PDPH – Post Dural Puncture Headache

Post dural puncture headache

Spinal anaesthesia developed in the late 1800s with the work of Wynter, Quincke and Corning. However, it was the German surgeon, Karl August Bier in 1898, who probably gave the first spinal anaesthetic. Bier also gained first‐hand experience of the disabling headache related to dural puncture. He correctly surmised that the headache was related to excessive loss of cerebrospinal fluid (CSF). In the last 50 yr, the development of fine‐gauge spinal needles and needle tip modification, has enabled a significant reduction in the incidence of post‐dural puncture headache. Though it is clear that reducing the size of the dural perforation reduces the loss of CSF, there are many areas regarding the pathogenesis, treatment and prevention of post‐dural puncture headache that remain contentious.1

PDPH Presentation

A Video on PDPH and epidural patch (Dr Barbara M Scavone)

PDF Articles on PDPH

International Journal of pain and palliative medicine

Dr PF Kotur’s Article in IJA

St George’s Hospital London Guidelines for PDPH

Dr James Bates Iowa

BJA Article

A very nice tutorial for PG students

Sciatic Nerve Block

Relevant Anatomy for Sciatic Nerve Block

Sciatic Nerve begins in the lower back and runs through the buttock and down the lower limb. It is the longest and widest single nerve in the human body, going from the top of the leg to the foot on the posterior aspect. The sciatic nerve supplies nearly the whole of the skin of the leg, the muscles of the back of the thigh, and those of the leg and foot. It is derived from spinal nerves L4 through S3. It contains fibres from both the anterior and posterior divisions of the lumbosacral plexus. The sciatic nerve is formed from the L4 to S3 segments of the sacral plexus, a collection of nerve fibres that emerge from the sacral part of the spinal cord. The fibres unite to form a single nerve in front of the piriformis muscle. The nerve passes beneath the piriformis and through the greater sciatic foramen, exiting the pelvis. From here, it travels down the posterior thigh to the popliteal fossa. The nerve travels in the posterior compartment of the thigh behind the adductor magnus muscle, and is itself in front of the one head of the biceps femoris muscle. At some point between the pelvis and popliteal fossa, the nerve divides into its two branches

  • The tibial nerve, which travels down the posterior compartment of the leg into the foot.
  • The common peroneal nerve, which travels down the anterior and lateral compartment of the leg into the foot.

The sciatic nerve is the largest nerve in the human body.

The sciatic nerve innervates the skin of the foot, as well as the entire lower leg (except for its medial side). The skin to the sole of the foot is provided by the tibial nerve, and the lower leg and upper surface of the foot via the common fibular nerve. The sciatic nerve also innervates muscles. In particular:

  • Via the tibial nerve, the muscles in the posterior compartment of the leg and sole of the foot.
  • Via the common fibular nerve, the muscles in the anterior and lateral compartments of the leg

Lumbar Plexus – Structure and Branches – Anatomy

Sciatic nerve block anatomy and approaches PDF

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Single Injection Subgluteal Sciatic Nerve Block

Tips for Sciatic Nerve Block

• A pillow may be placed between the legs at the level of the knee.

• Appropriate positioning is critical to establish the proper site for the introduction of the needle.

• Already at this level, the sciatic nerve is separated into the common peroneal and the tibial nerves, and the posterior femoral cutaneous nerve of the thigh has branched.

• The stimulation of the sciatic nerve is almost always preceded by the stimulation of the gluteus maximus.

• A bone contact usually indicates that the needle is too lateral.

• Stimulation of the piriformis muscle indicates that the needle is too cephalad.

• A motor response at the level of the toes increases the likelihood of success.

• When patients complain of pelvic discomfort, it suggests that the needle is too anterior and is going through the greater sciatic notch.

• Because the sciatic nerve is found at a depth of 8 to 13 cm, no redirection of the needle should be attempted after it passes the skin to avoid bending the needle.

• This approach can be uncomfortable for the patient and therefore requires appropriate local anesthesia with a 38-mm needle and an appropriate sedation.

• This approach is not recommended in anticoagulated patients.

• A new posterior approach has been described in adults: The patient is positioned either prone or in the lateral position. The site of introduction of the needle is 10 cm lateral from the midpoint of the intergluteal sulcus.

