The reported incidence of neurologic deficits in obstetric patients varies widely depending on the source and the complications that are being measured. Many surveys have attempted to assess the incidence of neurologic complications of neuraxial anesthesia, but these surveys share common limitations, including low response rates, lack of control groups that did not receive neuraxial anesthesia, and inaccurate diagnosis ( Box 31.1 ). Moreover, bias is created when more attention is paid to patients who received neuraxial blockade than to those who did not. Some of the more relevant surveys are listed in Table 31.1 . Although each survey is distinct in its population, measurements, and reporting, some generalizations can be made. Most of the neurologic complications in these reports were transient, most occurred in patients who labored, and only a very small minority were attributable to neuraxial anesthesia. Peripheral nerve damage was more common than central cord or plexus damage.

One of these reports from Leeds in the United Kingdom involved 3991 women who delivered in one center in a 1-year period. Twenty-one women who self-reported neurologic symptoms, defined as areas of numbness or motor weakness in the lower extremities, after neuraxial blockade were matched with 21 patients who reported no symptoms after neuraxial blockade and a third group of 21 patients who did not receive neuraxial blockade for delivery and also did not report any neurologic symptoms. Among the women in the first group reporting symptoms, typical peripheral neuropathies occurred among those who delivered vaginally; sacral numbness was most commonly detected after cesarean delivery. All changes were transient, and none could be attributed to neuraxial anesthesia. Interestingly, similar neurologic deficits were detected on physical examination among the groups of patients who did not report symptoms, regardless of whether they had received a neuraxial block or not. These results demonstrate that minor neurologic deficits are frequently found postpartum, if sought, regardless of anesthetic intervention. Permanent or significant neurologic deficits after childbirth are rare with or without the use of neuraxial anesthesia.

A prospective survey among 6057 women who delivered in 1 year in Chicago corroborates the findings of the Leeds study. The incidence of lower limb nerve injuries was approximately 1% (24 lateral femoral cutaneous nerve, 22 femoral nerve, 3 peroneal nerve, 3 lumbosacral plexus, 2 sciatic nerve, 3 obturator nerve, and 5 radicular injuries). Significant risk factors identified by logistic regression analysis included nulliparity and a prolonged second stage of labor but not neuraxial anesthesia.

A national audit of neuraxial blocks from the United Kingdom, without controls, published in 2009, found that the risk for major complications was 6- to 14-fold higher for perioperative than for obstetric procedures. Among the obstetric patients, the risk was highest for combined spinal-epidural (CSE), intermediate for spinal, and lowest for epidural procedures. Finally, the Serious Complication Repository (SCORE) project sponsored by the Society for Obstetric Anesthesia and Perinatology collected data from 30 institutions and more than 250,000 neuraxial blocks in the United States over a 5-year period (2004 to 2009); the incidence of anesthesia-related nerve injury for obstetric patients was approximately 1 in 35,000 deliveries. Four cases of epidural abscess/meningitis and a single case of epidural hematoma were reported.

Several conclusions can be drawn from these surveys. Despite an increased cesarean delivery rate in the past several decades, obstetric palsies still occur. Additionally, the reported frequency of neurologic sequelae depends on how hard one seeks them. The risk for transient mild deficits after childbirth may be quite high. Permanent or persistent injury is extremely rare. A 2006 review, which included some of the previously mentioned surveys, reported an incidence of persistent neurologic injury of four per million. However, a completely accurate figure for anesthetic complications cannot be calculated, even from thorough surveys because (1) the diagnosis is rarely accurate and (2) definitions, severity, and duration are often ill defined. Although we have some reliable data of neurologic complications after neuraxial anesthesia in nonobstetric populations, this cannot accurately extrapolated to the obstetric population due to confounding variables. Table 31.1 demonstrates a variation in the incidence of neurologic sequelae from 1 in 3 for mild symptoms with no neuraxial block to 1 in 250,000 for epidural hematoma.

