General Indications

The indications for spinal puncture have been reduced with the introduction of noninvasive diagnostic procedures—magnetic resonance imaging (MRI) and computed tomography (CT). A few clinical situations require early or even emergency spinal puncture. The primary indication for an emergency spinal tap is the possibility of central nervous system (CNS) infection (meningitis), with the exception of a suspected brain abscess or a parameningeal process. The need for early detection of meningitis results in the performance of many more lumbar punctures than ultimate diagnoses of infection.⁵ No other method can be used to completely exclude meningitis.

The mere presence of a fever does not mandate lumbar puncture. However, CSF should generally be examined for evidence of infection in patients with a fever of unknown origin, especially if consciousness is altered or the immune system is impaired, even in the absence of meningeal irritation. Meningeal signs may not be present in patients who are old, debilitated, or immunosuppressed; are receiving antiinflammatory drugs; or have had partial treatment with antibiotics.6,7 In a newborn, even a fever is not a dependable sign because temperatures may be normal or even subnormal. For infants younger than 1 year, a high index of suspicion is required to make the diagnosis of meningitis.

Approximately 25% of infants with meningitis will not have nuchal rigidity, but many appear toxic or moribund. A tense and bulging fontanelle is somewhat more reliable, although this sign may be absent in a dehydrated child. Neonatal meningitis occurs in 25% of sepsis cases. In addition, 15% to 20% of infants with meningitis have negative blood cultures.8,9 In a child between the ages of 1 month and 3 years, fever, irritability, and vomiting are the most common signs of meningitis. Typically, handling is painful for the child, and the child cannot be comforted. In addition, an older child may complain of a headache. At all ages, patients generally appear ill and drowsy with a dulled sensorium. Physical signs become more useful in diagnosing meningitis in children older than 3 years¹⁰ and include nuchal rigidity, Kernig’s sign (effort to extend the knee is resisted), and Brudzinski’s sign (passive flexion of one hip causes the other leg to rise, and effort to flex the neck makes the knees come up). The jolt accentuation test is a more sensitive sign of meningeal irritation.¹¹ This test is considered positive when the patient’s pain is exacerbated by lateral rotation of the head to either side. A petechial rash in a febrile patient should also raise suspicion for Neisseria meningitis.¹² Previous use of antimicrobial agents may modify the clinical and CSF findings; partially treated children are less likely to be febrile or exhibit an altered mental status. In addition, patients in the early stages of meningitis may lack the classic features associated with advanced disease.

The second indication for emergency spinal puncture is suspected spontaneous subarachnoid hemorrhage (SAH). The diagnosis is usually made by imaging (head CT) or by the direct finding of blood in CSF obtained by spinal puncture.13,14 The sensitivity of CT has been estimated to be as high as 95% soon after hemorrhage, but it drops in patients evaluated later than 24 hours after the event to 76% after 48 hours and to about 50% at 1 week. Before a major hemorrhage, 20% to 60% of patients with aneurysmal SAH have had a “sentinel thunderclap” or “warning leak” headache (i.e., an unusual sudden headache caused by a “minor” leak of blood from the aneurysm). The headache may precede a major rupture by hours to months. The goal of early clinical recognition is surgical or other interventional therapy before a recurrent major hemorrhage. After a warning leak, head CT is more likely to be negative, thus giving added importance to the performance of a lumbar puncture. Migraine or “vascular” headache is a common misdiagnosis in patients with SAH who initially have negative findings on head CT.

The usual clinical picture of SAH is an instantaneous excruciating headache. Patients generally recall the exact moment that the headache occurred. The location of the headache is variable and does not necessarily indicate the site of hemorrhage. Nausea, vomiting, and prostration are common symptoms, with approximately one third of patients becoming unconscious at the onset. Examination reveals an acutely ill patient with irritability or overt altered mental status. Meningeal signs are commonly present at the time of initial examination and usually develop within 2 to 3 days. The meningeal signs may become more severe during the first week after hemorrhage and correspond to the breakdown of blood in CSF. During the first week many patients are febrile, a reflection of chemical hemic meningitis.¹⁵ Failure to detect blood radiographically in an awake patient may indicate a small hemorrhage or a predominant basal accumulation of blood. If a patient is initially seen several days after the hemorrhage, the blood may have become isodense with brain tissue and may no longer be visible on CT. The proper diagnosis would then require spinal puncture.

Newer CT scanners detect recent SAH quite accurately.¹⁶ However, because acute SAH is not detected by the initial CT scan in at least 2% to 5% of all patients, lumbar puncture is appropriate to rule out the diagnosis with certainty.^17–19 If the neurologic picture demonstrates localizing findings, the presence of a large intracranial hematoma should be suspected, and spinal puncture is contraindicated until imaging studies delineate the nature of the lesion.

Other nonemergent reasons for examination of CSF include evaluation for CNS syphilis or unexplained seizures, instillation of chemotherapy and contrast agents, assessment for a suspected demyelinating or inflammatory CNS process, and treatment of headache from SAH. Carcinomatous meningitis and suspected spinal cord compression from metastatic disease may require spinal puncture for myelography and cytologic examination. MRI is a suitable alternative for identifying compressive myelopathy and has largely replaced contrast-enhanced myelography in developed countries.

