Hydrocephalus with shunt

Hydrocephalus may be congenital and present at birth, or it maybe acquired and

arise later in life. Congenital hydrocephalus can be due to blockage at the
aqueduct (aqueductal stenosis), congenital anomalies such as a Chiari
malformation or Dandy Walker malformation, or secondary to an inflammatory
process when premature birth causes bleeding within the brain. The treatmen for
this condition is placement of a lumboperitoneal, ventriculoperitoneal, or
ventriculoatrial shunt.
Neuraxial anesthesia has been safely used for the management of patient with
a shunt without complications.46,47 Although some have argued that radiologic
studies should be performed in order to ascertain the exact location of the shunt
prior to initiating a neuraxial technique,48 others have performed neuraxial
techniques safely without the aid of imaging studies.46 there are no reported
cases of trauma to the spinal portion of a lumboperitoneal shunt. Shunts are
tipically located at a low intervertebral space (L3-L4 or L4-L5) and the tubing
runs laterally to the peritoneum.46 common sense dictates the insertion of
needle at an intervertebral space below or above the scar, depending on the
location of the shunt. There is also concern that drugs in the CSF may leak into
the atrium or peritoneum, depending on the shunt type.47 therefore,,
theoretically, a single shot spinal is not preferred neuraxial technique. Because
of the risk of shunt infection, it has been recommended that prophylactic
antibiotics be administered prior to initiating neuraxial techniques.47
Symptoms of shunt failure, such as headache and increased ICP, may be
confused with postdural puncture headache.49 safe and successful performance
of an epidural blood patch has been reported in a patient with a lumboperitoneal
shunt. 47 although there are no reported case of patients with third
ventriculostomy receiving neuraxial techniques, nauraxial anesthesia is not
contraindicated and the decision as to the type of anesthesia should be based on
surgical considerations and the neurologic status of the patient.50

Neuraxial Anesthesia and Anticoagulation

Anticoagulation increase the risk of spinal-epidural hematoma after neuraxial

anesthesia (see chap 6). Neuraxial anesthesia in the presence of anticoagulation
has been addressed by a consensus conference of the American Society of
Regional Anesthesia and Pain Medicine (ASRA) and this information is
summarized later.51 As always, the decision to perform neuraxial anesthesia in
the presence of anticoagulation should use a risk-benefit analysis. If the risk level
warrants it, frequent lower extremity neurologic assessment should be
performed during neuraxial anesthesia/ analgesia and for a period of time after
catheter removal. Consideration should be given to using low concentration local
anesthetic techniques, when possible, to facilitate neurologic assessment.

Antiplatelet Drugs
Platelets are instrumental in primary hemostatis, leading to a platelet plug, and
providing the membrane surface on which activation of the clotting cascade
occurs. Therefore, any platelet abnormality secondary to disease or medication
has the potential to lead to significant bleeding complications, including a spinal-
epidural hematoma. There are multiple antiplatelet agents including aspirin
(ASA), nonsteroidal anti-inflammatory drugs (NSAIDs), thienopyridines
(ticlopidine and clopidogrel), and GP Iib-IIIa receptor antagonists (abciximab,
eptifibatide, and the tirofiban).
 ASA and NSAIDs impair platelet aggregation by inhibiting cyclooxygenase
(COX) and preventing the formation of thromboxane, which is a potent platelet
aggregator (Table 5.3). while the action of ASA on platelet COX is permanent,
lasting the life span of the platelet (7-10 days), the effect of other NSAIDs is
shorter (3 days). COX consists of two different enzymes: COX-1 is a constitutive
enzyme and COX-2 is an inducible isoform. 52 COX-1 is present in the platelets,
whereas COX-2 is not. The anti-inflammatory and analgesic properties of the
COX-2 inhibitors, celecoxib, and valdecoxib, are attributed to the dicreased
synthesis of prostaglandin H2 by selectively inhibiting COX-2. 52
The thienopyridines exert their antiplatelet effect by irreversible inhibition of
adenosine diphosphate (ADP). These drugs inhibit platelet fibrinogen binding and
subsequent platelet-platelet interaction.51,53 Ticlopidine has a longer effect on
platelet function and should be stopped 10-14 days prior to surgery, whereas
clopidogrel should be discontinued 7 days prior to surgery.51
Platelet GP IIb-IIIa receptor antagonists inhibit platelet aggregation by
interfering with the binding of fibrinogen and von Willebrand factor (vWF) to GP
IIb-IIIa receptor sites on activated platelets.54 The platelet function returns to
normal about 8 hours after discontinuation of eptifibatide and tirofiban, and 24-
48 hours after abciximab.51
Neuraxial analgesia performed in the presence of ASA and NSAIDs alone is
considered safe, as the risk of spinal epidural hematoma in these patients is
low.51 A retrospective analysis of 61 case reports of epidural hematoma and
neuraxial techniques found that most cases (68%) occured in patients with
impaired coagulation.3 Three cases followed neuraxial techniques performed in
the presence of a single antiplatelet agent, such as ASA, ticlopidine, or
indomethacin. However, no specific details were given about each individual
case.3 The concurrent use of antiplatelet therapy and other medications that
affect clotting may increase the risk of bleeding and, therefore, caution should be
exercised.
Thienopyridines and neuraxial anesthesia should be approached with more
caution. These agents, unlike ASA and NSAIDs, also affect primary platelet
aggregation to the subendothelium, thus preventing hemostatic plug formation
and the effects on platelet function are irreversible.51 Therefore, the use of
neuraxial techniques should be avoided until there is platelet recovery. Platelet
GP IIa-IIIa receptor antagonists block the final common pathway to platelet
aggregation for a short period of time and neuraxial techniques are
contraindicated during this period.

