Introduction


Neurological Sequelae


About forty years ago, Foster Kennedy published an article entitled: THE GRAVE SPINAL CORD PARALYSES CAUSED BY SPINAL ANESTHESIA, which anecdotically described cases of spinal cord injury after spinal anesthesia. This article received much publicity and nearly caused abandonment of spinal anesthesia, especially in Europe.


It was only after Dripps and coworkers in 1956 published the results of their three year study: LONG-TERM FOLLOW UP OF PATIENTS WHO RECEIVED 10,098 SPINAL ANESTHETICS, that the incidence of serious complications of spinal anesthesia was found to be 1 in 10,000.


In 1975 Usubiaga reviewed 750, 000 epidural anesthetics and found an incidence of severe neurological complications of 1:11,000. A more recent study by Hellman who reported on more than 20,000 epidural anesthetics for cesarian sections without one single serious neurological complication.


The majority of complications were attributed to contamination of needles by detergents or toxic drug injection through the needle, causing ascending arachnoiditis.


In 1980 case reports by Reisner and Ravindran described prolonged neurologic deficits following intrathecal 2-chloroprocaine. This complication followed the accidental subarachnoid injection of large doses of 2-chloroprocaine which contained sodium metabisulfite for epidural anesthesia. Sodium metabisulfite is a stabilizing agent in equilibrium with sulfur dioxide and water, and it is the sulfur dioxide which freely crosses cell membranes. There it forms sulfurous acid which can damage cells directly together with the low pH of 3 % chloroprocaine (3.1) Sodium metabisulfite was removed from 2-chloroprocaine solutions, which were then labeled "methylparabenfree".




Bacterial Meningitis following Epidural Anesthesia


Epidural infection is a rare complication of epidural anesthesia. Usually the source of infection arises from blood-born spread secondary to infection elsewhere in the body. In fact , Baker in a review of 39 cases of epidural abscess over a period of 27 years reported only one case which was associated with epidural anesthesia. A review in 1985 by Verner of spinal epidural abscess indicated that the incidence of epidural abscess has not risen in the last two decades, despite the increased use of epidural anesthesia during this period.


Two recent case reports by Ready and Helfer in December 1989 of two obstetrical patients describe one infection following the use of a hospital prepared block tray, but the source of infection was believed to be blood-borne since the alpha hemolytic streptococcus cultured from the CSF was found in the urine and vaginal cultures of this patient. The second infection developed after an uncomplicated epidural anesthetic and streptococcus faecalis was cultured from the CSF with uncertain source.


Meticulous aseptic sterile conditions have to be used when during the administration of epidural anesthesia especially outside of the operating room.




Symptoms and Signs of Epidural Infection 


SEVERE BACK PAIN USUALLY WITHIN 24 HRS 

SEVERE HEADACHE WITH MARKED NUCAL RIGIDITY 

LOCAL TENDERNESS 

FEVER 

LEUCOCYTOSIS 

CSF : ELEVATED PROTEIN, MARKED LEUCOCYTOSIS EPIDURAL ABSCESS 

LOWER LIMB WEAKNESS, (4 DAY INTERVAL) 

PARAPLEGIA (24 HRS AFTER WEAKNESS)

Early diagnosis and aggressive antibiotic treatment will prevent the progression to epidural abscess formation and the necessity for surgical drainage.




Peripheral nerve damage


In order to evaluate a patient with postepidural neurological deficits one has to be knowlegable of the occurrence of these complications unassociated with epidural anesthesia.




Obstetrical Peripheral Nerve Palsies


Injury to each nerve crossing the pelvic brim has been reported after complicated deliveries and in 25 % of normal deliveries. Hill 1962 reported an incidence of traumatic nerve injuries of 1: 2,600 deliveries unassociated with regional anesthesia.




Lumbosacral Trunk (L4,L5)


Trauma to the lumbosacracal trunc carrying fibers from L4 and L5 to join S1 occurs in women with flat platypeloid pelveces from trauma by forceps blades or pressure from the fetal head. This is the most common peripheral nerve lesion in child birth.