IIH (Pseudotumor Cerebri)

Idiopathic intracranial hypertension (IIH) is a rare condition of unclear etiology. Patients with IIH have a marked elevation in intracranial pressure (ICP; usually to 250 to 450 cm H₂O) without hydrocephalus or mass lesions in the setting of normal CSF composition. Findings on neuroimaging studies are typically normal, and most cases are idiopathic. Because of the nonspecific signs and symptoms, many cases initially escape detection by clinicians. IIH has been associated with hypervitaminosis A, tetracycline, estrogen therapy, and a plethora of other conditions such as sarcoidosis, tuberculosis, and carcinomatosis. Because of the nonspecific findings, many cases initially escape detection by clinicians. IIH is most common in obese adolescent girls and young women, but it can also occur in children and men. Patients suffer from chronic headaches, typically worse with maneuvers that increase ICP (e.g., Valsalva maneuver, squatting, bending, coughing). Papilledema is frequently present. Cranial nerve palsies, particularly of the sixth cranial nerve, are due to increased ICP alone and may be falsely localizing.²⁰

IIH may regress spontaneously after a few months. The major concern is visual loss, which may be permanent. The diagnosis can be made only by lumbar puncture performed after neuroimaging. This condition underscores the need to measure opening pressure during lumbar puncture whenever possible. Many cases can be controlled with medication, but occasionally, lumbar puncture is required to lower ICP. One way to lower ICP in the ED is to drain CSF via lumbar puncture by removing 5- to 10-mL aliquots of CSF and checking ICP after each removal until a pressure lower than 200 mm H₂O is achieved. Herniation does not occur despite the elevated pressure in IIH, probably because ICP is uniform in all CNS compartments. Since spinal fluid is regenerated rapidly, the procedure may need to be repeated every few days to keep CSF pressure at this level. Analysis of CSF should demonstrate all parameters to be normal. Drug therapy, in the form of acetazolamide, glycerol, diuretics, or corticosteroids, has been advocated and may negate the need for repeated lumbar puncture. Resistant cases may require shunting procedures.

Lateral Approach for Lumbar Puncture

The supraspinal ligament might be calcified in older persons, thus making a midline perforation difficult. A calcified ligament may deflect the needle. In this case, use a slightly lateral approach. Because the lower lamina rises upward from the midline, direct the needle slightly cephalad to miss the lamina and slightly medially to compensate for the lateral approach. The needle passes through the skin, superficial fascia, fat, the dense posterior layer of the thoracolumbar fascia, and the erector spinae muscles. The needle then penetrates the ligamentum flavum (bypassing the supraspinal and interspinal ligaments), the epidural space, and the dura before CSF is obtained (Fig. 60-12). Lateral cervical puncture is an alternative approach that can be performed utilizing an insertion site 1 cm inferior and 1 cm dorsal to the mastoid process.³⁹

Lumbar Puncture in Infants

Lumbar puncture in infants is usually performed to exclude meningitis or encephalitis. The sitting position may allow the midline to be identified more easily. Use of a needle without a stylet has been suggested for small infants because this device allows the pressure to be estimated as the needle punctures the dura.⁴⁰ However, failure to use a stylet may cause the subsequent development of an intraspinal epidermoid tumor.⁴¹ Use of a butterfly infusion set needle simplifies the procedure, which is helpful when managing a squirming or hyperactive patient.⁴⁰ In general, a stylet is recommended primarily at the time of skin penetration and on needle withdrawal, although many operators use the stylet during any advancement of the needle.

If the child’s neck is very tightly flexed, CSF might not be obtained. However, if the head is held in midflexion, CSF usually flows briskly. If CSF fails to flow, gently suction with a 1.0-mL syringe to exclude a low-pressure syndrome. Because pressure readings are inaccurate in a struggling child, measurement of pressure is not commonly attempted in infants and young children.⁴²

Avoid prolonged severe flexion of the neck in an infant because it may produce dangerous airway obstruction. If the infant suddenly stops crying, check the airway immediately.⁴³ Proper positioning is best accomplished by an assistant, who maintains the spine maximally flexed by partially overlying the child and using the chest and body weight to immobilize the thorax and hips while holding the child behind the shoulders and knees.⁴⁴ Infants have poor neck control; therefore, the assistant must also ensure that the child maintains an open airway. Pay particular attention to avoiding marked neck and trunk flexion. Incorrect positioning usually results in multiple punctures and a bloody tap.

Newborn and preterm infants may experience significant hypoxia and clinical deterioration during lumbar puncture; a sitting position appears to be preferable.⁴⁵ Lumbar puncture in infants with respiratory distress syndrome may pose greater risk than benefit.⁴⁶ This is a problem primarily in neonates but may also apply to younger infants with sepsis. Closely monitor all infants with serious cardiopulmonary disease during the procedure. Preoxygenation with or without monitoring oxygen saturation may be used as a precaution.

Although local anesthesia or sedation has not been a routine practice during lumbar puncture in an infant or child, it is being reconsidered.47,48 Neonates perceive pain, and local anesthesia neither produces physiologic instability nor makes the procedure more difficult.^49,50 The use of topically applied EMLA (eutectic mixture of local anesthetics) (AstraZeneca) reduces the pain associated with needle insertion in newborns.⁵¹ Sedation of an anxious child may be considered, but sedatives are relatively contraindicated in an obtunded patient without a protected airway and in the setting of hemodynamic instability.

