|
 
 |
| CASE REPORT |
|
| Year : 2016 | Volume
: 6
| Issue : 1 | Page : 22-24 |
|
Syncopal attack: A rare complication just after spinal needle insertion during spinal anesthesia
Sandeep Loha, Ghanshyam Yadav, Amrita Rath, Rajesh Meena
Department of Anesthesiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India
| Date of Web Publication | 22-Apr-2016 |
Correspondence Address:
Dr. Ghanshyam Yadav
Department of Anesthesiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi - 221 005, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2249-4472.181069
A syncopal attack is a sudden loss of consciousness and muscle tone that may be due to various reasons. Vasovagal attack is one of the reason that leads to an unanticipated syncopal attack. A case is described in which a high level of anxiety and pain during insertion of the spinal needle caused a vasovagal attack. A 36-year-old female patient was posted for exploratory laparotomy. During the insertion of a 25-gauge spinal needle she became unconscious with the loss of muscle tone. The spinal needle got bent when it was still present inside the patient. The spinal needle was removed immediately with restoration of airway and circulation. A patient undergoing elective surgery with adequate anxiolysis can still have a rare chance of a syncopal attack. Keywords: Spinal anesthesia, spinal needle, syncopal attack, vasovagal syncope
How to cite this article:
Loha S, Yadav G, Rath A, Meena R. Syncopal attack: A rare complication just after spinal needle insertion during spinal anesthesia. J Obstet Anaesth Crit Care 2016;6:22-4 |
How to cite this URL:
Loha S, Yadav G, Rath A, Meena R. Syncopal attack: A rare complication just after spinal needle insertion during spinal anesthesia. J Obstet Anaesth Crit Care [serial online] 2016 [cited 2021 Sep 16];6:22-4. Available from: https://www.joacc.com/text.asp?2016/6/1/22/181069 |
| Introduction | |  |
A syncope or collapse is a sudden loss of consciousness and postural tone. Any condition that jeopardizes cerebral oxygenation can lead to a syncope. The most common mechanism of syncope is reflex mediated, which is designated "neurally" or "vasovagally," and it typically develops in the upright position but may occur in supine or sitting positions as well. [1],[2] It is characterized by a rapid onset, short duration, and spontaneous recovery. Anxiety and apprehension of the patient before the surgery or any anesthesia procedure can lead to vasovagal syncope, especially in young females. [3]
Medline search did not reveal any case report regarding the vasovagal syncope just after spinal needle insertion in young females undergoing spinal anesthesia. A case of syncopal attack with sequence of events, during the insertion of spinal needle, is discussed here.
| Case Report | | |
A 36-year-old female patient, primigravida, 14 weeks pregnancy with dermoid cyst of uterus size 20 cm × 13 cm, American Society of Anesthesiology (ASA)-I was scheduled for elective exploratory laparotomy in obstetrics and gynecology operating room (OR). Preoperative investigations were within normal limit. After taking written and informed consent spinal anesthesia was planned. The patient was instructed to fast as per institutional protocols (solid food-8 h and clear liquid-3 h). Premedication included oral alprazolam (0.5 mg), ranitidine (150 mg), and metoclopramide (10 mg) at night and 2 h before surgery with sips of water. After arrival of the patient in the OR, the ASA standard monitors- electrocardiograph (ECG), noninvasive blood pressure (NIBP), and pulse oximetry (SpO 2 ) were attached. An 18-gauge intravenous (IV) catheter was secured in the left forearm and the patient was preloaded with 500 mL of ringer lactate. The patient was placed in the sitting position for subarachnoid block. During this whole procedure, the patient was a bit apprehensive and anxious. Vitals were pulse rate (PR) - 130/min, NIBP - 120/84 mmHg, and SpO 2 - 99%. With proper aseptic precautions a 25 G Quincke spinal needle was introduced in L3-L4 intervertebral space, and just after 1 cm of insertion the patient suddenly complained of light-headedness with nausea, following which she collapsed within a few seconds over the assisting technician in front of her. The spinal needle was still present inside the patient's back at that moment. Removal of the needle immediately met with a lot of resistance as it was bent inside the patient. With repeated semicircular motions and gentle pulling, we were able to extricate the needle from the back of the patient, which was bent in a "U" shape [Figure 1].