Nysora Article on Sciatic Nerve block anterior approach

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Continuous Sciatic Nerve Block

Continuous Sciatic nerve block article andre boezart NYSORA


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NYSORA Article on Sciatic Nerve block both approaches

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USG Guided anterior and posterior approach explained in great detail

Anterior Approach Posterior Approach

More Articles on Regional Anesthesia

Femoral Nerve Block – Landmarks, Technique and Videos

Femoral Nerve Blocks

Before learning Femoral Nerve Block, one has to first understand the relevant anatomy. The femoral nerve, the largest branch of the lumbar plexus, arises from the dorsal divisions of the ventral rami of the second, third, and fourth lumbar nerves (L2-L4). It descends through the fibers of the psoas major muscle, emerging from the muscle at the lower part of its lateral border, and passes down between it and the iliacus muscle, behind the iliac fascia; it then runs beneath the inguinal ligament, into the thigh, and splits into an anterior and a posterior division. Under the inguinal ligament, it is separated from the femoral artery by a portion of the psoas major.

Anatomy of Femoral Triangle

Nerve Supply Of Lower Limb


Patient position: Supine.


  • Femoral Nerve Block Landmarks
    Femoral Nerve block Landmark


  • Line between ASIS and pubic tubercle (PT).
  • Parallel line at the inguinal crease.
  • 1 cm lateral to the femoral artery pulse.

Video Showing Landmark Based Nerve Stimulator Approach


  • If the femoral artery pulse cannot be felt, the puncture point will be approximately 1 cm lateral to a point located 5 cm caudally on a perpendicular line at the midpoint of the line ASIS-PT.
  • A contraction of the vastus medialis indicates a medial and anterior approach of the nerve.
  • To obtain a contraction of the vastus intermedius (upward movement of the patella), the needle is directed posterior and laterally.
  • Single stimulation = the total dose of local anesthetic is injected when contraction of the vastus intermedius is elicited.
  • Multistimulation = injections of 5 to 7 mL local anesthetic, respectively, when a contraction of the vastus medialis, vastus intermedius, and vastus lateralis is elicited.
  • Distal pressure and large volume can procure a 3-in-1 block (the obturator nerve is missed most of the time).
  • For surgeries below the knee, a saphenous nerve block can be obtained when a vastus medialis contraction is elicited.
  • A catheter can be inserted for a continuous femoral block.

NYSORA Article on Femoral Nerve Block

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NYSORA Video of USG Guided Femoral Nerve Block

SONOSITE video of USG Guided Femoral Nerve Block


Also read ASRA Guides for Anticoagulation before Anesthesia

ASRA Guidelines
ASRA Guidelines Anticoagulation

Regional Anesthesia in a patient recieveing Anticoagulants – ASRA Guidelines

This is a collection of articles and guidelines from various online sources. If  you find it violating copyright laws then please inform and we shall remove it.

Regional Anesthesia in the Anticoagulated Patient

This article is taken from NYSORA website. Original article here . http://bit.ly/1o0RLBA

Intraspinal Hematoma

The incidence of intraspinal hematoma is approximately 0.1 per 100,000 patients per year.(1) It is more likely to occur in anticoagulated or thrombocytopenic patients, patients with neoplastic disease, or in those with liver disease or alcoholism.(2) The incidence of neurologic dysfunction resulting from hemorrhagic complications associated with neuraxial blockade is estimated to be

Antiplatelet Therapy

Antiplatelet medications inhibit platelet cyclo-oxygenase and prevent the synthesis of thromboxane A2. Thromboxane A2 is a potent vasoconstrictor and facilitates secondary platelet aggregation and release reactions. An adequate, although potentially fragile, clot may form.(5) Platelet function in patients receiving antiplatelet medications should be assumed to be decreased for 1 week after treatment with aspirin and 1 to 3 days with nonsteroidal anti-inflammatory drugs (NSAIDs). New platelets are produced every day, and these new platelets partly explain the relative safety of per- forming neuraxial procedures in these patients.

Although Vandermeulen et al (6) implicated antiplatelet therapy in 3 of the 61 cases of spinal hematoma occurring after spinal or epidural anesthesia, the results of several large studies demonstrated the relative safety of neuraxial blockade in combination with antiplatelet therapy. The Collaborative Low-Dose Aspirin Study in Pregnancy Group(7) included 1422 high-risk obstetric patients who were administered 60 mg aspirin daily and underwent epidural anesthesia without any neurologic sequelae. The studies of Horlocker et al,(8,9) of approximately 1000 patients in each study, showed no spinal hematomas, although blood was noted during needle or catheter placement in 22% of the patients. A later study in patients who were on NSAIDs and underwent epidural steroid injections did not develop the signs and symptoms of intraspinal hematoma.(10) A review of the case reports of intraspinal hematoma in patients on aspirin and NSAIDs showed complicating factors that in luded concomitant heparin administration, epidural venous angioma, and technical difficulty when performing the procedure.(11)