Symptoms and Signs of Lumbosacral Nerve Injury 


PARALYSIS OF THE DORSIFLEXORS OF THE ANKLE WITH FOOTDROP 

HYPALGESIA OVER THE LATERAL ASPECT OF THE CALF AND FOOT 

SLIGHT WEAKNESS OF THE QUADRICEPS (L4) 

SLIGHT WEAKNESS OF THE HIP ADDUCTORS (L4,L5)

This lesion is usually unilateral , recovery may take months and may be incomplete.




Femoral nerve L2,L3 and L4 (RARE)


THIS LESION IS ATTRIBUTED TO KINKING AND ISCHEMIC PRESSURE AT POUPARDS LIGAMENT FROM PROLONGED FLEXION IN THE LITHOTOMY POSITION




Symptoms and Signs of Femoral Nerve Injury 


QUADRICEPS PARALYSIS 

LOSS OF PATELLAR REFLEX 

HYPALGESIA OVER THE FRONT OF THE THIGH AND

MEDIAL ASPECT OF THE CALF



Lateral Femoral Cutaneus Nerve L2,L3 


NUMBNESS OF THE ANTERIOLATERAL PART OF ONE THIGH

This transient lesion is as frequent as the damage to the lumbosacral trunc. Compression of the lateral femoral cutaneous nerve is usually believed to arise from prolonged position in lithotomy stirrups leading to partial ischemia from kinking as the nerve passes under the inguinal ligament. This condition is known as meralgia paresthetica and is rare after normal vaginal delivery.




Common Peroneal Nerve L 4,L5,S1,S2


Damage to the common peroneal nerve may occur from pressure at the lateral aspect of the fibula by falsely positioned stirrups.




Symptoms and Signs of Peroneal Nerve Damage 


FOOT DROP 

HYPOESTHESIA OVER LATERAL ASPECT OF LOWER LEG



Obturator Neuropathy L3,L4


This neuropathy may be caused by a pelvic tumor, hematoma or difficult labor. The obturator nerve is formed by fibers from the third and fourth lumbar roots along the pelvic wall underneath the psoas muscle. It emerges over the pelvic brim,where it can be compressed by the fetal head or high forceps,which is accompanied by sharp pain in the groin and upper thigh.




Symptoms and Signs of Obturator Nerve Damage 


WEAKNESS OF HIP ADDUCTION AND ROTATION

HYPOESTHESIA OVER UPPER INNER THIGH



Differential Diagnosis of Postepidural Neurological Sequelae.




POSSIBLE SITE OF INJURY: 


SPINAL CORD 

PERIPHERAL NERVES 

MUSCLES



POSSIBLE NATURE OF INJURY 


TRAUMA 

ISCHEMIA 

INFECTION 

HEMORRHAGE 

DEGENERATION



POSSIBLE CAUSE OF NERVE INJURY 


ANESTHESIA (NEEDLE TRAUMA, TOXIC DRUGS, HYPOTENSION) 

SURGERY (ISCHEMIC PRESSURE BY RETRACTORS, FORCEPS, POSTURE) 

EXACERBATION OF PREEXISTING DISEASE (DIABETIC NEUROPATHY, PROLAPSED INTERVERTEBRAL DISC)



MANAGEMENT OF POSTEPIDURAL NERVE TRAUMA


HISTORY 


TIME OF ONSET (IMMEDIATE OR SLOW) 

DESCRIPTION OF PAIN, PARESTHESIA 

LOSS OF MOTOR POWER

Sudden onset and rapid progression suggests trauma to the roots and expansion of cord compressing progress, such as hematoma or abscess. Slow onset suggests chronic inflammation or degenerative disease. immediate diagnosis and surgical treatment may prevent permanent paralysis.




