More severe and is accompanied by low levels of fibrinogen.

mucocutaneous bleeding is more severe with type 1, and the disorder is

confirmed by platelets that do not aggregate in the presence of activators such
as epinephrine. Acquired GT is rare and is characterized by normally expressed
glycoprotein IIb-IIIa that is nonfunctional due to autoantibodies.

Bernard-Soulier syndrome is another disease characterized by abnormal

platelet aggregation as a result of abnormal adhesion.it is an autosomal
recessive disorder with quantitative receptor for vWF.Similiar to GT,the syndrome
presents with mucocutaneous bleeding.The ristocetin induced platelet
aggregation (RIPA) test,which measures the ability of vWF to support
aggregation,is abnormal.Platelet aggregation to agonists the require fibrinogen
for binding is abnormal in patients with GT,but unchanged with those with
Bernard-Soulier syndrome.

There are no reports in the anesthesia literature of patients with GT or

Bernard-Soulier syndrome receiving neuraxial techniques.In part,this may be
due to the rarity of these disorders.In addition,most of these patients have a
history of mucocutaneus consistent with a platelet abnormality ,and most
anesthesiologist avois neuraxial techniques in these patients.The treatment of
choice is platelet transfusion,but repeated transfusions predispose to the
development of antiplatelet antibodies making it difficult to predict which
patients will respond.

Measurement of Platelet Function

Altough the bleeding time is likely increase in patients with abnormal

platelet function, bleeding time determination has many limitations. it is operator
dependent and difficult to standardize and reproduce. The thromboelastogram
(TEG) provides a global assesment of coagulation, including clotting factor and
platelet function, and their interaction. TEG can determine the clot strength, the
rate of clot formation and strengthening, and fibrinolysis. TEG values include R
time (time to first clot formation), K time and angle (rate of clot strengthening),
MA (maximum strength of developed clot), and LY30 (percent lysis 30 min after
MA is reached) (Fig.5-2). K time, angle, and MA are more spesific for fibrinogen
and platelet function and are use to assess the based line clot strength as well as
the change in response to platelet transfusions. In addition, there is a strong
correlation between the MA and the platelet count. Platelet counts above 75 x
103/mm3 are associated with a normal MA.

The platelet function analyzer (PFA-100) is a relatively new technique for

differentiating normal from abnormal platelet function and evaluating primary
hemostasis. It measures the required for whole blood to occlude an aperture of a
bioactive membrane coated with the platelet agonist epinephrine and ADP
(closure time). Altough an increased aperture time correlates with decreased
platelet function, it is difficult to differentiate a quantitative from qualitative
defect. The PFA , however, can be used to follow the response of platelet
transfusion in patients with thrombasthenia. Similiar to TEG, the closure time of
the PFA-100 correlates with the platelet count. A platelet count greater than 70 x
103/mm3 is associated with a normal closure time. Results from TEG and PFA-100
farther support the notio that a platelet count greater than 75 x 10 3/mm3, and
the absence of significant findings on history and physical examination, is likely
to be associated with normal platelet function and, therefore, normal primary
hemostasis. Thus, it would seem reasonable to proceed with neuraxial
anesthesia if teh TEG or PFA results are normal.

Inherited Hemorrhagic Disorders

Von Willebrands Disease

Von Willebrands disease (vWD) is the most common inherited

hemorrhagic disorder to affect both sexes. The exact prevalence of the disease is
not known because of the variable expressivity and reduced penetrance, but it
has been estimated to be present in 2-3% of the general population. it is
characterized by quantitatively decreased (type 1 and type 3) or qualitatively
abnormal vWF (type 2;table 5-8). There is a defect in platelet interaction in the
subendotelium (adhesion) and with other platelets (aggregation). in addition,
vWF carries factor VIII in the circulation, and protects it from inactivation and
clearance. Therefore, patients with vWD also have a defect in fibrin formation.
Patients with vWD present with signs of platelet impairment manifested as
mucocutaneous bleeding, including epistaxis, gingival bleeding, easy bruising,
and menorrhagia.

Type 1 vWD is the most common type and has an autosomal dominant
inheritance. It is the milder form of the disease , and accounts for 70% of all
cases. There is a deccrease in plasma levels of vWF and factor VIII. it usually
responsive to desmopressin (DDAVP), which increases the release of vWF from
paltelets and endothelial cells. symptoms usually improve during pregnanc due
to the phisiologic increase in plasma factor VIII and vWF.

