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Table of Contents
LETTER TO EDITOR
Year : 2021  |  Volume : 5  |  Issue : 2  |  Page : 143-144

Transient severe hypertension following spinal anesthesia in a patient undergoing caesarean delivery: A rare experience


1 Department of Anaesthesiology, Institute of Medicine, Tribhuvan University Teaching Hospital, Tribhuvan University, Kathmandu, Nepal
2 Department of Anaesthesiology, National Trauma Centre, National Academy of Medical Sciences, Kathmandu, Nepal

Date of Submission16-Oct-2020
Date of Decision06-Nov-2020
Date of Acceptance11-Nov-2020
Date of Web Publication16-Apr-2021

Correspondence Address:
Dr. Utsav Acharya
Department of Anaesthesiology, Institute of Medicine, Tribhuvan University Teaching Hospital, Kathmandu 44600
Nepal
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bjoa.bjoa_228_20

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How to cite this article:
Acharya U, Yadav RK. Transient severe hypertension following spinal anesthesia in a patient undergoing caesarean delivery: A rare experience. Bali J Anaesthesiol 2021;5:143-4

How to cite this URL:
Acharya U, Yadav RK. Transient severe hypertension following spinal anesthesia in a patient undergoing caesarean delivery: A rare experience. Bali J Anaesthesiol [serial online] 2021 [cited 2021 Jun 23];5:143-4. Available from: https://www.bjoaonline.com/text.asp?2021/5/2/143/313888



Sir,

The hemodynamic response to the subarachnoid block (SAB) has been extensively studied. The common response is hypotension, accompanied by reflex tachycardia. Bradycardia may be observed if the level of block is high enough to involve cardioaccelerator fibers. We, however, encountered severe transient hypertension immediately following SAB in a healthy parturient undergoing cesarean delivery (CD), which we would like to share.

A 28-year-old healthy female was scheduled for elective CD. In the operating room, her blood pressure (BP) was 116/78 mmHg, heart rate (HR) was 92/min, and SpO2 was 94% in room air. After establishing intravenous (IV) access, SAB was given with all aseptic precautions, at L3–L4 interspace with 2.2 ml 0.5% heavy bupivacaine in sitting position. She was then positioned supine. The BP immediately after was 94/52 mmHg and HR 94/min. The BP responded well to a fluid bolus and did not require the use of a vasopressor. The level of the block was at T5 after 3 min, which was confirmed by loss of temperature sensation. The BP was 114/77 mmHg and HR 74/min. The surgeons were then asked to proceed.

Immediately after incision, the patient complained of headache. HR was 63/min and BP was 201/112 mmHg. Nitroglycerin IV 50 μg bolus was administered. She was talking normally and complained only of headache. BP now was 181/104 mmHg and HR was 67/min. Again, IV nitroglycerin 50 μgs was administered. After 1 min, BP was 155/96 mmHg and HR was 71/min. After 5 min, she said that the headache had disappeared completely. The BP was 126/66 mmHg and HR was 92/min. Thereafter, BP was normal and there was no complaint of headache. The surgery was uneventful thereafter. We reviewed the patient's history and medical documents. However, no apparent cause for the hypertension could be identified. The patient was observed in postanesthesia care unit for 1 h. After ensuring that there was no neurological deficit, she was transferred to the ward. A computed tomography (CT) scan of the head was done and intracranial bleeding was ruled out.

After discharge from the obstetric unit, the patient was sent for further evaluation to identify the cause of the transient hypertension. The electrocardiogram and echocardiography revealed no abnormalities. To rule out neuroendocrine tumors, a CT scan of the abdomen was performed, which was normal. Her hormonal studies were also within normal limits. After thorough workup, no apparent cause for the transient hypertension could be identified.

Neuraxial anesthesia is the most common and the safest choice of anesthesia for cesarean section, among which, single-shot spinal anesthesia is most widely practiced.[1] Spinal anesthesia-associated hypotension may occur in up to 64%–100% of pregnant women undergoing cesarean delivery.[2] The most frequent response to spinal anesthesia for elective cesarean section is a marked decrease in systemic vascular resistance and partial compensation from increased stroke volume and HR.[3] This partial compensation is usually not adequate, resulting in hypotension. Hypertension following SAB, however, is extremely rare and has not been explained so far.

In our case, the noninvasive blood pressure cuff was of appropriate size. A urinary catheter had been placed and the flow of urine was good, ruling out urinary bladder distention. The patient was calm and cooperative. She was previously normotensive and did not have pregnancy-induced hypertension till date. She was not under steroids or thyroxine and had normal thyroid function tests. No prophylactic vasopressors were given before or after SAB.

An alternative explanation could be autonomic dysreflexia (AD), usually seen in patients with spinal cord injury. It is commonly triggered by afferent stimuli below the level of injury, such as distension of hollow viscera (bladder, uterus, gallbladder, and bowel), uterine contractions during obstetric delivery, cutaneous stimulation, and surgical procedures involving pelvic organs or lower extremities.[4] The incidence of AD is about 50%–70% in patients with spinal cord lesions above T6.[5] The principal factor for unopposed hypertension in AD is the disinhibition of the descending inhibitory pathways due to cord injury, leading to unopposed sympathetic activity below the level of injury. The descending inhibitory pathways, in contrast, are intact following SAB.

Another possibility could be a compensatory sympathetic overactivity above the level of blockade. Extensive vasoconstriction above the level of the blockade could lead to reflex bradycardia. It was transient and responded well to vasodilator, suggesting vasoconstriction could be the reason for hypertension. So far, only one case report has been published on transient hypertension after spinal anesthesia.[6] The cause of increased BP, in that case, was attributed to the full bladder which went unnoticed. In our case, however, no obvious reason for transient hypertension could be identified. Although the physiological response to spinal anesthesia has been well studied, some corners still need to be explored.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Parikh KS, Seetharamaiah S. Approach to failed spinal anaesthesia for caesarean section. Indian J Anaesth 2018;62:691-7.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Nikooseresht M, Seif Rabiei MA, Hajian P, Dastaran R, Alipour N. Comparing the hemodynamic effects of spinal anesthesia in preeclamptic and healthy parturients during cesarean section. Anesth Pain Med 2016;6:e11519.  Back to cited text no. 2
    
3.
Langesæter E, Dyer RA. Maternal haemodynamic changes during spinal anaesthesia for caesarean section. Curr Opin Anaesthesiol 2011;24:242-8.  Back to cited text no. 3
    
4.
Leão P, Figueiredo P. Autonomic hyperreflexia after spinal cord injury managed successfully with intravenous lidocaine: A case report. Patient Saf Surg 2016;10:10.  Back to cited text no. 4
    
5.
Petsas A, Drake J. Perioperative management for patients with a chronic spinal cord injury. BJA Educ 2015;15:123-30.  Back to cited text no. 5
    
6.
Bhavsar R, Luy A, Kuhnt R, Jakobsen CJ. Severe hypertension after spinal anaesthesia: A case report. ARC J Anesthesiol 2018;3:20-2.  Back to cited text no. 6
    




 

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