Management of Post dural puncture headache by Dr. Kolawole Kazeem Shorunke
KolawoleShorunke1
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Aug 22, 2024
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About This Presentation
Post Dural Puncture Headache
Size: 39.84 MB
Language: en
Added: Aug 22, 2024
Slides: 42 pages
Slide Content
POSTDURAL PUNCTURE HEADACHE Dr. Shorunke Kolawole Kazeem Medical Officer Department of Anesthesia Garki Hospital Abuja
Outline Introduction Pathogenesis and anatomy Clinical presentation and Characteristics Risk Factors Prevention Diagnosis and Differential diagnosis
Introduction “Toward the evening I was forced to take to bed and remained there for nine days, because all the manifestations recurred as soon as I got up. At midnight a violent headache set in that quickly became insupportable.” August Bier, 1898: a personal experience of Postdural puncture headache
first described by August Bier in 1898 and classically presents as a postural headache following therapeutic or diagnostic interventions of the epidural or spinal space. incidence varies, estimated to be 36% or more following lumbar puncture, 0-10% following spinal anaesthesia , and 81% following accidental dural puncture during epidural insertion. Rates of accidental dural puncture during epidural insertion in pregnancy are estimated to be 0.04%-6%. Although PDPH usually resolves spontaneously, it may interfere with a mother’s ability to care for her newborn and may extend the length of hospital stay. More rarely, PDPH may be associated with serious complications such as subdural haematoma , seizures, sagittal sinus thrombosis, and cranial nerve palsies. Introduction
Pathogenesis and Anatomy
Pathogenesis and Anatomy
The pathogenesis of PDPH remains unclear but is thought to be caused by cerebrospinal fluid (CSF) leakage into the epidural space via a tear in the meninges. The CSF loss leads to a reduction in intracranial pressure and downward traction on pain-sensitive intracranial structures, resulting in a headache that is classically worse in the upright position. The fall in intracranial pressure may also cause compensatory cerebrovascular venodilation contributing to the headache. Pathogenesis and Anatomy
Onset: Onset of symptoms is generally delayed, with headache usually beginning 12–48 hours and rarely more than 5 days following meningeal puncture An onset of symptoms within 1 hour of neuraxial procedures is suspicious for pneumocephalus , especially in the setting of an epidural loss of-resistance technique using air. Presentation: The cardinal feature of PDPH is its postural nature, with headache symptoms worsening in the upright position and relieved, or at least improved, with recumbency Clinical Presentation and Characteristics
Presentation ( Contd ): the International Headache Society (IHS) diagnostic criteria further describe this positional quality as worsening within 15 minutes of sitting or standing and improving within 15 minutes after lying. Headache is always bilateral, with a distribution that is frontal (25%), occipital (27%), or both (45%). Headaches are typically described as “dull/aching,” “throbbing,” or “pressure type.” Although there is no universally accepted severity scale, one practical approach is to have patients simply rate their headache intensity using a 10-point analog scale, with 1–3 classified as “mild,” 4–6 “moderate,” and 7–10 “severe.” Clinical Presentation and Characteristics
Associated Symptoms The IHS criteria for PDPH are as follows: Headache accompanied by at least one of these symptoms: neck stiffness tinnitus hypoacusia photophobia nausea Clinical Presentation and Characteristics
Patient Characteristics Age : It is uncommon in patients less than 10 years of age; peak incidence is in the teens and early 20s. Gender : Nonpregnant females have twice the risk compared to age-matched men. Pregnancy BMI Patients with other forms of headache Previous history of PDPH Previous history of ADP Risk Factors
Procedural Details Needle size Needle tip design (Cutting vs noncutting) Insertion of cutting needles with the bevel parallel to the long axis of the spine experience/comfort/skill of the operator Risk Factors
Spinal needles of different manufacturers with same external diameter . A: Whitacre type. B: Spinal type. C: Sprotte type. D, E: Quincke type. Scanning electron microscopy. Magnification ×40. (Atlas of Functional Anatomy for Regional Anesthesia and Pain Medicine. Heidelberg: Springer; 2015.)