Type 2 vWD also has an autosomal dominant mode of inheritance, but with
qualitatively abnormality of vWF. It accounts for up to 20-30% of all cases of
vWD, and is characterized by various subtypes. Type 2A vWD has an absence of
large and itermediate size multimers and RIPA. Type 2B vWD has an absence of
large size multimers, and the interaction between platelets and vWF is increased.
Thrombocytopenia is a unique feature of this type of vWD, but does not predict
clinical severity. TYPE 2M vWD has normal size multimers but with decreased
platelet-dependent vWF function. Type 2N vWD has a defect in the binding of
factor VIII to vWF.

Type 3 vWD has an autosomal recessive mode of inheritance and is rarely seen.
It is the more severe form of vWD and is characterized by a minimal amount of
vWF and low plasma levels of factor VIII. It usually presents with severe bleeding,
is not responsive to DDAVP, and does not improve with pregnancy.

All patients with a history resembling vWD should have coagulation

screening test, including platelet count, Pt, and aPTT to rule out other causes of
bleeding. Specialized testing for vWD is important to confirm the diagnosis , and
to establish a proper sub-classification and treatment options. The ristocetin
cofactor avictivity assay (vWF:Rco) measures vWF binding to platelet Gplb or
vWF activity. Plasma vWF antigen (vWF:Ag) quantifies the deficiency of vWD, and
factor VIII activity is measured in a functional assay. The RIPA test assesses the
ability of the platelet-associated vWF to support aggregatin. Gel electrophoresis
aids in delineation of the vWF multimer structure.

DDAVP is synthetic analog of antidiuretic hormone and transiently

increases the levels of factor VIII and vWF by causing their release from the
endothelial cells (Table 5-9). It is most effective for type 1 vWD with a response
rate of approximately 80%. The response with Type 2 vWD is unpredictable.
DDAVP is contraindicated in cases of type 2B disease as it can precipitate or
worsen thrombocytopenia. There is no response in patients with type 3 disease
as there is minimal if any vWF. DDAVP is administered intravenously at a dose of
0.2-0.4 g/kg body weight over 30 min. The plasma factor VIII and vWF plasma
levels increase three to five times, and remain elevated for 8-20 h after DDAVP
administration. Repeat doses are recommended every 12-24 hour.
Antihemophilic factor/vWF complex(Humate P) is a heat inactivated concentrate
thaet contains more vWF activity than factor VIII (2.5:1 IU) and is indicated for
type 3 and some cases of type 2 vWD. Factor VIII plasma levels should be
monitored during therapy,as this is the main predictor of surgical hemostasis.
Peak plasma levels of factor VIII are achieved after 6-8 h of treatment.

The management of a patient woth vWD is best performed witha

multydisciplinary approach that includes the surgeon/obstetrician,
hematologist,and anesthesiologist. There is a direct correlation among
vWF:Ag,vWF:Rco, and factor VIII levels and normal hemostasis, and is often
difficult to decide wheter to perform neuraxial techniques for these patients.
Neuraxial techniques are contraindicated if the coagulation screen is abnormal,
as in cases with more severe types of vWD where the vWF is markedly reduced
or abnormal. There are several reports of neuraxial anesthesia administered to
patients with mild forms of type 1 vWD without any complications following
normalization of factor VIII and vWF plasma levels during pregnancy or after
DDAVP treatment. Of note, it is important to understand that while type 1 vWD
may becorrected temporarily during pregnancy or with DDAVP the level of vWD
decreases after the delivery of the placenta 8-10 hour following of neuraxial
techniques, as the removal of an epidural catheter may occur at the time when
vWF and factor VIII levels are decreasing.

Factor Deficiencies

Common factor deficiencies include factor VIII,IX, and XI. Hemophilia of

factors VIII and IX, respectively. The diseases are present almost exclusively in
males (1/10,000), and carier females are usually free of any bleeding
compliacations. Unlike platelet disorder, bleeding is usually deep, causing
hemarthrosis. Factor XI deficiency has an autosomal recessive mode of
inheritance and is common in ashkenazi Jews. Bleeding complications are more
common in females, including menorrhagia, postpartum hemorrhage. All of this
factor deficiencies are associated with an elevated aPTT that is highly suggestive
of an abnormality in the intrinsic pathway, as these factors are essential to the
activation of Factor Xa, which in turn converts prothrombin to thrombin.