Compression of the lumbosacral trunk by the fetal head at the pelvic brim ( Fig. 31.3 ) preferentially affects the more medial fibers that make up the peroneal rather than the tibial nerve. In addition to weakness that predominantly affects ankle dorsiflexion (foot drop), compression of the lumbosacral trunk produces sensory disturbance mainly involving the L5 dermatome (see Fig. 31.1 ). This palsy most often results from cephalopelvic disproportion and is therefore typically seen after prolonged labor and difficult vaginal delivery.

The Principal Nerves in the Pelvis.

The lumbosacral trunk (L4 to L5) and obturator nerve (L2 to L4) are vulnerable to pressure as they cross the pelvic brim, particularly in cases of cephalopelvic disproportion. The femoral (L2 to L4) and lateral femoral cutaneous (L2 to L3) nerves are particularly vulnerable in the lithotomy position, where they pass beneath the inguinal ligament.

Modified from Cole JT. Maternal obstetric paralysis. Am J Obstet Gynecol . 1946;52:374.

The obturator nerve is susceptible to compressive injury as it crosses the brim of the pelvis and within the obturator canal (see Fig. 31.3 ). The patient may complain of pain when the damage occurs, followed by weakness of hip adduction and internal rotation, with sensory disturbance over the medial thigh (see Fig. 31.1 ) and may have an abnormal gait secondary to weakness of thigh adduction. Cases are reported after both labor and cesarean delivery ; three of 66 new nerve injuries detected in a prospective study by Wong et al. were obturator nerve injuries. The most likely cause of obturator nerve palsy is compression of the nerve between the pelvis and fetal head or forceps applied to the fetal head.

The femoral nerve does not enter the true pelvis and is therefore not vulnerable to compression by the fetal head but rather is vulnerable to stretch injury as it passes beneath the inguinal ligament. The femoral nerve may be injured proximal to or at the inguinal ligament. Proximal injuries are associated with weakness of hip flexion, whereas more distal injuries spare the motor supply to the iliopsoas muscle. The patient with a femoral neuropathy may walk satisfactorily on a level surface but may be unable to climb stairs; the patellar reflex is diminished or absent. Although the incidence of femoral nerve palsy has decreased because of changes in obstetric management (e.g., fewer deliveries with prolonged second stage), it is still one of the most common obstetric nerve injuries. Approximately one-third of the postpartum palsies detected by Wong et al. were femoral nerve palsies. Dar et al. detected five cases in their small population, although the symptoms were transient. Damage may result from prolonged flexion, abduction, and external rotation of the hips during the second stage of labor and also during procedures conducted in an excessive lithotomy position. To avoid this injury, the hips should never remain continuously flexed during the second stage of labor and position changes or breaks should be encouraged.

Meralgia paresthetica is a neuropathy of the lateral femoral cutaneous nerve, a purely sensory nerve also known as the lateral cutaneous nerve of the thigh. First described more than 100 years ago, meralgia paresthetica is commonly encountered in pregnancy and childbirth. It is the most common nerve injury of pregnancy. The palsy may arise both during pregnancy, typically at about 30 weeks’ gestation, and intrapartum. The distribution is unlike that of a nerve root lesion (see Fig. 31.1 ), yet the disturbance is commonly misattributed to neuraxial blockade. Meralgia paresthetica manifests as numbness, tingling, burning, or other paresthesias affecting the anterolateral aspect of the thigh. The most likely cause is entrapment of the nerve as it passes around the anterior superior iliac spine beneath or through the inguinal ligament, where its vulnerability is increased by a gravid uterus or by retractors used during pelvic surgery. The compressive effect of edema may also contribute. The condition can be expected to resolve after childbirth.