PHYSICAL EXAMINATION


Careful neurological exam to define the site and extent of the lesion to identify the nerve structures involved. Examination of the back will reveal any local tenderness in case of acute spinal infection. Attention should be directed to other organ systems (lung, breast and prostate), to exclude metastatic lesions. Neuropathies from undetected diabetes mellitus or porphyria have to be excluded.




LABORATORY TESTS


X -Ray of the spine in two planes 

Coagulogram 

Electromyography 

Lumbar puncture 

Myelogram - Arteriogram 

CT Scan

EPIDURAL VEIN PUNCTURE Intravascular injection of local anesthetic


Inadvertent intravascular injection of local anesthetic may occur at any time during continuous epidural anesthesia. A test dose using a small amount of local anesthetic : either lidocaine 45 mg with epinephrine or 2-chloroprocaine 90 mg must be given before any therapeutic epidural dose. Bupivicaine is 4 times more toxic than lidocaine and not a good indicator when given iv.


Foldes , in a study done in human male volunteers compared procaine ,2-chloroprocaine, tetracaine , and lidocaine given as continuous infusion.They noted the tolerated duration of the infusion to be the longest for 2-chloro- procaine , time of onset and disappearance of signs and symptoms the shortest for 2-cp (4.7 min.)


Negative aspiration of the catheter is not an assurance that the tip is extravascular! Observe the patient closely! Wait at least 3-5 minutes before reinjection. Inject only 5 ml increments of the drug!


Symptoms of intravascular injection are: 


Ringing in the ears 

Metallic taste 

Overall warmth 

Sedation and/ or dizziness

2-chloroprocaine is the least toxic drug and is broken down to p-aminobenzoic acid in the blood by the plasma pseudocholinesterase in seconds (half-life 23 seconds). In contrast , when epinephrine is used ,the patient experiences nausea , vomiting and anxiety, which may last for 15 minutes and causes the patient to refuse to have the procedure repeated. Intravenously administered epinephrine decrease uterine blood flow in a dose dependent magnitude and will cause fetal distress.




Prevention of Epidural Vein Puncture and Intravascular Injection 


Midline insertion of epidural needle 

Choose other interspace, if blood was aspirated

Large doses of local anesthetics administered intravenously cause seizures and cardiac arrhythmias.


Bupivicaine in larger than 1 mg/kg iv causes seizures and cardiac arrest. Resuscitation is difficult and prolonged and in animal studies only responded to massive amounts of epinephrine.


The combination of bupivicaine and epinephrine was found to be additive in decreasing uterine blood flow in a study done by Hood et al. While bupivicaine or epinephrine alone decreased uterine blood only 10-30 % the combination of both caused a decrease of 50% in uterine blood flow.While a healthy baby may tolerate these changes,an alreadycompromised fetus of a preeclamptic mother may be seriously harmed.




Total Spinal


Massive subarachnoid injection of local anesthetic may occur at any time during reinjection of an epidural catheter,because of migration of the catheter tip,especially after the patient has been moved.


Negative aspiration of CSF is no assurance that the catheter is not subarachnoid!




Prevention


Again, a test dose, using a small amount of local anesthetic (3 ml of 3% 2 cp) is mandatory before each reinjection. It is necessary to wait at least 5 minutes and have the patient move her legs to assure a negative test. If high spinal block occurs after the test dose attention has to focus on maintaining maternal blood pressure with left lateral tilt, intravenous fluids and vasopressors .The block usually wears off within the hour and analgesia may be maintained with small amounts of local anesthesia as a continuous spinal.


If massive paralysis occurs, maintenance of the airway and artificial ventilation via an endotracheal tube has to be begun immediately while treating hypotension and monitoring for fetal distress.




Subdural Injections


This potential space lies between the dura mater and the pia-arachnoid membrane. Boys and Norman have obtained radiographic evidence of an epidural catheter placed into the subdural space, the incidence of subdural injection is reported to be 10-16% in the radiology literature. Slow onset of block and massive, patchy spread of small local anesthetic dose with and without negative CSF aspiration seems to be indicative of subdural injection. It is recommended that after obtaining CSF, the needle should be carefully rotated in all four quadrants to assure free flow of CSF.