Neuraxial techniques can be used in carriers of hemophilia that have

normal factor levels and are free of bleeding complications. Altough neuraxial
techniques are best avoided in homozygous patients with known factor
deficiencies , there are reported cases of neuraxial techniques in patients with
normal aPTT and factor levels after replacement therapy. In addition, there is a
report of two pregnant patients with mild to moderate factor XI deficiency and a
normal aPTT who received neuraxial techniques without any complications. Of
note,factor XI is one of the few factors that decreases as pregnancy progresses.
It is important to understand that isolated case reports of neuraxial techniques in
these patients should not be equated with safety, as epidural hematoma has a
low prevalence in the general population (1:150,000-1:220,00). Factor XII
deficiency leads to an elevated aPTT without any known bleeding complications.
Patients with this factor deficiency should have a complete hematologic workup
to rule out other cause of elevated aPTT, and neuraxial techniques are
permissible in the absence of bleeding tendencies.

Antiphospholipid Antibodies

Lupus anticoagulants (LAC) and anticardiolipin antibodies (ACA) are auto

antibodies against phospholipid-protein complexes and may result in abnormal
platelet aggregation and thrombocytopenia. in addition, circulating LACs
interfere with phospholipid dependent coagulation test resulting in prolongation
of the aPTT. LAC elevates aPTT invitro, but increases clottin in vivo and,
therefore, patients with LAC are more likely to experience a thrombotic event
with phospholipids of the platelet membrane may contribute to venous, arterial,
and placental thrombosis.

The challenge arises when these patients are treated with heparin to
prevent these complications, as the aPTT is likely to remain elevated even after
heparin has been dicontinued. If the decision is made to perform a neuraxial
techniques, blood heparin assays, activated clotting test, or thrombin time have
been used to monitor the heparin levels. The determination of baseline aPTT
levels is recommended prior to initiating heparin anticoagulation. Another option
is to check anti-XA levels, but controvesy exists regarding the use of anti-Xa
monitoring to predict heparin response. The abnormal phospholipid that
contributes to this artificially elevated aPTT can be confirmed by measuring ACA
with an enzyme-linked immunosorbent assay (ELISA). A careful history and
phisical examination, as well as the determination of the platelet count and PT
are important to the rule out any other coagulopathy.

Neuraxial Anesthesia or Catheter Insertion Under General Anesthesia

There is a great deal of controversy over the insertion of subarachnoid or

epidural catheters, or the initiation of neuraxial anesthesia while patients are
undergoing general anesthesia. While most series have demonstrated an
absence of neurologic injury when patients received intrathecal opioid injection,
spinal drainage, or lumbar epidural catheters under general anesthesia. The
incidence of neurologic complications related to neuraxial techniques us too
small to allow determination of actual risk of their practice. Neuraxial anesthesia
for children may only be possible under heavy sedation or general anesthesia;
however, in adult it is usually possible to perform these techniques with minimal
to no sedation. serious complications during neuraxial anesthesia are more likely
to occur after a paresthesia during needle puncture, or with pain during injection
of local anesthetics. Closed claims analyses demostrated that 39% of
lumbosacral nerve root injuries were associated ith paresthesia during needle
insertion, and another 13% were associated with pain during drug injection.
Cases of permanent loseof cevical spinal cord function due to direct spinal cord
injection of local anesthetics when intescalene blockswere perform under general
anesthesia have been reported. Therefore, close communication with the
patients is essential in order to recognize a paresthesia during needle insertion
or pain during injection of a drug . Rosenquist and birnbach have argued that the
risk-benefit ratio does not support the use of neuraxial techniques under general
anesthesia, even when performed at the lumbar level. There is a wide vertebral
level range at which the spinal cord terminates, and anesthesiologist often
inaccurately identify specific lumbar interspaces(see Chap.1). Current data
supporting the practice of inserting needles and catheters into the epidural or
subarachnoid space of adults with minimal to no sedation in order to recognize
pain or paresthesias during needle or catheter placement, or drug injection.