Sciatic nerve palsy arises from compression of the nerve, usually in the buttock. It is not commonly mentioned in surveys or generally recognized as a complication of childbirth, possibly because it is mistaken for a lesion of the lumbosacral trunk. It gives rise to loss of sensation below the knee with sparing of the medial leg, and loss of movement below the knee. Posterior cutaneous nerve and gluteal function are preserved, implying damage distal to the lumbosacral plexus, where the gluteal nerves branch off the sciatic nerve ( Fig. 31.4 ). Three cases out of 66 new nerve injuries were detected by Wong et al. It has occurred during childbirth with neuraxial blockade, either from sitting in one position too long or from a hip wedge misplaced during cesarean delivery. It has also been reported after iliac artery balloon placement for cesarean delivery in a woman with placenta accreta spectrum.

The Sacral Plexus.

The dorsal divisions of the anterior primary rami are shaded.

From Silva M, Mallinson C, Reynolds F. Sciatic nerve palsy following childbirth. Anaesthesia . 1996;51:1144–1148.

The common peroneal nerve is vulnerable to compression as it passes around the head of the fibula below the knee. It is also susceptible to damage while it still forms part of the sciatic nerve as it leaves the pelvis. When the peroneal nerve is damaged at the knee, there is sensory impairment on the anterolateral calf and the dorsum of the foot. Foot drop may be profound, with steppage gait and weak ankle eversion, but plantar flexion and inversion at the ankle are preserved. Peroneal nerve palsy may be caused by prolonged squatting, sometimes popular in “natural childbirth,” by excessive knee flexion for any reason, by compression of the lateral side of the knee against any hard object, even the patient’s hand, by prolonged use of the lithotomy position, and even by tight compression stockings in patients under spinal anesthesia. The incidence of peroneal nerve palsy is lower than that of lateral femoral cutaneous and femoral nerve palsy.

During pregnancy, nerve compression caused by edema may be a factor in the genesis of several peripheral neuropathies, such as carpal tunnel syndrome, Bell’s palsy, and meralgia paresthetica. Neuraxial blockade may indirectly contribute to compression injuries because it may decrease the ability of a woman to perceive that their legs are in a position that contributes to compression-induced neuropathy. Practices that providers should observe to lessen the risk for compression-induced neuropathy are listed in Box 31.2 .

The subject of postdural puncture headache (PDPH) is discussed in detail in Chapter 30 . Other neurologic sequelae of dural puncture include meningitis (see later discussion), cranial nerve palsies, and subdural hematoma. These often present as a headache but are distinct from disorders that should be included in the differential diagnosis for postpartum headache, including tension/stress and migraine headaches, cortical vein and venous sinus thrombosis, preeclampsia, hypertensive encephalopathy, intracerebral or subarachnoid hemorrhage, internal carotid artery dissection, and posterior reversible encephalopathy syndrome. It can be difficult to distinguish PDPH from other serious causes of a headache because signs and symptoms overlap.

Insertion of a spinal needle or epidural catheter may be accompanied by paresthesia that is sometimes painful. However, such a paresthesia is neither sensitive nor specific for nerve injury. If a paresthesia is encountered, advancement of the needle or catheter should be halted. It is generally deemed appropriate to continue spinal or epidural catheter placement after the paresthesia subsides. Continued paresthesias should prompt removal and redirection of the needle. Although a flexible catheter is unlikely to do lasting damage to a nerve root in the epidural space, nerve roots in the subarachnoid space may be more vulnerable.

