|Year : 2017 | Volume
| Issue : 4 | Page : 1075-1078
Role of oral prednisolone in the management of postdural puncture headache after spinal anesthesia in urological patients
Sunana Gupta1, Nandita Mehta1, Arti Mahajan2, Mohd Reidwan Dar3, Neeraj Gupta4
1 Department of Anaesthesiology and Intensive Care, Acharya Shri Chander College of Medical Sciences and Hospital, Sidhra, Jammu, Jammu and Kashmir, India
2 Government Medical College and Hospital, Jammu, Jammu and Kashmir, India
3 Department of Anaesthesiology and Intensive Care, Shri Mata Vaishno Devi Narayana Superspeciality Hospital, Katra, Jammu, Jammu and Kashmir, India
4 Fortis Escorts, Okhla, Delhi, India
|Date of Web Publication||28-Nov-2017|
Mohd Reidwan Dar
Room No. 104, Sushruta, Shri Mata Vaishno Devi Narayana Superspeciality Hospital, Katra, Jammu - 182 320, Jammu and Kashmir
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background and Aims: Postdural puncture headache (PDPH) is a frequently encountered complication of spinal anesthesia and may be associated with significant morbidity in some patients. Parenteral corticosteroids have been used in the management of PDPH both prophylactically and after the occurrence of headache. The aim of this study was to evaluate the effect of oral prednisolone in the management of PDPH after spinal anesthesia in urological patients. Materials and Methods: Sixty adult patients who developed PDPH after spinal anesthesia for urological surgeries were randomly allocated to two groups. Group C patients (n = 30) were managed conservatively, and Group P patients (n = 30) were given 20 mg of oral prednisolone for 4 days in addition to the conventional treatment. The intensity of headache was measured using visual analog scale (VAS). VAS score was taken just before the start of treatment (0 h) and at 12, 24, 48, 72, and 96 h after the start of treatment. Statistical Analysis: Statistical analysis was performed using Statistical Packages for Social Science version 19 (SPSS, Inc., Chicago, IL, USA). Results: There was no statistically significant difference in the VAS score in patients before the start of treatment (0 h) and at 12 h after the start of treatment. The VAS scores were less and statistically significant in Group P at 24, 48, 72 and 96 h after the start of treatment (P < 0.05). Conclusion: The use of oral prednisolone is effective in reducing the severity and duration of PDPH.
Keywords: Corticosteroids, postdural puncture headache, prednisolone, spinal anesthesia
|How to cite this article:|
Gupta S, Mehta N, Mahajan A, Dar MR, Gupta N. Role of oral prednisolone in the management of postdural puncture headache after spinal anesthesia in urological patients. Anesth Essays Res 2017;11:1075-8
|How to cite this URL:|
Gupta S, Mehta N, Mahajan A, Dar MR, Gupta N. Role of oral prednisolone in the management of postdural puncture headache after spinal anesthesia in urological patients. Anesth Essays Res [serial online] 2017 [cited 2019 May 25];11:1075-8. Available from: http://www.aeronline.org/text.asp?2017/11/4/1075/183565
| Introduction|| |
Postdural puncture headache (PDPH) as defined by the international headache society, is the headache that develops within 5 days of dural puncture, improves within 15 min of assuming the supine position and worsens within 15 min of assuming a sitting or erect posture, and may be associated with features such as nausea, vomiting, dizziness, tinnitus, photophobia, or neck stiffness. It usually resolves spontaneously and PDPH that persists even after 14 days of dural puncture is called as cerebrospinal fluid (CSF) fistula headache. It is an important cause of morbidity after spinal anesthesia, dural tap during attempted epidurals for anesthesia or pain management, and after a diagnostic lumbar puncture.
The history of PDPH dates back to 1898 when Sir August Bier performed spinal anesthesia on himself and eight other subjects using 10–15 mg of cocaine. Four of nine people, including Sir Bier himself, developed headache. Risk factors for the development of PDPH are young age, female sex, lower body mass index (BMI), taller height, reduced pre procedure intravenous hydration, h/o chronic or recurrent headache, high stress during the procedure, and multiple lumbar punctures.
Before making a diagnosis of PDPH other causes such as spinal abscess, intracranial hematoma, meningitis, intracranial mass lesion, cerebral aneurysm, cerebral edema, myofascial syndrome, arachnoiditis caused by intrathecal steroids, neural toxicity of drugs, and anterior spinal artery syndrome should all be ruled out.
The incidence of PDPH ranges from 4% to 18% after spinal anesthesia in nonobstetric patients. Conservative management of PDPH includes good hydration, bed rest, abdominal binders, analgesics such as paracetamol and nonsteroidal anti-inflammatory drugs. Pharmacological management includes the use of drugs such as methylxanthines (caffeine, aminophylline, and theophylline), sumatriptan, and adrenocorticotropic hormone. Gamma-aminobutyric acid analogs such as pregabalin or gabapentin  have also been used for the treatment of PDPH. Few researchers have also used corticosteroids for the management of PDPH., PDPH resistant to all medical therapies is treated with invasive techniques such as autologous epidural blood patch.