Neuraxial Techniques Following Dural Puncture or Epidural Blood Patch

it has been postulated that a previous epidural blood patch for a postdural
puncture headeche may lead to obliteration of the epidural space.
Reorganization of the blood clot has been hyphotesized to cause fibrous tissue
formation around the dura, leading to obstruction to spread of local anesthetics
in the eidural space. Some authors have reported theat previous dural puncture
was associated with a higher incidence of subsequent inadequate epidural
anesthesia, requiring larger does of local anesthetics. Possible explanations for
this observation include the presence of a preexisting abnormality in the epidural
space causing difficulty with the initial epidural technique (resulting in breach of
dura), or that dural puncture may result in rearrangement of dural arcitecture,
resulting in changes in the epidural space.
 In contrast to the above reports, other authors have reported succesful
epidural analgesia following a previous dural tap or epidural blood patch. These
studies found no association between a history of prior epidural blood patch and
subsequent unsuccessfull neuraxial anesthesia. The history of prior dural
puncture, however was reported to increase the likelihood of a subsequent
puncture.

Because the data are conflicting as the subsequent effects of prior dural
puncture and epidural blood patch, it may be prudent to disclose to patients that
a prior dural puncture may be associated with more difficult initiation of epidural
enesthesia, with an increased likelihood of inadvertent dural puncture and
adequate or failed anesthesia.

Gross Anatomic Abnormalities

Previous spinal surgery

Harrington originally described the use of disraction and compression rods

for the treatment of scoliosis in 1962. Current surgical techniques employ
Harrington, Luque, and Cotrell- Doubousset metal rods. Common to these rods
is the removal of spinous processes and interspinous ligaments, the decortication
of vertebrae, and the placement of bone graft material over the vertebrae.

Although neuraxial anesthesia is not contraindicated in patients with prior

spinal instrumentation, technical difficulty due to fused areas from scar tissue or
bone grafting are often encountered. Other problems that may contibute to a
greater degree of difficulty performing neuraxial techniques include further
degenerative spine changes below the area of fusion, the involvement of the L4
and L5 vertebral levels in up to 20% of patients, and the possibility of an injury to
the ligamentum flavum during the surgical procedure, resulting in adhesions in
the epidural space. Potential problems include the inability to locate the epidural
space (see Chap. 2), limited spread of local anesthetic above the level of the
spinal fusion, and an increased incidence of dural puncture. In a small series of
nine patients with Harrington rods receiving epidural analgesia for labor,
successful analgesia was achieved in seven patients despite close to 50% having
some of complication mentioned earlier. Although these patients suffer from
postdural puncture headache following an unintentional dural breech, an
epidural blood patch will be as difficult as the original technique and there is the
possibility that the epidural space has been obliterated.

Conventional radiographs and a copy of the surgical report are helpful

prior to initiating neuraxial anesthesia in patients with any type of rods.
Anteroposterior and lateral radiographs demonstrate the position of the spinal
elements, the instrumentation itself, the presence of graft material, and
evidence of gross anatomic abnormalities. A spinal technique may be preferred
over an epidural, as it is less likely to be affected by distortions of the epidural
space , has a more specific endpoint, and is more reliable. Should an extended
period of analgesia or anasthesia be required, the use of a continuous spinal
catheter following intentional or unintentional dural breech has been described.
Ultrasonography has been suggested as an aid to identify landmarks and locate
the midline. The rod and the vertebra to which it is anchored are usually
positioned in the midline; however; this may not be true in the middle part of the
rod, as the vertebral columnmay be significantly displaced laterally. Interestingly,
the rods may be the only visible image on the ultrasound to aid midline location.

In concludion, neuraxial techniques can be offered to patients with prior

spinal instrumentation. These patients may be reluctant to accept neuraxial
techniques due to anxiety, back pain, or simply because they have been told to
avoid any instrumentation of their back. reassurance that these techniques are
safe and generally effective is very important, while at the same time disclosing
the increased incidence of comlications.

Lower Back Disease

Neuraxial anesthesia is often performed in patients with known back

disease , ranging from commonly occuring low back pain without any anatomic
etiology, to lumbar spinal stenosis. Other common causes of low back pain
include spondylosisthesis and herniated disc. A thorough history and physical
examination is important in order to identify any preexisting muscular or
neurologic disease prior to an attemted neuraxial techniques. Although
permanent neurologic injury as a result of a neuraxial technique is very low,
ranging from 0.01 to 0.03% (see Chap.6), any undocumented pathology prior to
a needle inserion may be attribbuted to the neuraxial technique.