The Difficult Lumbar Puncture

The traditional approach to lumbar puncture depends on palpation of bony landmarks to determine the correct location for insertion of the needle. However, landmarks are difficult to palpate in overweight and obese patients.⁵² When lumbar puncture fails, the usual alternative has been fluoroscopic guidance, which necessitates movement of the patient out of the ED, as well as the availability of an appropriately trained radiologist.⁵² Bedside ultrasound is increasing being used in emergency and critical care medicine, and its scope of practice has expanded to include guidance for a number of procedures, including lumbar puncture (see Ultrasound Box).^53–56 Ultrasound can be used in adults, as well as in neonates and infants.⁵⁷

Headache after Lumbar Puncture

A number of complications from lumbar puncture have been reported.⁵⁸ One of the most common is headache, which occurs after 1% to 70% of spinal taps.^59–66 In general, the development of postpuncture headache can be neither prognosticated nor prevented. The syndrome most commonly starts within the first 48 hours after the procedure (although a case occurring 12 days after the procedure has been reported)⁶⁷ and usually lasts for 1 to 2 days (occasionally as long as 14 days). Cases lasting months have been described. The headache usually begins within minutes after the patient arises and characteristically ceases as soon as the patient lies down. The pain is mild to incapacitating and is generally cervical and suboccipital in location but might involve the shoulders and the entire cranium. Exceptional cases include nausea, vomiting, vertigo, blurred vision, ear pressure, tinnitus, and stiff neck. The headache may change to a positional backache or neck ache.

The technique of spinal puncture probably has little to do with the development of a postprocedure headache. The syndrome is widely thought to be caused by leakage of fluid through the dural puncture site. This results in a reduction in CSF volume below the cisterna magna and downward movement of brain tissue, along with displacement and stretching of pain-sensitive structures such as the meninges and vessels, and causes a traction headache. The recumbent position brings relief because the weight of the brain is shifted cephalad. Another proposed mechanism is cerebral vasodilation. A more recent hypothesis suggests that the headache is caused by an altered distribution of craniospinal elasticity and acute intracranial venous dilation.⁶⁸ Some authors have commented on the incidence and severity of post–dural puncture headache as being related to the orientation of the spinal needle bevel and its type and size.^69–79 It is clear that the incidence of post–dural puncture headache is lower when the bevel of the needle is oriented parallel to the longitudinal axis of the spine. Until relatively recently the explanation for this was that the parallel bevel would separate rather than cut the longitudinal dural fibers and thus produce a smaller dural hole and less CSF leakage. However, it is now known that the dural fibers are oriented randomly, not longitudinally.⁸⁰ Even with random fiber orientation, back flexion is more likely to close a dural hole in the longitudinal plane than a hole in the horizontal plane.

The two basic types of spinal needles are cutting (Quincke) and noncutting or pencil point (Sprotte and Whitacre). Noncutting needles cause a lower incidence of headache after dural puncture, perhaps because the tip of the needle tends to separate rather than cut the dural fibers. It has traditionally been thought that the dural hole resulting from puncture with a noncutting needle is smaller than that created by puncture with a cutting needle; however, this may not be true. The important difference may be that the cutting needle causes a clean-cut opening in the dura whereas the noncutting needle produces a jagged opening with rough edges.⁸¹ The jagged opening may produce a more intense inflammatory response that results in edema and more complete closure of the hole. The use of atraumatic spinal needles is not routine.⁸² As more spinal kit manufacturers include them in kits, their use might increase.⁸³ A single-institution study suggested that routine use of noncutting needles yields a potential cost savings.⁸⁴ However, in thick-skinned individuals, passage of a thin, noncutting needle may be technically difficult. Making the initial pass with a thicker cutting needle to the level of the interspinal ligament, followed by removal and advancement of a noncutting needle in the same soft tissue tract, can be helpful.

Use of a smaller-diameter needle is one intervention that will probably cause a lower incidence of postpuncture headache because it creates a smaller dural hole. If diameter were the only consideration, as small a needle as possible would be used. However, a needle must provide adequate CSF flow rates to allow timely CSF collection and pressure measurement. With a very small needle, a syringe may be needed to withdraw fluid, and pressure cannot be recorded easily. In addition, technically, a small needle such as a 26 gauge is difficult to place and manipulate into a position in which it does not become intermittently obstructed by nerve roots. When these characteristics are considered, a 20- to 22-gauge atraumatic needle seems to be the best overall choice for diagnostic lumbar puncture.⁷²

Despite common beliefs about techniques and postprocedure interventions, lumbar puncture headaches may not be completely preventable. Studies of the influence of directives such as strict bed rest on postpuncture headache have yielded contradictory results, with no consensus on any specific preventive intervention forthcoming concerning the worsening of, improvement in, or effect on the incidence. Brocker reported a reduction in the incidence of headache from 36.5% to 0.5% when patients lie prone instead of supine for 3 hours after puncture with an 18-gauge needle.⁸⁵ He postulated that the prone position caused hyperextension of the spine and disrupted alignment of the holes in the dura and the arachnoid, thus making leakage less likely. Thoennissen and coworkers concluded that there was no evidence that longer bed rest after lumbar puncture was better than immediate mobilization or short bed rest in reducing the incidence of headache.⁸⁶ There appears to be no reason to enforce bed rest following lumbar puncture.