Corticosteroids have been widely used for the relief of postoperative pain and cancer pain. There is a strong Grade A evidence supporting the use of corticosteroids in multimodal analgesia protocols for managing postoperative pain. Few researchers have used injectable dexamethasone, methylprednisolone, and hydrocortisone  for the management of PDPH, but there has been no study regarding the use of oral prednisolone for the same. Prednisolone has been widely used in the treatment of a low-pressure headache associated with the syndrome of spontaneous intracranial hypotension (SSIH). The signs and symptoms of the headache associated with SSIH are similar to that of PDPH. Hence, we hypothesized that if prednisolone can improve the headache associated with SSIH, it may be beneficial in PDPH also.
| Materials and Methods|| |
This double-blinded, randomized prospective study was done after taking clearance from the Ethical Committee of the hospital. Sixty adult patients (the American Society of Anesthesiologists [ASA] I and II) in the age group 18–65 years who developed PDPH after urological surgery were included in this study. Exclusion criteria include patients having a history of migraine or other type of headache, cerebrovascular accident, previous neurological disease, any systemic infection and diabetes mellitus (June 2014–December 2015).
Any patient who reported headache following spinal anesthesia in hospital or reported within maximum up to 5 days after the procedure was included in the study. The diagnosis of PDPH was made according to the guidelines of the international headache society. All these patients had received spinal anesthesia in the sitting position through midline approach with 25-gauge Quincke needle, and 0.5% hyperbaric bupivacaine was used.
These sixty patients were randomly divided with the help of computer-generated random number table into two groups. Every participant was assigned a sequential number for the study, and the four tablets of prednisolone or placebo (multivitamin tablets) were placed in a small sequentially numbered medication packets. An assistant, not involved in the study, prepared the packets, and anesthetist blinded to the content gave the packet to the patient Group C received conventional treatment in the form of recumbent positioning, good hydration, stool softener, a combination of paracetamol and caffeine tablet thrice daily, and a placebo tablet once daily. Group P received tablet prednisolone 20 mg once daily in addition to the conventional treatment.
Headache intensity was measured with the help of a visual analog scale (VAS) graded 0–10. Zero was considered as no pain and 10 as severe pain: 0–1 (no headache), 2–4 a mild headache, 5–7 moderate headache, and 8–10 a severe headache. VAS was measured and recorded at the start of treatment (0 h), at 12, 24, 48, 72, and 96 h after the commencement of treatment. If VAS score was more than 5 in both groups additional tablet diclofenac was given eight hourly, and the number of diclofenac tablets given over 96 h was recorded in both the groups.
Any other coexisting symptoms such as nausea, vomiting, dizziness, neck stiffness, diplopia, and photophobia were recorded. Patients who had a severe headache even after 4 days of treatment were planned for an autologous epidural blood patch.
All statistical analysis was performed using Statistical Packages for Social Science version 19 (SPSS, Inc., Chicago, IL, USA). Demographic data were compared using Chi-square test. Quantitative data were compared using un-paired t-test. Statistical significance was considered if P < 0.05.
| Results|| |
There was no statistically significant difference among the groups regarding their age, sex, ASA status, and BMI [Table 1]. No patient withdrew from the study and no patient developed any adverse effect attributable to the study drug. There was no statistically significant difference in the VAS score in patients before the start of treatment (0 h, P = 0.387) and at 12 h (P = 0.192) after the start of treatment. The VAS scores were less and statistically significant in Group P at 24 h (P = 0.008), 48 h (P < 0.001), 72 h (P < 0.001), and 96 h (P < 0.001) hours after the start of treatment. The group comparison for mean VAS score at different time intervals is shown in [Figure 1].
|Figure 1: Comparison for visual analog scale score at different time intervals|
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None of the patients in Group P required epidural blood patch, whereas two patients of Group C were symptomatic even after day 4 and they were treated with epidural blood patch. Number of diclofenac tablets given was significantly less in Group S as compared to Group C [Table 2]. The number of patients who had nausea and vomiting after the start of treatment was more in Group C (n = 10) as compared to Group P (n = 4).
|Table 2: Comparison of mean number of diclofenac tablets required and nausea and vomiting in both groups|
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| Discussion|| |
PDPH is still a very common cause of morbidity following dural puncture for spinal anesthesia or attempted epidurals. Often the headache is so distressing that it restricts the patient to bed for a prolonged period. This is especially true for most of the urological endoscopic surgeries where the patients are discharged early. The occurrence of PDPH in such patients leads to delayed recovery, adds to their hospital stay, cost, and ultimately increases the workload of attending doctor and hospital. PDPH is mostly benign in nature and headache usually resolves spontaneously after a few days in most of the patients, but the morbidity of the patient increases during this period. Despite several innovative techniques for performing spinal anesthesia and invention of different kind of spinal needles, the question of optimal management of PDPH remains unanswered.