Trauma Associated With Spinal Anesthesia

Insertion of a spinal needle below the level of the spinal cord sometimes causes brief radiating pain or paresthesia, which may be associated with persistent paresthesia in the same dermatomal distribution. Prolonged symptoms involving more than one spinal segment suggest damage to the spinal cord itself. Damage to the terminal portion of the cord (the conus medullaris) without intracord injection has also been reported in healthy conscious parturients receiving spinal or CSE anesthesia using a pencil-point needle. Typically, the patient complains of pain on needle insertion before any fluid is injected, often followed by the normal appearance of CSF from the needle hub, easy injection of the local anesthetic agent, and a normal onset of neural blockade. On recovery, there is unilateral numbness, which is followed by pain and paresthesia in the L5 to S1 distribution and foot drop, and in some cases urinary symptoms; sensory symptoms may last for months or years. The MRI appearance is one of a small syrinx or hematoma within the conus on the same side as the pain at insertion and subsequent leg symptoms ( Fig. 31.7 ). In most reported cases, the anesthesia provider believed the interspace selected was L2 to L3. In one patient who subsequently died of other causes, hematomyelia was confirmed at autopsy. After a rash of cases of conus damage in the 1990s, increasing awareness of this phenomenon may have led providers to conscientiously choose a lower interspace than they otherwise might have, but an abnormally long cord may still be damaged with the best of techniques.

(A and B) Magnetic resonance images of a conus medullaris lesion (arrows) .

From Reynolds F. Damage to the conus medullaris following spinal anaesthesia. Anaesthesia . 2001;56:238–247.

These injuries may have occurred for the following reasons:

• •

  Identification of lumbar interspaces is far from accurate. Studies showed that it is common to select a space that is higher than assumed by one, two, or even more segments ( Fig. 31.8 ). In a study of 125 obese women, 21% of epidural and intrathecal catheters were unintentionally placed at the L1 to L2 interspace level or above. Even the use of ultrasound did not improve accuracy of level placement.

  

  Identification of Lumbar Interspaces by Oxford Anesthetists.

  The horizontal axis shows the position of the actual interspace identified on magnetic resonance imaging, relative to the assumed space, in 200 observations.

  Data from Broadbent CR, Maxwell WB, Ferrie R, et al. Ability of anaesthetists to identify a marked lumbar interspace. Anaesthesia . 2000;55:1122–1126.

• •

  Although the spinal cord typically ends level with the lower body of L1 or the L1 to L2 interspace, the length varies ( Fig. 31.9 ). From the L1 to L2 interspace, the needle tip can easily reach the conus in 27% of men and 43% of women.

  

  Variation in the level of the tip of the conus medullaris assessed by magnetic resonance imaging of the lumbar spine among 504 consecutive adults. L , Lower third of vertebral body listed; M , middle third of vertebral body listed; T12/L1 , interspace between T12 and L1; U , upper third of vertebral body listed.

  Data derived from Saifuddin A, Burnett SJ, White J. The variation of position of the conus medullaris in an adult population: a magnetic resonance imaging study. Spine . 1998;23:1452–1456.

• •

  The standard method of identifying lumbar interspaces involves the use of Tuffier’s line, the imaginary line joining the two iliac crests. This method can be inaccurate, however, particularly in obese or pregnant women ( Fig. 31.10 ). Moreover, even when accurately assessed, Tuffier’s line is an inconstant landmark. Although typically at the level of the L4 spinous process, it may lie anywhere between the L3 to L4 and L5 to S1 interspaces.

  

  Error that may arise if Tuffier’s line is judged in a pregnant patient in the lateral position, when a line is drawn perpendicularly from the upper iliac crest rather than through both iliac crests. In pregnant patients at term, the hips may have a greater width than the shoulders. The resulting cephalad pelvic tilt may lead to an error in the cephalad direction.

• •

  Pencil-point spinal needles must be advanced further than cutting needles before the orifice is within the subarachnoid space, at which point the tip may impinge on the spinal cord.

Given the inaccuracy of identification of lumbar interspaces and the variability of the position of the conus, it is both logical and prudent to insert a spinal needle into a lower lumbar interspace. Although entry into the intrathecal space is frequently accompanied by a transient paresthesia, injection of spinal medication should not occur if there is a persistent paresthesia or pain with initial injection. Box 31.3 summarizes the problems and precautions in identifying lumbar interspaces and avoiding damage to the conus medullaris. In cases in which there is doubt about the level of lumbar interspace for injection, ultrasound guidance may be useful in accurately identifying the correct interspace.

