Year : 2010  |  Volume : 13  |  Issue : 1  |  Page : 73--74

ST elevation in a head-injured patient for emergency neurosurgery: Do we routinely need a cardiac evaluation?


Hemant Bhagat1, Himanshu Chauhan2, Hari H Dash2,  
1 Department of Anesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Neuroanesthesiology, All India Institute of Medical Sciences, New Delhi, India

Correspondence Address:
Hemant Bhagat
Department of Anesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh
India




How to cite this article:
Bhagat H, Chauhan H, Dash HH. ST elevation in a head-injured patient for emergency neurosurgery: Do we routinely need a cardiac evaluation?.Ann Card Anaesth 2010;13:73-74


How to cite this URL:
Bhagat H, Chauhan H, Dash HH. ST elevation in a head-injured patient for emergency neurosurgery: Do we routinely need a cardiac evaluation?. Ann Card Anaesth [serial online] 2010 [cited 2022 Aug 14 ];13:73-74
Available from: https://www.annals.in/text.asp?2010/13/1/73/58843


Full Text

The Editor,

We have the experience of treating a head-injured patient with ST elevations in an intensive care setting. [1] ST elevations in the electrocardiography (ECG) of a head-injured patient may mimic myocardial infarction and lead to diagnostic dilemma. [1] On one hand there may be need for emergency neurosurgery while on the other, it may be necessary to evaluate the patient in view of ST elevation. Cardiac evaluation for ST elevation in ECG of head-injured patient demands time and the resultant delay in emergency neurosurgery may adversely affect the overall outcome. Evidence is lacking to support a priority in these groups of patients-emergency neurosurgery or a cardiac evaluation. We report a case management of a head-injured patient with marked ST segment elevation in the ECG prior to emergency surgery. Here is an example: A 47-year-old male patient admitted in an unconscious state following a road traffic accident. He was hemodynamically stable and was localizing only to the painful stimuli. Computed tomography (CT) scan revealed left frontal subdural hemorrhage with significant midline shift. The patient was transported immediately to the operation room for hematoma evacuation. ST elevations in leads II and V5 were detected on ECG monitor connected in the operation theater. Though cardiac evaluation was contemplated, it was decided to go ahead with the surgery since urgent evacuation of the hematoma was thought to benefit him more. Additionally, during our earlier experience about a similar case, cardiological assessment yielded no conclusive results, while the neurosurgical intervention probably helped the patient. [1] Anesthesia was induced with fentanyl and thiopentone, while tracheal intubation was facilitated with rocuronium. Within few minutes of induction ECG changes reverted to normal. The mechanism of such normalization is unknown to us. Hypotension ensued after induction of general anesthesia, which required dopamine infusion, helped to stabilize the blood pressure. Anesthesia was maintained with nitrous oxide in oxygen, isoflurane, fentanyl and vecuronium. Following surgery the patient was mechanically ventilated. Postoperative 12-lead ECG was unremarkable and Troponin T-test was negative. Dopamine infusion was tapered off in 12 hours. The patient regained consciousness over the next two days. The patient was extubated after 54 hours and was discharged after three weeks.

Occurence of ST segment elevation following head injury has been described. [1],[2] ST elevation suggestive of acute myocardial infarction normalized following anesthetic induction. The raised intracranial pressure (ICP) and the consequential sympathetic activation could have led to coronary vasospasm along with myocardial dysfunction. [3] Anesthetic agents during induction might have decreased the ICP and sympathetic activity, thereby reversing the adverse effect on coronary arteries. Hypotension after anesthetic induction which was noted in our case may have been due to myocardial dysfunction following administration of thiopentone. It is known that such myocardial dysfunction will get reversed following ionotropic stimulation; the same was observed in our patient also. The ST segment elevations in the ECG reverted to normal corresponding to improvement in cerebral dynamics. It is probable that reversible neurogenic myocardial dysfunction was the cause of ST segment elevations following head injury. [1] Since the patient had an unremarkable postoperative course and based on our previous experience, [1] the need for specialized cardiac evaluation was not pursued with. The occurrence of ST elevation in perioperative setting may have clinical implications regarding the management of patient. Since the literature on the outcome of head-injured patients with ST elevation is little known, the question whether cardiac evaluation should precede early surgical management of head injury remains to be answered. This case is being reported to promote such a discussion.

References

1Bhagat H, Narang R, Sharma D, Dash HH, Chauhan H. ST Elevation: An indication of reversible neurogenic myocardial dysfunction in patients with head injury. Ann Card Anaesth 2009;12:149-51.
2Wittebole X, Hantson P, Laterre PF, Galvez R, Duprez T, Dejonghe D, et al. Electrocardiographic changes after head injury. J Electrocardiol 2005;38:77-81.
3Yuki K, Kodama Y, Onda J, Emoto K, Morimoto T, Uozumi T. Coronary vasospasm following subarachnoid hemorrhage as a cause of stunned myocardium. J Neurosurg 1991;75:308-11.