There has been significant controversy in the obstetric literature regarding

epidural techniques and postpartum backache. Even though retrospective
reviews have demonstrated an association, prospective studies have
demonstrated that the majority of parturients had similiar back pain during
pregnancy and prior to the epidural technique. Futhermore, the incidence of
postpartum back pain was similiar regardless of the performance or avoidance of
neuraxial techniques.

A paresthesia is often present following a spinal needle insertion into the

subarachnoid space or during epidural catheter advancement. Altough a
paresthesia is more common in patients with known spine pathology or
complaints it is not associated with any long-term neurologic condition.
However,extreme caution should exercised in the presence of a paresthesia
during needle or catheter insertion. A persistent,recurrent,or reproducible
paresthesia, or pain during injection is more likely to be associated with lasting
radiculopathy in the same dstribution. variable distribution of medication in the
epidural space, and delayed onset of anesthesia have been demonstrated in
patients with sciatica. Delayed onset of anesthesia accours when comparing
patients with known spinal pathology to healthy patients, as well as between
affected and unaffected nerves and nerve root in patients with known pathology.

Regional techniques are not contraindicated in the presence of back pain

and are not likely to exacerbate it. A care demonstrate that the cause of back
pain is not of neurologic origin.Scatica may occur in the presence of lumbar disc
herniation with radicular symptoms, and patients should be informed that
neuraxial tecjniques might reproduce these symptoms.An imaging study such as
a MRI is helpfull in the presence of radicular symptoms and will help identify the
location of the injury. The L4-L5 and L5-S1 interspaces are implicated in over
95% of cases of lumbar spine pathology, and it is best to perform a neuraxial
technique at a different interspace. Finally,it is important to discuss with patients
that any significant pathology in the lumbar spine may result in a technically
more difficult neuraxial procedure,with the possibility of reproducing pathologic
symptoms, and inadequate anesthesia due to uneven distribution of medication
in the epidural space.

Localized Infection

The administration of neuraxial techniques in patients with a localized

infection, particularly near the site of skin puncture, has been viewed with some
skepticism. There is a concern that sinal-epidural abscess or spinal meningitis
may result. While hematogenous spread of the localized infection to the CSF has
been implicated as a possible cause of meningitis and spinal-epidural abscess,
direct inoculation of bacteria at the same time of block initation may also
account for neuraxial infection. Epidural anesthesia has been used in the
presence of distant abscess or infected wounds without any complacations. Of
note, deep or superficial epidural infections are more likely in patients on
intensive care units, with long duration of epidural catheterization, receiving
immunosuppression or low-dose anticoagulation,or with diabetes or cancer.
Other idintifiable risk factors include chronic renal failure, steroid administration,
herpes zoster, and rheumatoid arthritis. Therefore, these factors should be taken
into consideration when deciding wheter to use neuraxial techniques in patients
who are febrile or with a localized infection. Specifically,any sign of infection in
close proximity to the insertion site should be viewed as a relative
contraindications to neuraxial techniques.

There are number of steps that are recommended in order to avoid

contamination during epidural catheter insertion(see Chap.2). Adequate time
must be allowed for drying of skin preparation fluid, the number of attempts
should be minimized , and the catheter site should be covered with a clear
occlusive dressing at the time of insertion. it is important to examine catheters
daily, remove them if there is any sign of infection at the puncture site, and
maintain a high index of suspicion for an epidural abscess when caring for
patients whose epidural catheters were placed at the time of a localized infection
or a febrile episode. In addition, there should be low threshold for suspicion of an
epidural abscess in presence of neurologic signs. A MRI scan should be obtained
and antibiotics that cover the most common organism, Staphylococcus aureus,
should be initiated (see Chap.6). This will enable prompt diagnosis and treatment
with reduced likelihood of permanent neurologic sequelae.

A risk-benefit analysis should be conducted in patients with a localized

infection before initiating neauraxial anesthesia and this should be discussed
with the patients. The risk factor that increase the risk of an epidural abscess in
predisposed patients should be taken into consideration. The use of antibiotics
prior to a neuraxial technique is currently recommended in patients with
evidence of a localized infection. Altough there is no evidence for a cause and
effect relationship between neuraxial techniques and meningitis or epidural
abscess in these patients, any serious neurologic complication may be attributed
to the neuraxial technique. The initiation of neuraxial analgesia for the treatment
of acute pain from herpes zoster infection is disccused in Chap.17.