Horners syndrome


Horners syndrome,(myosis, ptosis, and enophtalmus) and engorgement of nasal mucosa occurs usually in patients with high epidural sensory blockade, but has also been reported with levels to only T 7. The preganglionic sympathetic outflow to the head leaves the spinal cord from the first three thoracic segments, but may receive sympathetic fibers as far down as T 9.


The syndrome is not serious, although many patients complain of inability to breathe through their nose and need reassurance.




Transient Postpartum Parethesias and Motor Dysfunction


Differentiation between obstetrical and anesthetic factors contributing to minor postpartum sensory and motor dysfunction is often difficult. A prospective study in 4,972 parturients by Abuleish in 1981 reported an incidence of paresthesias of 42.3/10,000 deliveries and motor dysfunction in 2.7/ 10,000 deliveries.


Ong reviewed charts from 23,827 postpartum patients and interviewed 15,414 parturients and found an incidence of 18.9/ 10,000 deliveries.




INCIDENCE OF PARESTHESIAS AND MOTOR DYSFUNCTION


Group per 10,000 deliveries P


Multiparas 11.7 -


Primiparas 27.9 <0.02*


Spontaneus vaginal 11.0 -


deliveries


Forceps/vacuum 28.5 <0,03+


No anesthesia 2.4 -


Inhalational analgesia 6.3 NS


Epidural anesthesia 36.2 <0.001


General anesthesia 34.7 <0.001


*Compared to multiparas


+Compared to spont.vaginal deliveries


Ong et.al. ANESTH ANALG 1987


COMMON Complications of Epidural Anesthesia




Arterial Hypotension


Sympathetic blockade causes complete dilation of the veins and venules partial relaxation of the arteries, and increased capillary blood flow. Venous return to the heart decreases resulting in diminished cardiac output. The degree of hypotension depends on the level of sympathetic block, the volume status of the patient and the position of the patient.


Shnider and coworkers report an incidence of hypotension of 29% in obstetrical patients during epidural anesthesia for cesarian section. Lumbar epidural anesthesia for labor with sensor levels up to T 10 is associated with hypotension in 18% of the patients. Hypotension in obstetrics is defined as a systolic arterial blood pressure below 100 mm/Hg or 20% below pre-block level.




Prevention


Prehydration of the patient with 20 ml/kg of balanced salt solution through a large bore cannula will decrease the incidence and severity of hypotension. Obstetrical patients have to be nursed in the the left lateral position to avoid aorto-caval compression. Placing the patient in 15 degree head down tilt assures venous return to the heart. Prophylactic vasopressor medication (iv or im) has not proven to be very effective in preventing hypotension, although it seems to ameliorate the severity.




Treatment


Immediate treatment of hypotension consists of increasing the left lateral tilt and the iv fluids. Incremental doses of ephedrine 5 mg iv usually restore the blood pressure within a minute. Failure of ephedrine treatment is usually indicative of the need for more intravenous fluid. Placement of a second intravenous catheter and pressure applied to the fluid bag by a bloodpump.




Drug interactions


Ephedrine and Ergotamine may cause severe maternal hypertension when administered in sequence. There is potential danger of stroke, because of severe hypertension. The awake patient will complain of excruciating headache and appear flushed.


Treatment of hypertension is achieved with the administration of a pure alpha antagonist such as nitroprusside.




Missed Segments (patchy block)


Unblocked segments ,usually one sided in an otherwise satisfactory field of anesthesia, , are encountered more often in obstetrical patients than in the general surgical population. The occurrence of residual pain in one area means failure of the total block since the pain in this area is just as agonizing as if no anesthesia existed in the neighboring segments. This complication seems to occur more often when small amount of local anesthetics are used as in segmental analgesia for labor . It is seen more frequent with the use of a catheter than with injections directly through the needle. The reasons for this complication are not completely clear and several factors may be involved.