The thienopyridine drugs, ticlopidine and clopidogrel, prevent platelet aggregation by inhibiting adenosine diphosphate (ADP) receptor-mediated platelet activation. Ticlopidine is rarely used because it causes neutropenia, thrombocytopenic purpura, and hypercholesterolemia. Clopidogrel is preferred because of its increased safety profile and proven efficacy. The maximal inhibition of ADP-induced platelet aggregation with clopidogrel occurs 3 to 5 days after the initiation of a standard dose (75 mg), but within 4 to 6 hours after the administration of a large loading dose of 300 to 600 mg.(12) There is a case report of spinal hematoma in a patient on ticlopidine(13) and a case of quadriplegia in a patient on clopidogrel, diclofenac, and possibly aspirin.(14)

Neuraxial blocks can be safely performed on patients taking aspirin or NSAIDs.(4) It is safe to perform neuraxial blocks on patients taking cyclo-oxygenase (COX)-2 inhibitors. For the thienopyridine drugs, it is recommended that clopidogrel be discontinued for 7 days and ticlopidine for 10 to 14 days before a neuraxial injection. It is possible for epidural catheters to be removed or neuraxial injections to be performed 5 days, and not 7 days, after clopidogrel is discontinued.(15) If a neuraxial injection is to be performed in a patient on clopidogrel before 7 days of discontinuation, a P2Y12 assay, a new assay of residual antiplatelet activity, can be performed;

Here is a summary of current recommendations:

1. Neuraxial blocks can be performed on patients taking aspirin or NSAIDs.(4)

2. It is safe to perform neuraxial blocks on patients taking COX-2 inhibitors.

3. For the thienopyridine drugs, the ASRA recommendation is that clopidogrel be discontinued for 7 days and     ticlopidine for 10 to 14 days before a neuraxial injection.

4. Epidural catheters can be removed safely and neuraxial injections can be performed 5 days (not 7 days, as once     advised) after clopidogrel is discontinued.(15)

5. If a neuraxial injection is to be performed in a patient on clopidogrel before 7 days of discontinuation, a P2Y12    assay, a new assay of residual antiplatelet activity, is performed;

Oral Anticoagulants

Warfarin exerts its anticoagulant effect by interfering with the synthesis of the vitamin K-dependent clotting factors (VII, IX, X, and thrombin).17 It also inhibits the anticoagulants protein C and S. Factor VII and protein C have short half-lives (6-8 hours), and the prolongation of the international normalized ratio (INR) during the early phase of warfarin therapy is the result of the competing effects of reduced factor VII and protein C.(18) Adequate anticoagulation is not achieved until the levels of biologically active factors II (half-life of 50 hours) and X are sufficiently depressed, that is, 4 to 6 days.

Few data exist regarding the risk of spinal hematoma in patients with indwelling spinal or epidural catheters who are subsequently anticoagulated with warfarin. Horlocker et al(19) and Wu and Perkins(20) found no neuraxial hemorrhagic complications in patients who received postoperative epidural analgesia in conjunction with low-dose warfarin after total knee arthroplasty. Because intraspinal hematomas have occurred after removal of the catheter,(6) some have recommended that the same laboratory values apply to placement and removal of an epidural catheter.(21) The current ASRA guidelines recommends an INR value of ≤1.4 as acceptable for the performance of neuraxial blocks.(4) The value was based on studies that showed excellent perioperative hemostasis when the INR value was ≤1.5. The concurrent use of other medications, such as aspirin, NSAIDs, and heparins that affect the clotting mechanism, increases the risk of bleeding complications without affecting the INR.

A controversy exists regarding whether or not the epidural catheter can be removed on postoperative day 1, or 12-14 hours after warfarin is started, when the INR is >1.4. In the absence of other risk factors for increased bleeding, the catheter can probably be removed. The factor VII activity should be determined if risk factors such as low platelets, advanced age, kidney failure, or intake of other anticoagulants are present.(18)

Warfarin is metabolized primarily by the CYP2C9 enzyme of the cytochrome P450 system. Mutations in the gene coding for the cytochrome P450 2C9 hepatic microsomal enzyme affect the elimination clearance of warfarin by impairing the patient’s ability to metabolize S-warfarin. Other genetic factors affecting the warfarin dose-response relationship include polymorphisms of the vitamin K oxide reductase (VKOR) enzyme. Mutations in the gene encoding for isoforms of the protein that can lead to enzymes with varied sensitivities to warfarin is rare, and the American College of Chest Physicians (ACCP) advises against pharmacokinetic-based initial dosing of warfarin at this time.(17)

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