Heparin
Heparin is a negatively charged, water-soluble acid. Its anticoagulant effect is
due to a unique pentasaccharide sequence. The pentasaccharide binds to
antithrombin III and accelerates the inactivation of factors II,IX,X,XI, and XII
(Figure 5.1). while long saccharide chains are needed to inhibit factor II, those
with less than 18 saccharide units inhibit factor X.55 The biological half-life of
heparin is dose and molecular size dependent and ranges from 1 to 2 hour for
intravenous unfractionated heparin, and from 3 to 6 hour for low molecular
weight heparins (LMWH).55 unfractionated heparins anticoagulant effect is
monitored with the aPTT. Patients on heparin for more than 4 days should also
have a platelet count measured due to the possibility of heparin-induced
thrombocytopenia.56 Subcutaneous prophylactic unfractionated heparin is
unlikely to cause an increase in the aPTT, and is not a contraindication to
neuraxial techniques (Table 5.4)51 epidural catheter placement or removal
should be delayed for at least 2-4 hour following the discontinuation of
therapeutic doses of unfractionated heparin. Confirmation of a return to normal
hemostatic function with an aPTT is indicated. When intravenous unfractionated
heparin is used intraoperatively, administration should be delayed for at least 1
hour after a neuraxial technique. The same guidelines should be used for
epidural catheter removal, as it has been suggested that catheter removal is a
traumatic as catheter placement.3