The patient was repositioned to a supine and the vitals were PR - 28/min, NIBP - 85/50 mm Hg, and SpO 2 - 99% on room air. The patient became unresponsive with decreased muscle tone. Immediately atropine 0.5 mg IV injection was given and as the patient was still spontaneously breathing, 100% oxygen was provided by Bain circuit. The patient was placed in a left lateral position and simultaneously jaw thrust was given. Blood was drawn for blood sugar and arterial blood gas (ABG) analysis. After 2 min of oxygenation and pharmacological resuscitation, the patient regained her consciousness. The vitals were recorded as PR - 105/min, NIBP - 102/60 mm Hg, and SpO 2 - 100%. She was kept under observation with oxygen supplementation by ventimask. Blood sugar was 84 mg/dL and ABG was within normal limit. The case was postponed and echocardioraphy (Echo) was done to rule out any structural or valvular cardiac abnormality. Echo revealed no abnormality and the case was rescheduled on the next day under general anesthesia. The general anesthesia was induced and maintained as per institutional protocols for pregnant patients. The vitals remained stable during the surgery. At the end of surgery she was extubated smoothly and shifted to postoperative care unit for further monitoring and observation.
| Discussion | | |
The common causes of syncope are hypoglycemia, [4] hypoxia, [5] seizure, [6] electrolyte disturbances, [7] cardiogenic abnormalities, [8] acute hemorrhage, intoxication, or vasovagal attack. In our case, as blood sugar, ABG, and SpO 2 were within the normal range, which excludes the chance of hypoglycemia, hypoxia, and electrolyte disturbances. During the preanesthetic check-up, the Metabolic equivalents (METS) was >4 and Echo was normal. There was no history of diabetes mellitus, or any other symptom of orthostatic hypotension. Local anesthetic was not infiltrated before spinal needle insertion because it assumed to be successful in a single attempt. The prodromal symptoms manifested during the insertion of needle suggest that it may be a case of vasovagal attack due to pain.
Vasovagal syncope is a reflex of the involuntary nervous system that causes the bradycardia and dilatation of blood vessels (pooling of the blood) in the legs [9] that leads to decrease cardiac output and cerebral perfusion. [10] All these events lead to hypoxia of brain and ultimately fainting episode occurs. It has three distinct phases: A prodromal phase, loss of consciousness, and a postsyncopal phase. Emotional stress, trauma, pain, sight of blood, prolonged standing, etc. are usually precipitating factors for vasovagal syncope. In our case, the cause of vasovagal syncope might be fear of anticipated pain induced by introduction of spinal needle in an already apprehensive patient.
The prodrome is characterized by diaphoresis, epigastric discomfort, extreme fatigue, weakness, yawning, nausea, dizziness, and vertigo; and results from increased parasympathetic tone, and may last seconds to several minutes. Lying down or removing the stimulus may abort the syncopal episode. The postsyncopal phase may last hours or, rarely, days and may include protracted confusion, disorientation, nausea, dizziness, and a general sense of poor health. [11] A prolonged postsyncopal phase may be associated with causes more serious than vasovagal stimulation and should prompt a more extensive evaluation.
| Conclusion | | |
An anxious patient, especially a female can develop syncopal attack due to a painful stimulus such as insertion of spinal needle.
Acknowledgment
We would like to thank technical staff who helped during this case management.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, et al.; Task Force on Syncope, European Society of Cardiology. Task force on syncope, European Society of Cardiology. Part 1. The initial evaluation of patients with syncope. Europace 2001;3:253-60.  |
| 2. | van Lieshout JJ, Wieling W, Karemaker JM, Eckberg DL. The vasovagal response. Clin Sci (Lond) 1991;81:575-86. |
| 3. | Bahrami F, Yousefi N. Females are more anxious than males: A metacognitive perspective. Iran J Psychiatry Behav Sci 2011;5:83-90. |
| 4. | Lagi A, Cencetti S, Lagi F. Incidence of hypoglycaemia associated with transient loss of consciousness. A retrospective cohort study. See comment in PubMed Commons belowInt J Clin Pract 2014;68:1029-33. |
| 5. | Lempert T, Bauer M, Schmidt D. Syncope: A videometric analysis of 56 episodes of transient cerebral hypoxia. Ann Neurol 1994;36:233-7. |
| 6. | Asadi-Pooya AA, Nikseresht A, Yaghoubi E. Vasovagal syncope treated as epilepsy for 16 years. Iran J Med Sci 2011;36:60-2. |
| 7. | Erden I, Yalcin S, Ozhan H. Syncope caused by hyperkalemia during use of a combined therapy with the angiotensin-converting enzyme inhibitor and spironolactone. Kardiol Pol 2010;68:1043-6. |
| 8. | Epstein AE, Miles WM, Benditt DG, Camm AJ, Darling EJ, Friedman PL, et al. Personal and public safety issues related to arrhythmias that may affect consciousness: Implications for regulation and physician recommendations. A medical/scientific statement from the American Heart Association and the North American Society of Pacing and Electrophysiology. Circulation 1996;94:1147-66. |
| 9. | Soteriades ES, Evans JC, Larson MG, Chen MH, Chen L, Benjamin EJ, et al. Incidence and prognosis of syncope. N Engl J Med 2002;347:878-85. |
| 10. | Nair N, Padder FA, Kantharia BK. Pathophysiology and management of neurocardiogenic syncope. Am J Managed Care 2003;9:327-34. |
| 11. | Kenny RA. Neurally mediated syncope. Clin Geriatr Med 2002;18: 191-210, vi. Review. |
[Figure 1]
|
Search Pubmed for