Other factors that might influence the incidence of a post–spinal puncture headache were reviewed by Fishman and by Lin and Giederman.21,87 The incidence is higher in young patients than in older patients and is also increased in females and individuals with a history of headache. Many medications have been advocated for the treatment of headache after lumbar puncture: barbiturates, codeine, neostigmine, ergots, diphenhydramine (Benadryl), dimenhydrinate (Dramamine), caffeine, amphetamine sulfate (Benzedrine), ephedrine, intravenous fluids (normal saline, lactated Ringer’s solution), magnesium sulfate, and vitamins.^21,88–90

Caffeine is a traditional common initial intervention for postpuncture headache, and it appears to be of benefit.⁹⁰ Caffeine can be administered in the ED, and pain relief can be seen within a few hours and is thought to result from caffeine’s vasoconstrictive effect on the cerebral vasculature. One suggested regimen is 500 mg of caffeine (sodium benzoate) diluted in 1000 mL of normal saline infused over a 1- to 2-hour period. A second dose can be given if the headache is not relieved. If successful, consumption of caffeinated beverages may be continued as an outpatient.

Most postpuncture headaches can be managed by bed rest with the head in the horizontal position. Avoid dehydration because it lowers CSF pressure and might aggravate the headache. Although dehydration should be avoided, the role of fluid supplementation in the prevention of post–dural puncture headache remains uncertain.

Simple analgesics are commonly prescribed, but they have no apparent advantage over bed rest and fluid intake. A patient with a prolonged headache after spinal puncture should be reassessed to rule out structural causes. Because a spinal headache has classic signs and symptoms, if the headache is not postural, consider other causes.

In summary, because most post–lumbar puncture headaches are mild and self-limited, conservative therapy for the first 24 to 48 hours is recommended. Bed rest and oral analgesics, including opioids, are usually effective, as well as perhaps oral caffeine drinks, but for those refractory to conservative measures, an epidural blood patch is recommended.

For patients with a prolonged low-pressure headache, placement of an epidural blood patch by experienced operators is highly successful and often provides dramatic relief.91–95 Consider a blood patch for all patients with seriously symptomatic spinal headaches. Perform an epidural tap at the level of the previous lumbar puncture. Use the loss-of-resistance technique with sterile saline to locate the epidural space.⁹⁶ Draw 10 to 20 mL of autologous blood into a syringe aseptically and slowly inject it (1 to 2 mL every 10 seconds) into the epidural space at the site of the dural puncture.⁹⁷ Slow or discontinue the injection if back pain or paresthesia develops. Keep the patient supine for 1 hour while hydration is administered intravenously. Relief usually occurs within 20 to 30 minutes after the procedure. Epidural patches are less likely to be effective if symptoms have been present for more than 2 weeks. Pain is relieved when the blood patch forms a gelatinous tamponade that stops the CSF leak and immediately elevates CSF pressure. Patch failures (15% to 20%) are believed to be caused by improper needle placement, injection of an inadequate quantity of blood (after which a second patch is usually successful), or an incorrect diagnosis.

Complications reported after placement of an epidural patch include back stiffness, paresthesia, radicular pain, subdural hematoma, adhesive arachnoiditis, and bacterial meningitis.⁹⁸ The procedure should be used in patients with refractory headaches that do not respond to conservative therapy, and it should be performed by clinicians trained in the procedure.

Infection

Spinal puncture is contraindicated in the presence of local infection at the puncture site (cellulitis, suspected epidural abscess, or furunculosis) because of the danger of inducing meningitis. A large concentration of bacteria in the bloodstream at the time of CSF examination is associated with meningitis. The meningitis could be coincidental (“spontaneous”) or could result from leakage of blood containing bacteria into the subarachnoid space after lumbar puncture (“induced”). It is likely that many cases of puncture-induced meningitis emerge after a cautious clinician performs a lumbar puncture early in the course of meningitis, before the infection has had time to be reflected in CSF. A recent review concluded that the majority of cases of postpuncture meningitis are probably caused by contamination of the site with aerosolized bacteria from medical personnel, contamination from skin flora, or least commonly, direct or hematogenous spread from an endogenous infectious site.³⁷ Suspected bacteremia is not a contraindication to lumbar puncture. Delay in diagnosis because of concern regarding the risks associated with lumbar puncture is probably more serious than the risk of causing meningitis with the procedure.^99,100

Herniation Syndromes after Lumbar Puncture

Lumbar puncture is of value in confirming a diagnosis of meningitis, encephalitis, or SAH. Generally, when the patient has symptoms consistent with bacterial meningitis but not increased ICP, it is safe to perform lumbar puncture before a head CT scan. Lumbar puncture may also be the best initial procedure to diagnose SAH, thus reducing the need for routine CT scanning in certain low-risk patients with acute sudden headache.¹⁰¹ However, in patients with focal findings, papilledema, or a suspected intracranial mass lesion, one should perform a CT scan before lumbar puncture. When meningitis remains in the differential diagnosis, antibiotics are best administered after blood is obtained for culture and before the CT scan.

Particularly in patients with supratentorial masses, there may be a large pressure gradient between the cranial and lumbar compartments. When brain volume is increased because of a mass or edema, rostrocaudal displacement may occur after lumbar puncture if the skull is intact.

The question of whether lumbar puncture precipitates brain herniation in cases in which herniation would not have occurred spontaneously cannot be answered with certainty. Controversy still exists regarding the risk for brain herniation from lumbar puncture in patients with acute bacterial meningitis, and data continue to be sparse.¹⁰² Herniation may occur in the absence of lumbar puncture in the setting of acute bacterial meningitis and has been temporally related to the procedure. Brain herniation occurs in about 5% of patients with acute bacterial meningitis and accounts for about 30% of the deaths associated with the disease.¹⁰² Although CT imaging may reveal contraindications to lumbar puncture, normal findings on CT do not eliminate the risk for herniation and do not necessarily mean that a lumbar puncture is safe.