Low melucular weight heparin differs from unfractionated heparin biochemically

and pharmacologically (Table 5.5). it has greater inhibitory effect againts factor
Xa than againts thrombin because of its shorter chain length. It has greater
bioavailability and a longer half-life than unfractionated heparin. After a
subcutaneous dose of low molecular weight heparin, the peak anti-Xa activity
occurs at 3-4 hour and decreases to 50% of peak activity by 12 hour. Low
molecular weight heparin is excreted by the kidney and the half-life is increased
in patient with obesity or renal failure. The aPTT is not a sensitive laboratory
measurement of low molecular weight heparin activity. The anti-Xa level
measures its anticoagulant effect, but is not predictive of bleeding complications.
There have been 60 reported cases of epidural hematoma associated with
neuraxial techniques and low molecular weight heparin since its introduction in
1993. Plausible explanations is include high doses of low molecular weight
heparin, twice a day dosing, and the performance of neuraxial techniques during
the time of peak low molecular weight heparin activity. These case were the
driving force behind the ASRA consensus conference on neuraxial anesthesia and
anticoagulation, first convened in 1998, and updated in 2002. Key points of these
guidelines include the delay of neuraxial techniques for at least 10-12 hour
following the administration of a prophylactic dose of LMWH, and 24 hour after a
therapeutic dose (Box 5.6). spinal anesthesia is preferred as it is less traumatic
than epidural anesthesia. Anti-Xa activity measurement is not recommended
because it has not been standardized. It is the authors belief that neuraxial
techniques should be avoided in the presence of increased anti-Xa activity, but
that normal activity in the setting of recent LMWH administration does not mean
that neuraxial techniques can be safely performed.
Fondaparinux, a new anticoagulant, is a synthetic pentasaccharide that
selectively binds to antithrombin, thus inducing a conformational change that
significantly increases the antifactor Xa activity without inhibition of factor IIa. It
is not associated with thrombocytopenia because it does not cross-react with
antibodies against heparin-platelet factor 4 complexes. Unlike other factor Xa
antagonists, it has a very long half-life (18 h) and it may take up to 96-120 hour
to completely eliminate this agent from the circulation. Until further data are
available, neuraxial anesthesia should be avoided in patients receiving this
medication for at least 4 days after the last dose. There are reported cases of
fondaparinux administered 2 hour after an atraumatic single spinal needle pass
or epidural catheter removal without adverse outcomes.
Warfarin
Warfarin blocks the vitamin-K-dependent gamma-carboxylation of factors II, VII,
IX, X, and anticoagulant proteins C and S. This leads to the inability of the
clotting factors to bind calcium, thereby leading to decrease formation of
thrombin. The PT is primarily related to factor VII and X levels. The initial increase
in PT (standardized as the international normalized ratio (INR) following the
initiation of warfarin therapy reflects the inhibitions of factor VII activity, the
vitamin-K-dependent factor with the shortest half-life. The full anticoagulant
effect of warfarin takes several days and depends on the respective half-lives of
factors II, IX, and X (Table 5.6). The opposite happens on discontinuation of
warfarin therapy, when the normalization of the INR reflects return of factor VII
activity before full recovery of the other vitamin-K-depenent factors. For any
given elevated INR, coagulation is more likely to be impaired when recovering
from the effects of anticoagulation than when initiating anticoagulation.
In anticipation of surgery, warfarin should be discontinued 4-5 days prior to
procedures and the INR measured on the day of surgery (Table 5.7).
Normalization of the INR is recommended prior to the performance of neuraxial
techniques. It is considered appropriate to perform neuraxial techniques at the
beginning of warfarin anticoagulation provided that a single low dose has been
administered less than 24 hour prior to the block. Patients on low-dose warfarin
(5 mg or less) with and indwelling epidural catheter should have daily
measurements of INR until catheter removal. Warfarin should be reduced or
withheld if the INR is greater than 3. The catheter is removed once the INR value
is less than 1,5. This number is based on data from trials that correlated
hemostatis with factor activity levels greater than 40%.
SUMMARY
Neuraxial anesthesia techniques have numerous benefits and are well accepted,
especially for certain surgical procedures or patient populations. In addition,
neuraxial anesthesia is now safer than ever before. Major complications are very
unsual. Certain patient characteristics, however, may increase the risks
associated with neuraxial anesthesia, and may even pose major risks to the
patient. An example is the introduction of LMWH in the early 1990s that led to
multiple cases of epidural hematoma. Therefore, it is essesntial to recognize and
understand the multiple circumstances where a neuraxial anesthesia technique
need to be tailored to certain physiologic or pathologic states, or when it should
be avoided altogether. As is true for almost all medical decision-making, a
thorough knowledge of the risks and benefits of the procedure and disease state
is necessary to make the best possible decision.

Lack Of Consent
The concept of informed consent is a hallmark of modern medical ethics and is
firmly grounded in the principle of respect for autonomy. The two key elements
for informed consent are patient understanding of the risks and benefits of a
particular procedure, and physician recommendation regarding the best
available options. However, patients may not be able to provide consent due to
an altered mental status, even when a neuraxial techniques may be in the best
interests of the patient. Therefore, implied consent is used in cases where there
is a medical emergency, in patients with an altered mental status, and where the
health-care proxy is unavailable. The anesthesiologist is choosing the best
available option based on scientific information and what is in the patients best
interests.
Some have argued that patients in severe pain may be unable to provide
informed consent. However, others have demonstrated that even patients with
significant labor pain were satisfied with the level of informed consent provied by
the anesthesiologist. Interestingly, patients felt that all neuraxial technique-
related complications should be disclosed, regardless of severity or risk. It has
also been argued that beneficence provides a moral requirement to relieve pain
and, therefore, relieving the pain is more important than the informed consent
per se unless there is explicit patient refusal. Although the use of sedatives or
analgesics for premedication does not appear to interfere with the informed
consent process as long as the patient is not too sedated to conduct an
intelligible conversation, common sense dictates that the consent be obtained
prior to the administration of these medications, if possible. Parents should be
able to provide consent for minors, and emancipated minors should be able to
provide consent themselves. Health-care proxy consent is allowable in cases
where there has been a proven lack of patient competency. However, the issue of
competency should not be dealt with at the time of the informed consent
process. Should the health-care proxy be unavailable, the best interests of the
patient should be taken into account, balancing the risks and benefits of
neuraxial techniques.
Informed consent is more than signing a piece of paper for medicolegal
protection. The patient should understand the risks and benefits of neuraxial
techniques compared to other options, and be directed toward the best and
safest technique.