Box 31.3

Points to Remember to Reduce Risk for Damage to the Conus Medullaris During Spinal Anesthesia

• •

  Tuffier’s line is not in a constant position relative to the spine.

• •

  The interspace chosen is usually higher than supposed.

• •

  The spinal needle should be inserted into a lower lumbar level.

• •

  Advancement of the spinal needle should be halted immediately, and the stylet removed to check for CSF, if entry of the needle tip into the subarachnoid space is suspected.

• •

  The procedure should be abandoned if the patient is unable to cooperate.

  CSF , Cerebrospinal fluid.

Catheters advanced into the intrathecal space theoretically would seem to place patients at risk for traumatic nerve injury. However, a retrospective study of 761 short-term intrathecal catheters placed over a 12-year period found no neurologic or serious complications. Transient paresthesias with catheter placement into the intrathecal space have been reported, but do not appear to be associated with long-term consequences.

Space-occupying lesions of the vertebral canal include intraspinal hematoma (epidural or subdural), epidural abscess, and intraspinal tumors, any of which, within the rigid confines of the bony spinal canal, can cause dangerous compression of nervous tissue and its blood supply. Urgent laminectomy is required to avoid permanent neurologic damage. Delayed recognition and treatment (>8 to 12 hours after onset of symptoms) may have a catastrophic outcome.

Epidural analgesia in labor does not normally behave like a space-occupying lesion and produces no lasting deformation of the thecal sac on MRI. Nevertheless, in the presence of vertebral stenosis or lumbar disc protrusion, a large volume injected into the epidural space may tip the balance and produce signs of nervous tissue compression that normally resolve in a few hours.

The neurologic deficit that may arise from a compressive lesion depends on the vertebral level; lower thoracic lesions are associated with leg weakness or paraplegia, and lumbar lesions with cauda equina syndrome, including urinary retention and incontinence. Back pain (often radiating to the legs) is a common feature.

Neuraxial infection (epidural abscess and meningitis) was identified as the most common cause of neuraxial injury in obstetric cases in the ASA Closed-Claims Project database between 1980 and 1999. Infections that have been reported include epidural abscess, paraspinal and other epidural-related infection, and meningitis.

Epidural Abscess

Frequency

Epidural abscess may occur spontaneously in pregnancy and the puerperium as at other times. An analysis of 915 reports of spinal-epidural abscess published between 1954 and 1997 found that epidural blockade had been performed in only 5.5% of cases. Epidural abscess, like neuraxial hematoma, appears to be rare after neuraxial blockade in obstetric patients. Seven cases were found among 1,462,631 epidural procedures listed in ten surveys summarized in Table 31.1 , a frequency of 0.479 per 100,000. The incidence among general surgical patients has been reported as 10-fold to 100-fold higher, with most cases arising in elderly and immunocompromised patients. A 4-year Australian study of 9482 obstetric patients who underwent childbirth in a center where correct sterile procedures were used found 49 epidural catheter–related infections (0.52%): 45 superficial, 2 epidural, and 2 paraspinal, giving an epidural infection rate of 21 per 100,000, which was 100-fold higher than the calculated frequency from larger, but potentially less sensitive, surveys.

Multiple case reports of epidural abscess after epidural analgesia in obstetric patients illustrate that even when the principal risk factors of prolonged catheterization, suboptimal aseptic technique, and traumatic insertion are avoided, epidural abscess still may occur. A comprehensive review of epidural abscess cases after neuraxial anesthesia found that all cases occurred after epidural catheterization, with three following CSE anesthesia; none followed spinal anesthesia alone.

Risk factors identified from these cases are summarized in Table 31.2 . An epidural abscess typically follows prolonged epidural catheterization, usually between 1 and 4 days in obstetric cases. Other possible etiologic factors are traumatic or difficult insertion of the catheter, and diabetes or immunosuppression from any cause. Inflammation at the epidural catheter entry point may presage epidural space infection. In light of these reports, it may be prudent to avoid epidural catheterization of more than 2 days in the patient with other risk factors for infection.