CSF is produced by the choroid plexus system, and it serves as a cushion for the brain and the spinal cord. Dural puncture-induced CSF leak is the most accepted mechanism of PDPH. CSF has a buoyant effect and when its volume is diminished it leads to sagging of the brain within the cranial cavity causing traction on cranial nerves and other pain sensitive structures, especially in the upright position. In addition, loss of CSF also activates adenosine receptors that subsequently dilate intracranial arteries and veins leading to clinical manifestations of PDPH. Even 10% loss of CSF volume can cause an orthostatic headache. Headache is relieved only when the CSF volume and pressure return to normal.
Some workers have used injectables corticosteroids for the management of PDPH prophylactically as well as therapeutically.,,, Alam et al. used intravenous hydrocortisone 100 mg thrice daily for 3 days in patients who developed PDPH after spinal anesthesia and found that hydrocortisone was effective in reducing headache.
The exact mechanism of action of corticosteroids in relieving PDPH is not clear. In response to the healing process at dural puncture site, various inflammatory mediators are released from immune cells in CSF, which in turn stimulate pain receptors and cause headache. Corticosteroids suppress the production of these immune mediators (allogenic prostaglandins and leukotrienes) by inhibiting arachidonic acid production through lipocortin-induced phospholipase inhibition. Hence, this anti-inflammatory action of corticosteroids at dural puncture site may be responsible for their analgesic action in PDPH. Steroids also favor the reabsorption of CSF from the extradural space and thus lead to increased CSF volume. Both these mechanisms may be interacting in combination to produce therapeutic effects in PDPH.
We used oral prednisolone for our study because of its wide usage and good response in the treatment of SSIH. Sign and symptoms, the presentation of headache, and the basic mechanism of headache are similar in both SIH and PDPH. Spontaneous intracranial hypotension is due to a CSF leak followed by decreased CSF volume and hydrostatic CSF pressure changes. Downward displacement of the brain due to decreased CSF volume causes traction on pain-sensitive venous sinuses and cranial nerves resulting in various symptoms of SSIH. Gentile et al. used oral prednisolone in three cases of headache attributed to spontaneous low-CSF pressure and found a good response. Similarly, prednisolone was used in a pregnant patient with a low-pressure headache and there was excellent response within hours of treatment.
Our study showed favorable effects of prednisolone on the severity of PDPH as was evident by statistically significant reduction of VAS score. The study drug prednisolone had no effect within 12 h of the start of treatment (P > 0.05), but the severity of PDPH was significantly reduced at 24 h and thereafter. The number of diclofenac tablets required in prednisolone group was also significantly less as compared to conventional group. Most of the patients in prednisolone group were pain-free at 72 h and 96 h as it is evident by the mean VAS score in both groups. Hence, the use of prednisolone has decreased the duration of PDPH also.
The main concern regarding the use of prednisolone in postoperative patients is its effect on wound healing and postoperative infections. For this reason, we have not included the patients with active infection, diabetes mellitus, tuberculosis in the study. It has been found in various studies that the side effects with the use of steroids are related to the high-mineralocorticoid activity and or long-term dosing. Studies clearly reflect the safety of short-term use of corticosteroids for acute postoperative analgesia and postoperative nausea and vomiting in relatively healthy individuals.,, Even studies on patients with severe asthma and ulcerative colitis who had undergone surgical procedures failed to reveal an increased wound infection rate in association with the use of perioperative steroids. Wang et al. reviewed the literature on the effects of corticosteroids on wound healing and concluded that high-dose corticosteroid administration (15–40 mg/kg/day) for <10 days has no effect on wound healing.
We decided to use 20 mg once daily prednisolone keeping in view that in most studies regarding the use of it in SSIH, researchers have used dose range starting from 40 mg. If the headache persisted after 4 days, it was presumed that the response to treatment is inadequate and such patient with severe headache was administered autologous epidural blood patch. Prednisolone was stopped without tapering as it is not recommended for therapy of <1 week.
In our study, two patients in conventional group required epidural blood patch for severe headache whereas none of the patients in prednisolone group required it. Invasive treatment options for PDPH includes the use of epidural autologous blood patch, epidural dextran or 0.9% saline, computed tomography-guided injection of fibrin glue, and the last resort is surgery to seal the leak. All these being invasive procedures are resorted to once pharmacological measures fail.
Limitation of our study is the small sample size because we included only those patients who developed PDPH after spinal anesthesia which is in contrast to those studies where corticosteroids were administered prophylactically in all patients undergoing spinal anesthesia. Review of literature shows that oral prednisolone has never been used before for the management of PDPH, and this is the first study of its type. Further studies with larger sample size and different doses may be advisable in future.
| Conclusion|| |
The occurrence of PDPH in a patient should not be taken lightly as it carries the risk of morbidity to the patient, especially in those patients who can be discharged early from the hospital. It adds to their hospital stay as well as increases the work burden of the attending doctor and hospital. The use of oral prednisolone was effective in relieving both severity and duration of PDPH after spinal anesthesia thus avoiding the use of invasive procedures for the same.
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Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2]