Lowering pressure in the lumbar spinal canal by removing CSF can increase the gradient between the cranial and lumbar compartments and thereby theoretically promote both transtentorial and foramen magnum (cerebellar) herniation. The frequency with which lumbar puncture causes or accelerates transtentorial herniation is unknown because herniation might have developed spontaneously in a seriously ill patient without the procedure. With the current use of small-caliber spinal needles, herniation appears to be extremely rare; nonetheless, it is fully predictable neither by CT nor by opening CSF pressure readings.

A careful neurologic examination should precede all spinal punctures. When the patient has a history of headache and fever with progressive deterioration in mental status and localizing neurologic signs, spinal puncture should not be performed as the initial diagnostic procedure. Gopal and colleagues identified three statistically significant predictors of new intracranial masses: papilledema, focal abnormalities on neurologic examination, and altered mental status.¹⁰³ Greig and Goroszeniuk made similar recommendations.¹⁰⁴ Hasbun and associates demonstrated that in adults with suspected meningitis, the presence of any of 13 clinical features is predictive of abnormal findings on CT (Box 60-1).¹⁰⁵ Theoretically, the presence of abnormal findings on CT portends potential herniation, with or without lumbar puncture. The absence of abnormal findings suggests the patient is a good candidate for immediate lumbar puncture because the risk for brain herniation as a result of the procedure is low (see Box 60-1). Joffe argues that clinical signs of impending herniation are the most appropriate criteria on which to base decision making regarding the timing of lumbar puncture in patients with acute bacterial meningitis.¹⁰² Such signs include a significantly decreased level of consciousness (Glasgow Coma Scale score ≤11), brainstem findings (pupillary changes, posturing, irregular respirations), and a very recent seizure.¹⁰² It is recommended that these patients undergo neuroimaging (CT or MRI) and receive antibiotics empirically while awaiting the results of imaging, which will help in assessment of the safety of a subsequent lumbar puncture. Measures to lower ICP before spinal puncture may also be considered. Appropriate cultures of blood and more easily accessible body fluids should be obtained before the administration of antibiotics. Blood cultures are positive in 80% of infants with meningitis.

Critically ill patients with acute bacterial meningitis often deteriorate rapidly and experience fatal brain herniation, both shortly after lumbar puncture and in the absence of the procedure. A direct cause-and-effect relationship between lumbar puncture and brain herniation in the setting of suspected meningitis is obscure and probably cannot be defined prospectively in the ED when clinical decisions must be made. A recent review identified 22 case reports of rapid deterioration and herniation after lumbar puncture in adults and children with acute bacterial meningitis.¹⁰² The general consensus is that less ill patients (clearly a subjective clinical judgment) with a clinical scenario that includes meningitis as a possibility can be evaluated safely with lumbar puncture. In critically ill patients, especially those with localizing neurologic signs, severely depressed level of consciousness, or papilledema, diagnostic lumbar puncture may be delayed until the risk for herniation is lower, and aggressive and empirical treatment with meningitis doses of antibiotics should proceed.

Head CT can identify hemorrhagic lesions and most neoplasms. Its results should contribute to the decision regarding the need for and the risk involved with spinal puncture. Head CT can identify patients with unequal pressure between intracranial compartments, who are at greater risk for cerebral herniation. Findings that suggest unequal pressure include (1) lateral shift of midline structures, (2) loss of the suprachiasmatic and perimesencephalic cisterns, (3) shift or obliteration of the fourth ventricle, and (4) failure to visualize the superior cerebellar and quadrigeminal plate cisterns with sparing of the ambient cisterns.¹⁰⁶ The presence of a mass in the posterior fossa is a strong contraindication to lumbar puncture. Unfortunately, because of bone and motion artifact, the posterior fossa may be a difficult area to visualize on CT.

Although there is no clear standard with respect to the use of CT before lumbar puncture, a reasonable and logical approach is to avoid initial lumbar puncture and first perform head CT when a mass lesion is suspected or if the patient has signs and symptoms of increased ICP (see Box 60-1). This approach correlates with the clinical policy promulgated by the American College of Emergency Physicians in 2002.¹⁰⁷

Epidermoid Tumor

An epidermoid tumor or cyst is a mass of desquamated cells containing keratin within a capsule of well-differentiated stratified squamous epithelium. Congenital lesions arise from epithelial tissue that becomes sequestered at the time of closure of the neural groove between the third and the fifth weeks of embryonic life, but such lesions are rare. Acquired intraspinal epidermoid tumors result from the implantation of epidermoid tissue into the spinal canal at the time of lumbar puncture performed with needles without stylets or with ill-fitting stylets. The clinical syndrome consists of pain in the back and lower extremities developing years after spinal puncture. Failure to use a stylet on needle withdrawal might also result in aspiration of a nerve root into the epidural space.

Backache and Radicular Symptoms

Minor backache from the trauma of the spinal needle occurs in 90% of patients. Frank disk herniation has been reported from passage of the needle beyond the subarachnoid space into the anulus fibrosus. Transient sensory symptoms from irritation of the cauda equina are also common.

Other reported complications include transient unilateral or bilateral sixth-nerve palsies caused by stretching or displacement of the abducens nerve as it crosses the petrous ridge of the temporal bone, SAH, subdural and epidural hematoma, epidural CSF collection, cauda equina syndrome, anaphylactoid reactions to local anesthetics, settling of cord tumors, and retroperitoneal abscess produced by laceration of the dura in patients with meningitis.108–114 Most of these complications are rare and seldom encountered; however, they should be considered if a patient returns after a lumbar puncture with worsening back pain or abnormal findings on neurologic examination.