Table 31.2

Possible Etiologic Factors for Epidural Abscess and Meningitis

	Epidural Abscess	Meningitis
Entry point	Through the epidural catheter or along its track	Via dural puncture
Usual causative organism	Staphylococcus aureus	Streptococcus salivarius
Possible source of infection	Patient’s skin, tracking along the catheter entry point Epidural equipment contaminated by operator’s skin Body fluids in the bed Injectate without racemic local anesthetic	Operator’s mouth Talking without a mask Blood-borne Vagina
Risk factors	Prolonged catheterization Poor aseptic technique Multiple attempts at insertion, traumatic insertion No bacterial filter Lying in a wet, contaminated bed Polyurethane occlusive dressing Immunocompromise: corticosteroids, diabetes, acquired immunodeficiency syndrome	Dural puncture Labor No proceduralist face mask Manual removal of the placenta Vaginal infection Bacteremia Immunocompromise

Clinical presentation

In contrast to epidural hematoma, symptoms of epidural abscess are more insidious. Backache (with local tenderness) and fever, with or without radiating or root pain, are the presenting features. The catheter entry point may be inflamed with some fluid leak, and a hematology screen typically reveals leukocytosis and increased C-reactive protein. Fever, neck stiffness, headache, and signs of inflammation serve to differentiate epidural abscess from hematoma. These signs and symptoms should prompt MRI, which may allow early diagnosis before the onset of neurologic symptoms ( Fig. 31.11 ). If untreated, symptoms may progress to leg weakness, paresthesias, bladder dysfunction, and other evidence of cauda equina syndrome. A blood culture may identify the organism before or without surgical drainage.

Epidural Abscess.

Midsagittal T1-weighted magnetic resonance image of the lumbar and lower thoracic region after intravenous gadolinium-DTPA. Note the dorsal epidural mass located at T12–L1 (arrows) , convex anteriorly but not compressing the conus. Normal epidural fat is flat anteriorly.

From Royakers AA, Willigers H, van der Ven AJ, et al. Catheter-related epidural abscesses—don’t wait for neurological deficits. Acta Anaesthesiol Scand . 2002;46:611–615.

Etiology

Staphylococcus aureus is the most common causative organism in cases of epidural abscess, with the occasional infection with Streptococcus and Pseudomonas species. The skin appears to be the most likely source of infection.

The skin is commonly colonized by Staphylococcus epidermidis and other weakly pathogenic bacteria and occasionally by S. aureus . The highest concentration of colonies is found in hair follicles, where organisms may be protected from poorly applied disinfectants. Infectious organisms from the skin can reach deeper tissue planes via the needle track or an implanted epidural catheter to create a localized abscess in the paraspinal or epidural space. Despite all aseptic precautions, some level of detectable bacterial colonization of the epidural catheter is very common, but robust host defenses normally prevent infection. When defenses are weak and infection containment breaks down, epidural abscess formation begins.

Management

As with spinal hematoma, once neurologic signs are present, early diagnosis with prompt laminectomy is essential to recovery. In the presence of mild symptoms without neurologic changes, successful conservative treatment with antibiotics and successful percutaneous needle drainage of epidural abscesses have also been reported, although only a laminectomy can ensure that all loculations are drained under direct vision. Prompt identification of the infectious organism(s) and directed antibiotic therapy are mandatory. The duration of antibiotic therapy should be determined on a case-by-case basis but is usually 4 to 6 weeks.

