.06.007

References

1. Healey K, Schrading W. A case of shaken baby syndrome with unilateral retinal hemorrhage with no associated intracranial hemor- rhage. Am J Emerg Med 2006;24(5):616-7.
2. Morad Y, Avni I, Capra L, et al. Shaken baby syndrome without intracranial hemorrhage on initial computed tomography. J AAPOS 2004;8(6):521-7.
3. Morad Y, Avni I, Benton SA, et al. Normal computerized tomography of

brain in children with shaken baby syndrome. J AAPOS 2004;8(5): 445-50.