The complications associated with lateral cervical and cisternal puncture are similar to those encountered with lumbar puncture. Perforation of a large vessel with resultant cisterna magna hematoma or obstruction of vertebral artery flow has been described. Puncture of the medulla oblongata may cause vomiting or apnea, and puncture of the cord may be associated with pain. Long-lasting side effects of cord puncture seem to be rare. A traumatic tap and postpuncture headache may occur.

Spinal Epidural Hemorrhage

Rarely, serious bleeding leading to spinal hematoma secondary to lumbar puncture can produce spinal cord compromise and permanent significant neurologic deficits, such as cauda equina syndrome.²⁷ This may occur more frequently in coagulopathic patients but can occur in those with a normal coagulation profile and a seemingly atraumatic tap. The bleeding is concealed and may be suspected only by persistent severe backache or neurologic findings. Weakness, numbness, and incontinence after spinal puncture must be investigated, usually with MRI for a possible spinal hematoma. Surgical intervention, including laminectomy and evacuation of blood, may be required and must occur in a timely manner to avoid permanent loss of neurologic function. Those with mild symptoms and progressive recovery may be managed conservatively with close monitoring.

Pressure

CSF pressure is clinically important.¹¹⁵ Measure it accurately whenever feasible. Unfortunately, in some cases it will be logistically impossible to obtain. If the lumbar puncture is being performed with the patient in a seated position, place the patient in the lateral decubitus position before a measurement is obtained. This may be done initially, before fluid is collected, or after fluid collection, in which case a closing pressure is obtained. By repositioning the patient and measuring the pressure after fluid is collected, the likelihood of the needle being displaced as a result of the repositioning is minimized.^13,17 Accurate measurement depends on cooperation of the patient. Measurements from struggling or agitated patients will probably be inaccurate; in such cases, sedation may allow more accurate readings to be obtained.

Normal CSF pressure is between 7 and 20 cm H₂O. Obese patients may have a CSF pressure of up to 25 cm H₂O. Elevated pressure is abnormal. Opening pressure is taken promptly, thereby avoiding falsely low values caused by leakage through and around the needle. Herniating cerebellar tonsils may occlude the foramen magnum and prevent increased ICP from being reflected in the lumbar pressure reading. Increased ICP can result from expansion of the brain (edema, hemorrhage, or neoplasm), overproduction of CSF (choroid plexus papilloma), a defect in absorption, or obstruction of flow of CSF through the ventricles. Cerebral edema may be associated with meningitis, CO₂ retention, SAH, anoxia, congestive heart failure, or superior vena cava obstruction. Pressure may be falsely elevated in a tense patient when the head is elevated above the plane of the needle and, possibly, in markedly obese patients and those experiencing muscle contraction.²¹ Pressure is not usually measured in neonates because a struggling or crying child will have a falsely elevated pressure. Avery and colleagues concluded that for most children (1 to 18 years of age), an opening pressure above 28 cm H₂O should be considered elevated.¹¹⁶

Low pressure suggests obstruction of the needle by the meninges. Low pressure can also be seen with a spinal block. Rarely, a primary low-pressure syndrome occurs in a setting of trauma, after neurosurgical procedures, secondary to subdural hematoma in elderly patients, with barbiturate intoxication, and in cases of CSF leakage through holes in the arachnoid.117,118

The Queckenstedt test is useful for demonstrating obstruction in the spinal subarachnoid space,4,21 but this test is seldom performed today because myelographic techniques have been refined and the availability of MRI has reduced the number of myelograms and associated lumbar puncture studies. However, because situations might arise when this simple and reliable test is important diagnostically, the technique is described here.

With the patient in the lateral recumbent position, compression of the jugular vein causes decreased venous return to the heart. This distends the cerebral veins and causes a rise in ICP, which is transmitted throughout the system and measured in the manometer. After 10 seconds of bilateral compression, CSF pressure usually rises to 15 cm H₂O over the initial reading and returns to baseline 10 to 20 seconds after release. If there is no change in lumbar pressure or if the rise and fall are delayed, one may conclude that the spinal subarachnoid space does not communicate with the cranial subarachnoid space. In this situation, to facilitate subsequent myelography, consider injecting Pantopaque before removing the needle. This is necessary because the lumbar dural sac may collapse and thus make it impossible to reenter the canal. If cervical cord disease is suspected, repeat the test with the neck in the neutral position, hyperextended, and flexed. When lateral sinus obstruction is suspected, use unilateral jugular venous compression (Tobey-Ayer test).