Preload-Dependent Conditions

Central neuraxial techniques lead to decreased preload and afterload

secondary to sympathetic blockade and its associatiated venous and arterial
dilation (see.Chap.4). Therefore,patients with condidtions such as aortic stenosis
(AS) and hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic
stenosis (IHSS)),which are associated with a fixed or dynamic left ventricular
outflow tract obstruction,are likely to deteriorate these conditions.

Aortic Stenosis

Patients with AS have compensatory left ventricular concenric

hypertrophic and a fixed stroke volume (Box5-8). Decrease afterload axacerbates
the left ventricular outflow tract gradient and decreases diastolic pressure
(upstream coronary artery perfusion pressure). Decreased preload leads to
decrased stroke volume. Tachycardia decreases left ventricular filling time and
also results in decreased stroke volume. Patients with AS have a noncompliment
left ventricle and are more dependent on atrial contraction to maintain
preload.Patients are at increased risk for myocardial decreased in the hyper
trophied heart. Therefore,decreases in afterload and preload, and tachycardia(or
a heart rhythm other than sinus) lead to a decreased cardiac output and
coronary artery perfusion pressure, worstening ischemia, and so on.

The acute sympathectomy induced by the rapid induction of neuraxial

anesthesia may cause acute decompensation in the patient with AS by acutely
decreasing preload and afterload. Therefore, a single-shot spinal anesthetic is
contraindicated. A carefully titrated neuraxial anesthetic is necessary in patients
with AS to avoid the sudden decrease in preload and SVR. A slowly titrated
neuraxial technique with continous monitoring and maintenance of arterial and
right atrial pressure or central volume status is permissible.

It is preferable to administer a direct acting vasopressor to restore the

SVR, rather than an intravenous fluid bolus, as this may perticipate left
vintricular failure. Phenylephrine is the vasoconstrictor of choice should
hypotension develop, as it does not increase heart rate or contractility. A slowly
titrated epidural technique may be used safely, especially in patients with mild to
moderate disease for whom low thoracic blockade is adequate. Other options
include a combined spinal-epidural or continuous spinal technique with a gradual
onset of a sympathectomy, allowing for careful titration of vasopressors, and
minimal fluid and minimal fluid resuscitation or pulmonary artery catheter. The
safe use of continuous spinal anesthesia has been described in patients with
severe AS scheduled for hip surgery. Blood and pulmonary artery pressure and
cardiac output meassurements, calculated SVR, and sensory level were used to
guide the infusion of subarachnoid local anesthetics.

Obstructive Hypertrophic Cardiomyopathy

Obstructive Hypertrophic Cardiomyopathy, sometimes referred to as

IHSS,is characterized by left ventricular and interventricular septum hypertrophy
leading to obstruction of the left ventricular outflow tract durimg systole.

Similiarto the management of AS, it is essential to maintain preload and

afterload and avoid tachycardia. reduction in preload and afterload increases the
levt ventricular tract gradient and decreases left ventricular filling, conditions
that may lead to hypotension and ischemia. Tachycardia and enhanced
contractility also worsen dynamic left ventricular outflow obstruction. Neuraxial
anesthesia is relatively contraindicated in these patients because of the rapid
onset sympathetic blockade decreases both preload and afterload, especially
after a single-shot spinal technique. Epidural and combined spinal-epidural
technique, however, have been used safely in these patients. The goals are to
maintain euvolemia , vascular resistance, and synus rythm , condition that are
accomplished with a slowly titrated neuraxial technique. Neuraxial labor
analgesia may be initiated with intrathecal opioid only (no local anesthetic),
folowed by an infusin of epidural local anesthetic. Invasive blood pressure and
central pressure monitoring via a central or pulmonary artery catheter are
recommended in more severe cases. Hypotension may be best treated with
incremental intravenous does of phenylephrine.

Lack of Consent

The concept of informed consent is a hallmark of modern medical ethics

and is firmly grounded in the principle of respet for autonomy.The two key
elements for informed consent are patient understanding of the risk