Speed of injection


Bromage tested the influence of speed of injection on the incidence of patchy sacral analgesia and found that slow injections (0.5 ml/sec) decreased the incidence from 30 % to 6 % in human volunteers.




Local Anesthetic pH


The carbonated solutions of lidocaine and prilocaine were found to have a very low incidence of persistent unblocked segments, when compared to plain bupivicaine and tetracaine.This is attributed to the fact that that carbon dioxide penetrates nerve cell membranes extremely fast which was proven by studies in animals and humans.


Migration of the catheter into an intervertebral foramen is usually the cause of persistent one sided block. This is occurs with increasing frequency the farther the catheter is inserted. Retraction of the catheter and reinjection of additional dose with the patient positioned on the side of the unblocked segment may help. Lately, adding a narcotic,(fentanyl or morphine) to the local anesthetic has markedly reduced the incidence of patchy analgesia.




Inadvertent Dural Puncture


This is a dreaded complication of epidural anesthesia,especially in obstetrics because of the high incidence of post dural puncture headache. It is also most likely to occur in parturients who are frightened and writhing in pain. Obesity and extreme lumbar lordosis in pregnant patients contribute to difficulties in locating the epidural space.




Prevention


Good communication with explanation of every step of the procedure in firm, reassuring language is often helpful. Positioning the patient in the sitting up position especially in obese patients and having an assistant holding them will stabilize the moving target. The oxytocin infusion should be temporarily discontinued and attempts of puncture should be performed between contractions.




Immediate Management of Dural Puncture


Options: 


ABANDON THE PROCEDURE 

INSERT CATHETER INTO SUBARACHNOID SPACE 

REINSERT IN A DIFFERENT SPACE

The first option is often unpractical and has to be weight against the risk of general anesthesia or an uncontrolled patient.


Inserting the catheter into the subarachnoid space and using it for subarachnoid analgesia has become more popular lately. The advantage of continuous spinal anesthesia are : the need for only small amounts of local anesthetic, the fast onset of analgesia or anesthesia in case of an emergency cesarian section especially in the morbidly obese patient and the ability to titrate local anesthetic doses to the desired level.


The third option used to be preferred in the past because the epidural catheter was left in place postpartum for prophylactic saline infusion.




Headache Prophylaxis


When the dura is pierced the most valuable advantage of epidural anesthesia is lost : The freedom of postdural puncture headache.The large bore epidural 16-18 gauge needle has an incidence of 76% of headache (Crawford 1972, Craft 1973) from leakage of CSF through the dural hole. About 38 % of headaches begin in the first 24 hours, another 38 % after 24 hours. Typical for post lumbar puncture headache is the dependency on posture and its relieve in the supine position. Conservative measurements include : bedrest, abdominal binder to increase epidural pressure to prevent leakage of CSF and analgesics.




Active Treatment 


EPIDURAL SALINE (50 ML/HR 24 HRS) IMMEDIATELY 

EPIDURAL BLOODPATCH (10-15 ML AUTOLOGOUS ) AFTER 24 HRS

Epidural saline reduces the incidence from 73% to 20% (Crawford). Epidural blood patch, because of its high success rate (98%) and safety which was de-termined in a study by Ostheimer 1974 is most commonly employed. Side effects include : Transient backache , paresthesias in the legs or thighs and stiff neck.




Backache, Headache and Urinary Retention


These complications are very common especially in obstetrical anesthesia. Grove,Crawford,Moir and Davidson in England studied the incidence of backache, headache and urinary retention in obstetrical patients with and without epidural. According to the results the postpartum incidence of headache without epidural is 10 - 23%, with epidural 18 -19%, backache occurs in 32 - 37% without epidural and 22 - 45% with epidural analgesia. Bladder dysfunction is most common after forceps delivery ranging from 20 -37% after non epidural to 25.8 -34%. Whether these data apply to the US population is not known.