Appearance

If CSF is not crystal clear and colorless, a pathologic condition of the CNS should be suspected. The examiner should compare the fluid with water and view down the long axis of the tube or by holding both tubes against a white background. A glass tube is preferred because plastic tubes are frequently not clear. CSF will appear grossly bloody if more than 6000 red blood cells (RBCs)/µL are present. Note that the fluid may appear clear with as many as 400 RBCs/µL and 200 WBCs/µL.²¹ Xanthochromia, a yellow-orange discoloration of the supernate of centrifuged CSF, is generally considered to be the result of SAH of at least a few hours’ duration and has been used to differentiate prior bleeding from a traumatic tap. A traumatic tap does not usually exhibit xanthochromia (see the later section “The Traumatic Tap”). Xanthochromia is produced by red cell lysis and is caused by one or more of the following pigments: oxyhemoglobin, bilirubin, or methemoglobin

Traditionally, CSF samples have been assessed for xanthochromia by visual inspection by a laboratory technician after centrifugation of a sample of CSF. Most hospitals still use this method.¹¹⁹ Recently, spectrophotometry, designed to demonstrate both oxyhemoglobin and bilirubin, has been advocated as a more precise way of determining xanthochromia. Oxyhemoglobin alone without bilirubin in a CSF sample is thought to be artifactual (traumatic). Visually, bilirubin and oxyhemoglobin cannot be differentiated. Therefore, detection of bilirubin by spectrophotometry should define xanthochromia and prompt additional investigation for SAH. Relying on spectrophotometry to identify xanthochromia without pigment differentiation will cause a high false-positive interpretation. The absence of both oxyhemoglobin and bilirubin by spectrophotometry does not support the diagnosis of SAH. Oxyhemoglobin causes red coloration; bilirubin, yellow; and methemoglobin, brown. Oxyhemoglobin is seen within 2 hours after subarachnoid bleeding and red cell lysis, but it may be detected immediately if the bleeding is profuse. Formation of oxyhemoglobin peaks 24 to 48 hours after hemorrhage, and the discoloration disappears in 3 to 30 days.⁴

Blood must be present in CSF (in vivo) for a number of hours for bilirubin to appear; it will not appear spontaneously once CSF is in the collection tube. The appearance of bilirubin in CSF involves the conversion of oxyhemoglobin by the enzyme heme oxygenase. The enzyme is found in the choroid plexus, the arachnoid, and the meninges. Enzyme activity appears approximately 12 hours after the hemorrhage.⁴ Bilirubin may persist in CSF for 2 to 4 weeks. Moreover, bilirubin in CSF caused by hepatic or hemolytic disease does not appear until a serum level of 10 to 15 mg of total bilirubin per 100 mL is reached, unless underlying disease associated with high CSF protein levels is present. Xanthochromia may also be seen with CSF protein values above 150 mg/dL. CSF may clot in patients with a complete spinal block and very high CSF protein.

Graves and Sidman noted that an RBC concentration of 5000/µL, created by adding RBCs to acellular CSF, will produce xanthochromia evident on spectrophotometry by 2 hours.¹²⁰ The addition of RBCs to achieve RBC concentrations of 20,000/µL and 30,000/µL will produce xanthochromia by 1 hour or immediately, respectively. Therefore, xanthochromia may occur with a traumatic tap and does not always indicate SAH.

Methemoglobin is a reduction product of oxyhemoglobin that is characteristically found in encapsulated subdural hematomas and in old intracerebral hematomas.

Cells

In adults, WBC counts higher than 5 cells/µL indicate the presence of a pathologic condition. A recent large study by Kestenbaum and colleagues determined 95th percentile WBC reference values in normal infants: 19 cells/µL for infants 28 days of age or younger and 9 cells/µL for those between the ages of 29 and 56 days.¹²¹ A median CSF WBC count of 271 WBCs/µL has been reported in infants with group B Streptococcus in the era of intrapartum antibiotic prophylaxis. The CSF WBC count in infants is higher with gram-negative meningitis than with gram-positive CNS infections. In general, polymorphonuclear leukocytes are never seen in normal adults. However, with use of the cytocentrifuge, an occasional specimen from an otherwise normal individual may show one to two neutrophils.¹²² More than three neutrophils is always abnormal in an adult. Moreover, as many as 30% of patients exhibit CSF pleocytosis after a generalized or focal seizure. Nonetheless, such a finding should prompt culture of CSF because the presence of neutrophilic pleocytosis is commonly associated with bacterial meningitis or the early stages of viral or tuberculous meningitis. Small lymphocytes may be seen in normal individuals. Small and large immunocompetent cells are found with a variety of bacterial, fungal, viral, granulomatous, and spirochetal diseases.

Eosinophils always indicate an abnormal condition, most commonly a parasitic infestation of the CNS. They may also be seen after myelography and pneumoencephalography and, to a minor degree, with other inflammatory diseases, including tuberculous meningitis and neurosyphilis. Normal CSF RBC counts are lower than 10 cells/µL. Herpes simplex virus (HSV) encephalitis may elevate the RBC count. Finally, myeloid and RBC precursors may contaminate CSF with bone marrow cells from an adjacent vertebral body.¹²³

Glucose

Glucose enters CSF by way of the choroid plexus, as well as by transcapillary movement into the extracellular space of the brain and the cord via carrier-mediated transport. It then equilibrates freely within the CSF subarachnoid space. Once in CSF, glucose undergoes glycolysis and there is an invariable rise in CSF lactate levels. Glucose levels remain subnormal for 1 to 2 weeks after effective treatment of bacterial meningitis.

The normal range of CSF glucose is 50 to 80 mg/dL, which is 60% to 70% of the glucose concentration in blood. Ventricular fluid glucose levels are 6 to 8 mg/dL higher than in lumbar fluid. A ratio of CSF glucose to blood glucose of less than 0.5 or a CSF glucose level below 40 mg/dL is invariably abnormal. The ratio is higher in infants, in whom a ratio of less than 0.6 is considered abnormal. Hyperglycemia may mask a depressed CSF glucose level; when present, the ratio of CSF glucose to blood glucose should be measured routinely. With extreme hyperglycemia, a ratio of less than 0.3 is abnormal.¹²⁴ Between 90 and 120 minutes is required before CSF glucose reaches a steady state with changes in blood glucose (e.g., after an intravenous injection of glucose). When CSF glucose is of diagnostic importance, obtain CSF and blood samples, ideally after a 4-hour fast.

