QJM: An International Journal of Medicine, 2016, 559–560 doi: 10.1093/qjmed/hcw088 Advance Access Publication Date: 11 June 2016 Clinical picture
CLINICAL PICTURE
Electrocardiogram helmet sign: an adverse clinical prognosis A 90-year-old male with a history of hypertension, diabetes mellitus type II and coronary artery disease status-post coronary artery bypass graft surgery in 2001 presented with a new onset seizure. On examination he was stuporous, afebrile, had a heart rate 85 beats per minute and blood pressure 148/70 mm of Hg. His pupils were reactive to light, had a supple neck and no focal neurological deficits. Had elevated jugular venous pressure 14 cm of H2O, diffuse bilateral rales on lung auscultation and III/VI holo-systolic murmur on left sternal border on auscultation of precordium. Had 2þ pitting edema on lower extremities. Laboratory results were significant for elevated white blood cell count 14 500/microliter, blood urea nitrogen 54 mg/dl, creatinine 1.9 mg/dl, Troponin-I 4.7 ng/ml (peak level 13 ng/ml), N-terminal pro b-type Natriuretic Peptide 28 100 pg/mL, blood glucose 427 mg/dl and serum osmolality of 332 mOsm/kg. Computed tomography of the head showed diffuse cerebral atrophy and no new intracranial hemorrhage, mass or infarct. Radiography of the chest showed moderate pulmonary vascular congestion. Electrocardiogram revealed normal sinus rhythm with left ventricular hypertrophy. Echocardiogram showed
moderately decreased left ventricular systolic function 35% with diffuse hypokinesis and moderate pulmonary hypertension. Patient was managed in intensive care unit for seizures, hyperosmolar state, Non-ST-elevation myocardial infarction, systolic heart failure and acute renal failure. Patient continued to have recurrent seizures and was started on anti-epileptic medications. On day 3 of hospitalization, patient went into pulseless electrical activity and he was successfully resuscitated following advanced cardiac life support protocol. He was started on vasopressor support, which was tapered off within 12 hrs. On day 4, he developed “spiked helmet sign” (Figure 1, black arrows) in inferior leads on electrocardiogram and disappeared spontaneously. Appearance of helmet sign resembling a German military spiked helmet on electrocardiogram more commonly in inferior leads was described earlier in very sick people suffering from non-cardiac ailments.1 Mechanism underlying the appearance of helmet sign is unknown but it was postulated to be due to sudden increase in intra-abdominal pressure or synchronized contraction of the diaphragm with heart.1,2 This was found to be associated with prolonged hos-
Figure 1. Electrocardiogram showing spiked helmet sign in leads II, III, and AVF (black arrows).
C The Author 2016. Published by Oxford University Press on behalf of the Association of Physicians. V
All rights reserved. For Permissions, please email: [email protected]
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pital stay and high in-hospital mortality.1 Awareness of this sign will assist in quick evaluation and management of critically ill patients. In the following days, his condition deteriorated, developed atrial fibrillation, had worsening of renal function and expired on day 8 of hospitalization. Photographs and text from: V. Namana and J. Patel, Department of Cardiology, Maimonides Medical Center, Brooklyn, NY, USA; N. Tripathi and P. Mathur, Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA Address correspondence to V. Namana, M.D., M.P.H, Department of Cardiology, Fellow in Cardiovascular Medicine,
4802 10th avenue, Brooklyn, [email protected]
NY
11219,
USA.
email:
Conflict of interest: None declared.
References 1. Littmann L, Monroe MH. The “spiked helmet” sign: a new electrocardiographic marker of critical illness and high risk of death. Mayo Clin Proc 2011; 86:1245–6. 2. Frye RL, Braunwald E. Bilateral diaphragmatic contraction synchronous with cardiac systole. N Engl J Med 1960; 263:775–8.
CLINICAL PICTURE
Electrocardiogram helmet sign: an adverse clinical prognosis A 90-year-old male with a history of hypertension, diabetes mellitus type II and coronary artery disease status-post coronary artery bypass graft surgery in 2001 presented with a new onset seizure. On examination he was stuporous, afebrile, had a heart rate 85 beats per minute and blood pressure 148/70 mm of Hg. His pupils were reactive to light, had a supple neck and no focal neurological deficits. Had elevated jugular venous pressure 14 cm of H2O, diffuse bilateral rales on lung auscultation and III/VI holo-systolic murmur on left sternal border on auscultation of precordium. Had 2þ pitting edema on lower extremities. Laboratory results were significant for elevated white blood cell count 14 500/microliter, blood urea nitrogen 54 mg/dl, creatinine 1.9 mg/dl, Troponin-I 4.7 ng/ml (peak level 13 ng/ml), N-terminal pro b-type Natriuretic Peptide 28 100 pg/mL, blood glucose 427 mg/dl and serum osmolality of 332 mOsm/kg. Computed tomography of the head showed diffuse cerebral atrophy and no new intracranial hemorrhage, mass or infarct. Radiography of the chest showed moderate pulmonary vascular congestion. Electrocardiogram revealed normal sinus rhythm with left ventricular hypertrophy. Echocardiogram showed
moderately decreased left ventricular systolic function 35% with diffuse hypokinesis and moderate pulmonary hypertension. Patient was managed in intensive care unit for seizures, hyperosmolar state, Non-ST-elevation myocardial infarction, systolic heart failure and acute renal failure. Patient continued to have recurrent seizures and was started on anti-epileptic medications. On day 3 of hospitalization, patient went into pulseless electrical activity and he was successfully resuscitated following advanced cardiac life support protocol. He was started on vasopressor support, which was tapered off within 12 hrs. On day 4, he developed “spiked helmet sign” (Figure 1, black arrows) in inferior leads on electrocardiogram and disappeared spontaneously. Appearance of helmet sign resembling a German military spiked helmet on electrocardiogram more commonly in inferior leads was described earlier in very sick people suffering from non-cardiac ailments.1 Mechanism underlying the appearance of helmet sign is unknown but it was postulated to be due to sudden increase in intra-abdominal pressure or synchronized contraction of the diaphragm with heart.1,2 This was found to be associated with prolonged hos-
Figure 1. Electrocardiogram showing spiked helmet sign in leads II, III, and AVF (black arrows).
C The Author 2016. Published by Oxford University Press on behalf of the Association of Physicians. V
All rights reserved. For Permissions, please email: [email protected]
559
560
|
QJM: An International Journal of Medicine, 2016, Vol. 109, No. 8
pital stay and high in-hospital mortality.1 Awareness of this sign will assist in quick evaluation and management of critically ill patients. In the following days, his condition deteriorated, developed atrial fibrillation, had worsening of renal function and expired on day 8 of hospitalization. Photographs and text from: V. Namana and J. Patel, Department of Cardiology, Maimonides Medical Center, Brooklyn, NY, USA; N. Tripathi and P. Mathur, Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA Address correspondence to V. Namana, M.D., M.P.H, Department of Cardiology, Fellow in Cardiovascular Medicine,
4802 10th avenue, Brooklyn, [email protected]
NY
11219,
USA.
email:
Conflict of interest: None declared.
References 1. Littmann L, Monroe MH. The “spiked helmet” sign: a new electrocardiographic marker of critical illness and high risk of death. Mayo Clin Proc 2011; 86:1245–6. 2. Frye RL, Braunwald E. Bilateral diaphragmatic contraction synchronous with cardiac systole. N Engl J Med 1960; 263:775–8.