Procedural Details ( contd ) A number of procedural details do not appear to influence the rate of development of PDPH, including patient position at the time of meningeal puncture, “bloody tap” during spinal anesthesia, addition of opiates to the spinal block, and volume of CSF removed (for diagnostic purposes). Risk Factors
General Measures appropriate patient selection Practitioners use of ultrasound Bed rest Aggressive oral and Intravenous hydration Caffiene Prevention
Spinal technique Needle selection Replacing the stylet after CSF collection but prior to needle withdrawal Continuous spinal anesthesia (CSA) Intravenous aminophylline Epidural Technique using the smallest feasible epidural needles air versus liquid for identification of the epidural space Bevel orientation for epidural needle insertion remains a matter of debate. Prevention
Stylet Replacement Subarachnoid Saline (10ml sterile preservative-free saline) Intravenous Cosyntropin Limiting/Avoiding Pushing Intrathecal Catheters Epidural Saline Epidural Opiates Prophylactic Epidural Blood Patch Measures to Reduce the Risk of PDPH After ADP
remains a diagnosis of exclusion. Although headache following meningeal puncture will naturally be suspected to be PDPH, it remains critical to rule out other etiologies While postpartum headaches occur in up to 40% of postpartum women, 50%-75% of postpartum headaches are tension or migraine headaches, and only 5%-15% are PDPHs. Importantly, one study found that 24% of postpartum headaches were due to preeclampsia, affirming the importance of ruling out serious causes. Other often-overlooked causes such as medication headaches ( eg ondansetron) should also be excluded. Diagnosis and Differential Diagnosis
A history and examination should be performed, taking into account the timing of the headache in relation to the neuraxial procedure and the nature of the headache, as well as other symptoms and signs. Since PDPH can present following an unrecognized dural puncture during an epidural, details of the epidural insertion should be reviewed including the difficulty of the procedure and number of attempts. Following a spinal procedure, PDPH is more likely with a larger-gauge ‘cutting’-tipped needle or after multiple attempts at spinal block which might result in a number of dural tears, increasing the chance of a CSF leak. Diagnosis and Differential Diagnosis
A careful history : known or possible meningeal puncture, delayed onset of symptoms (but within 48 hours), bilateral postural headache possibly accompanied by associated symptoms if moderate or severe. Physical examination plays a limited role in the diagnosis of PDPH. Vital signs (normal blood pressure and absence of fever) basic neurologic exam (gross motor and sensory function plus ocular and facial movements) should be documented. Diagnosis and Differential Diagnosis
Physical examination ( contd ) Firm bilateral jugular venous pressure, applied briefly (10–15 seconds), tends to worsen headaches secondary to intracranial hypotension. Conversely, the “sitting epigastric pressure test” may result in transient relief of PDPH symptoms. For this test, the patient is placed in a sitting position until headache symptoms become manifest. Firm, continuous abdominal pressure is applied with one hand, while the other hand is secure against the patient’s back. In cases of PDPH, some improvement is usually noted within 15–30 seconds with prompt return of symptoms on release of abdominal pressure. ( Gutsche sign) Skin over the epidural or spinal puncture site should be inspected for inflammation and tenderness Diagnosis and Differential Diagnosis
Investigations Laboratory studies are usually not necessary for the diagnosis of PDPH and, if obtained, are generally unremarkable LP may reveal low opening pressures and increased CSF protein Imaging: most commonly, MRI may show meningeal enhancement and Brain decent Diagnosis and Differential Diagnosis
Diagnosis and Differential Diagnosis
Once a diagnosis of PDPH has been made, patients should be provided a straightforward explanation of the presumed etiology, anticipated natural course (factoring in the time from meningeal puncture), and a realistic assessment of treatment options (with consideration of needle gauge). Treatment considerations are presented individually next Treatment are the forms of: Conservative management Pharmacological management Invasive management Treatment
Reassurance : in the untreated patients a median duration of symptoms of 5 days with a range of 1–12 days Bed Rest Oral and Intravenous hydration Abdominal binders Conservative Management
Analgesics (acetaminophen, NSAIDs, opiates, etc.) Methylxanthines These agents include aminophylline, theophylline, and—the most familiar—caffeine. Caffeine is thought to treat PDPH by inducing cerebral vasoconstriction. Doses from 75 to 500 mg, orally and intravenously, both one-time and repeated Caffeine is associated with adverse events including cardiac arrhythmias and seizures, and high doses may enter breast milk and lead to neonatal irritability. Corticosteroidogenics (corticotropin [ACTH] and its synthetic analogues [ ie , cosyntropin / tetracosactin ]). Postulated mechanisms include CSF retention through mineralocorticoid-mediated sodium reabsorption, and a direct analgesic effect via its glucocorticoid activity Pharmacological Management
Other Medications Numerous other reports exist in the literature with for a variety of other pharmacological agents, most with a mechanism involving vasoconstriction. Some of these include serotonin agonists ( egsumatriptan ), methylergonovine, gabapentin, theophylline, and hydrocortisone Pharmacological Management
SPGB is a recent treatment option for PDPH that has been used in the past for treating migraines. The sphenopalatine ganglion is a collection of parasympathetic cells located in bilateral nares posterior to the middle nasal concha in the nasopharynx. The proposed mechanism of action is a block of the sphenopalatine ganglion parasympathetic-induced cerebral vasodilation. Sphenopalatine Ganglion Block
Technique Have the patient lie supine in a sniffing position. Soak a long cotton-tipped applicator in local anaesthetic (2%-4% lidocaine, 0.5% ropivacaine, or 0.5% bupivacaine). Insert cotton-tipped applicator into patient’s nare aiming straight back. Advance until the posterior nasopharynx wall is reached and resistance is felt. Leave applicator in place and in contact with sphenopalatine ganglion for 10 minutes, then remove. Sphenopalatine Ganglion Block
Sphenopalatine Ganglion Block Adverse events include: nausea, bitter taste, discomfort during insertion of applicator, nasal or throat pain.