Low CSF glucose levels may be associated with several diseases of the nervous system (Box 60-2). Only low concentrations of glucose are of diagnostic value; elevated CSF glucose levels generally have little significance and usually reflect hyperglycemia. A rapid estimate of the CSF glucose level can be obtained by using bedside reagent strip testing with a commercial autoanalyzer. Formal laboratory testing is recommended for confirmation of the bedside levels.

Protein

The normal range of lumbar CSF protein is 15 to 45 mg/dL. Infants normally have a lower level than adults do, and protein levels may drop after lumbar puncture. The concentration is lower in the ventricles (5 to 15 mg/dL) and the basilar cisterns (10 to 25 mg/dL) as a result of a gradient in the permeability of capillary endothelial cells to proteins in blood. Levels of CSF protein in premature infants and full-term neonates are higher than in adults, with a mean of 90 mg/dL; protein levels decline by the age of 8 weeks because of maturation of the blood-brain barrier.

Most of the proteins in CSF come from blood, which normally has a protein concentration of up to 8000 mg/dL. Protein entry is determined by its molecular size and the relative impermeability of the blood-CSF barrier. A full range of serum proteins is found in CSF at a several hundred–fold dilution.

An increase in the total CSF protein level is a nonspecific abnormality associated with many disease states. Levels higher than 500 mg/dL are uncommon and seen mainly with meningitis, subarachnoid hemorrhage, and spinal tumors. The high levels that occur with cord tumors result from an increase in local capillary permeability. With high levels (generally 1000 mg/dL), CSF may clot (Froin’s syndrome).

Hemorrhage into CSF or the introduction of blood by a traumatic tap increases CSF protein levels. If the serum protein concentration is normal, the CSF protein level should theoretically rise by 1 mg/dL for every 1000 RBCs, but this relationship varies. The inflammatory effect of hemolyzed RBCs may also significantly increase CSF protein.

Selective measurement of immunoglobulin fractions in CSF has proved to be of diagnostic value in suspected cases of multiple sclerosis. Elevated CSF immunoglobulin levels may reflect disruption of the blood-brain barrier or a local antibody response to a CNS immune response.¹²⁵ Stimuli may be infectious or antigenic and produce an inflammatory response. Elevated immunoglobulin levels have been found in many conditions, including syphilis, viral encephalitis, subacute sclerosing panencephalitis, progressive rubella encephalitis, tuberculous meningitis, sarcoidosis, cysticercosis, and acute inflammatory demyelinating polyneuropathy (Guillain-Barré syndrome).

The Traumatic Tap

The incidence of a traumatic tap is 10% to 30%, depending on the criteria used to define the condition.126–128 Currently, there is no consensus on what constitutes a traumatic tap. Traditionally, the number of RBCs in CSF, the rate of clearance of RBCs from tube 1 to tube 3 or 4, and the presence or absence of xanthochromia have guided clinicians in attempts to define the need for further investigation for SAH when blood is detected during lumbar puncture.

CSF Analysis with Infections

CSF Analysis in Immunocompromised Patients

The number of immunocompromised individuals is increasing because of the HIV epidemic and the increased survival of patients with cancer and autoimmune disorders. The nervous system is a major target of the HIV virus: neurologic disease develops in 40% to 60% of infected individuals during their lifetime. One third of HIV-infected patients have neurologic complaints as the initial manifestations of AIDS, and an even higher incidence of nervous system involvement is found at autopsy.¹⁵³ The risk for CNS infection depends on the underlying disease, treatment, duration, and type of immune abnormality. Abnormalities include defects in T-lymphocyte and macrophage cellular immune function, defects in humoral immunity, defects in the number and function of neutrophils, and loss of splenic function with an inability to remove encapsulated bacteria.¹⁵⁴ The major neurologic manifestations of HIV infection, including clinical characteristics, are summarized in Table 60-5.

Patients with defective cell-mediated immunity include those with lymphoma, organ transplants recipients, those taking corticosteroids daily, and patients with AIDS. These individuals are vulnerable to infections with microorganisms that are intracellular parasites. A common source of acute bacterial meningitis in such patients is L. monocytogenes. Clinical findings include fever, headache, seizures, focal neurologic deficits, and brainstem encephalitis.

Patients with defective humoral immunity include those with chronic lymphocytic leukemia, multiple myeloma, and Hodgkin’s disease after radiotherapy or chemotherapy. These patients have difficulty controlling infection by encapsulated bacteria. A fulminant meningitis caused by S. pneumoniae, H. influenzae type B, or N. meningitidis may develop. After splenectomy, patients are at risk for the development of meningitis for the same reason. Neutropenic patients are at risk for meningitis caused by Pseudomonas aeruginosa and the Enterobacteriaceae.

Establishing a specific diagnosis in HIV and organ transplant patients may be difficult or impossible because of overlapping clinical and radiographic findings, the presence of simultaneous infections with more than one organism, and changes in CSF that may be nonspecific. The immune response may be altered, with absence of the usual signs of meningeal irritation. Patients may have diffuse encephalopathy or focal neurologic deficits. CSF is abnormal in 60% of asymptomatic HIV-infected individuals, thus complicating correlation of the CSF and clinical findings.¹⁵³

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