Meningitis

Although not consistently included in surveys, post–spinal meningitis has become a cause for concern and is a serious neurologic complication of neuraxial labor analgesia. It was suspected in two cases in the prospective survey of 108,133 epidural procedures and 14,865 spinal anesthetic procedures reported by Scott and Tunstall, although the specific type of anesthesia was not stated. Palot et al. reported three cases of meningitis among 288,351 obstetric epidural procedures but did not state whether they followed dural puncture. One case was identified in a survey of spinal and CSE anesthesia (1/42,000 procedures). A 2008 review found an incidence derived from surveys of spinal and CSE anesthesia in obstetrics of 1 in 39,000. Table 31.3 summarizes 55 published reports of post–spinal meningitis in obstetric patients.

Table 31.3

Case Reports of Post–Dural Puncture Meningitis Among Obstetric Patients

	References	Number of Cases	Organism; Comments
Spinal Analgesia for Labor (11 cases)	Gibbons, 1969	3	Case cluster, no growth, “chemical meningitis,” CSF findings suggested bacterial etiology
	Phillips, 1970	1	No growth, CSF findings suggested bacterial etiology
	Corbett and Rosenstein, 1971	3	Case cluster, single anesthesiologist, unsterile technique, Pseudomonas aeruginosa
	Newton et al., 1994	1	S. salivarius
	Lurie et al., 1999	1	Streptococcus viridans
	Centers for Disease Control and Prevention, 2010 137	2	Case cluster, single anesthesiologist, S. salivarius , one death
Spinal Anesthesia for Cesarean Delivery (24 cases)	Bugedo et al., 1991	1	Signs of bacterial meningitis following cesarean delivery, labor unknown
	Lee and Parry, 1991	1	No growth, CSF findings suggested bacterial etiology, in labor, three attempts at epidural analgesia
	Stallard and Barry, 1995	1	No growth, CSF findings suggested bacterial etiology, in labor, three attempts at epidural analgesia, spinal anesthesia at same interspace
	Donnelly et al., 1998	1	No growth, CSF findings suggested bacterial etiology, membranes ruptured
	Thomas and Cooper, 2001	1	Preeclampsia, labor unknown, patient died
	Rodrigo et al., 2007	6	Aspergillus , five elective cesarean deliveries, one in labor, three patients died
	Celik et al., 2014	1	No growth, CSF findings suggested aseptic meningitis
	Ersoz et al., 2014	12	Serratia marcescens , elective cesarean deliveries, extrinsic vial contamination
Spinal Anesthesia for Retained Placenta (1 case)	Roberts and Petts, 1990	1	Two attempts at spinal anesthesia, no growth, CSF findings suggested bacterial etiology
CSE Analgesia for Labor (9 cases)	Harding et al., 1994	2	No growth, CSF findings suggested bacterial etiology
	Cascio and Heath, 1996	1	S. salivarius (dismissed as contaminant)
	Bouhemad et al., 1998	1	S. salivarius
	Duflo et al., 1998	1	S. viridans
	Vernis et al., 2004	1	One case in the course of a randomized trial
	Centers for Disease Control and Prevention, 2010 137	3	Cluster, single anesthesiologist, S. salivarius
CSE Anesthesia for Cesarean Delivery (1 case)	Gordon et al., 2022	1	CSF-cutaneous fistula, recognized on postoperative day 2
Unintentional Dural Puncture in Labor (3 cases)	Berga and Trierweiler, 1989	1	Streptococcus sanguis
	Sansome et al., 1991	1	No growth, CSF findings ambivalent
	Baer, 2006	1	S. simulans and S. salivarius; patient died
“Uncomplicated” Epidural Analgesia for Labor (6 cases)	Neumark et al., 1980	1	Coxsackievirus B
	Ready and Helfer, 1989	2	1 Streptococcus uberis 1 Streptococcus faecalis (epidural inflammation)
	Davis et al., 1993	1	Group B streptococcus
	Goldstein et al., 1996	1	Group B streptococcus
	Choy, 2000	1	Two attempts at epidural analgesia, no growth, CSF findings suggested bacterial etiology, patient died
Total (55 cases)	49 known dural punctures 18 elective cesarean deliveries, all with extrinsic contamination of medication or equipment 7 deaths

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