After the observation that patients with bloody spinal taps at lumbar puncture were less likely to develop PDPH, the first EBP was performed in 1960. Just 2 mL of the patient’s blood was injected during the first EBP and the headache was relieved. Epidural blood patching involves injection of autologous blood into the epidural space. The mechanism of action of the EBP, while not entirely elucidated, appears to be related to the ability to stop further CSF loss by the formation of clot over the defect in the meninges as well as a tamponade effect with cephalad displacement of CSF (the “epidural pressure patch”). Epidural Blood Patch
Epidural Blood Patch
Epidural Blood Patch
Epidural Blood Patch An EBP should be performed by two personnel Contraindications: sepsis, coagulopathy, and patient refusal. Timing of EBP performance is somewhat controversial, with limited evidence pointing to less failure when performed more than 48 hours after PDPH onset. Volumes of between 2 and 60 mL of blood have been described in literature. Standard volume used is 20ml Most anesthesiologists recommend the patient lie flat for 1 to 2 hours after the procedure and avoid heavy lifting for 48 hours.
Epidural Blood Patch Safety Strict asepsis must be maintained during an EBP. Do not perform in the presence of leucocytosis or fever due to the risk of meningitis. Minor complications include backache, neck ache, and transient bradycardia. Major complications are rare and include meningitis, subdural haematoma , seizures, arachnoiditis, and dural puncture.15,16 An EBP may be unacceptable to Jehovah’s Witness patients, so thorough informed consent detailing the procedure,alternatives , risks, and benefits should be performed in these and all patients. If an EBP fails to relieve a PDPH, it may be prudent to consider head imaging to exclude other pathology prior to a repeat EBP.
Treatment algorithm for established PDPH. Patient education, reassurance, and supportive measures. Triage by severity of symptoms. Resolution over time without further treatment. Worsening symptoms or failure to improve substantially within 5 days. Choice of EBP or pharmacologic measures based on patient preference. Definitive treatment (EBP) is recommended (bold arrow). Caffeine or other agents. Failure, worsening of symptoms, or recurrence. Patch materials other than blood remain preliminary. Generally performed no sooner than 24 hours after a first EBP. Serious reconsideration of diagnosis. Radiologic guidance is recommended if another epidural blood patch (EBP).
Persistent or Recurrent PDPH Persistent or recurrent headaches following the EBP, while not necessarily requiring consultation, warrant follow-up and thoughtful reevaluation The EBP is associated with nearly immediate symptomatic relief in greater than 90% of cases, but appropriate follow-up reveals a number of patients experiencing incomplete relief, failure, or recurrence of symptoms.
When to seek further consultation seek neurological consultation if: symptoms have failed to resolve after an arbitrary duration ( eg , 7–10 days) or number of EBPs (usually two or three). serious non-PDPH is suspected or cannot reasonably be ruled out lateralizing neurologic signs, fever/chills, seizures, or change in mental status are not consistent with a diagnosis of PDPH or benign headache any headaches with atypical features. headaches that worsen over time and no longer have a positional nature
Summary In summary, PDPH is usually a self-limited, positional headache that can occur following dural puncture but may be very painful and have a significant impact on a patient’s functional ability. A broad differential diagnosis is critical when evaluating a suspected PDPH as there are many alternative causes, including serious and life-threatening conditions. While there are multiple potential pharmacological treatments, many lack strong evidence to support their efficacy. The SPGB is a newer treatment modality that offers an alternative to an EBP. However, further evidence is required to determine its true efficacy. An EBP remains the most effective treatment for PDPH.
References Van Zundert AAJ, Reina MA, Lee RA. Prevention of post- dural puncture headache (PDPH) in parturients . Contributions from experimental research. Acta Anaesthesiol Scand. 2013;57:947–9. Reina MA, Prats- Galino A, Sola RG, Puigdellívol -Sánchez A, Arriazu Navarro R, De Andrés JA. Structure of the arachnoid layer of the human spinal meninges: a barrier that regulates dural sac permeability. Rev Esp Anestesiol Reanim . 2010;57:486–92. Spanish. Reina MA, López A, Badorrey V, De Andrés JA, Martín S. Duraarachnoid lesions produced by 22 gauge Quincke spinal needles during a lumbar puncture. J Neurol Neurosurg Psychiatry. 2004;75893–7. Reina MA, de Leon- Casasola OA, Lopez A, De Andres J, Martin S, Mora M. An in vitro study of dural lesions produced by 25-gauge Quincke and Whitacre needles evaluated by scanning electron microscopy. Reg Anesth Pain Med. 2000;25:393–402. Dittmann M, Reina MA, López García A. New results in the visualization of the spinal dura mater with scanning electron microscopy. Anaesthesist . 1998;47:409–13. German. Reina MA, Dittmann M, López Garcia A, van Zundert A. New perspectives in the microscopic structure of human dura mater in the dorsolumbar region. Reg Anesth . 1997;22:161–6.