Postoperative Complications of Spine Surgery

Accepted Manuscript
Postoperative Complications of Spine Surgery
Matthew C. Swann, MD, Kathryn S. Hoes, MD, Salah G. Aoun, MD, David L.
McDonagh, MD, Professor & Vice Chair
PII: S1521-6896(16)00003-3
DOI: 10.1016/j.bpa.2016.01.002
Reference: YBEAN 886
To appear in: Best Practice & Research Clinical Anaesthesiology
Received Date: 16 November 2015

Revised Date: 5 January 2016
Accepted Date: 12 January 2016
Please cite this article as: Swann MC, Hoes KS, Aoun SG, McDonagh DL, Postoperative Complications
of Spine Surgery, Best Practice & Research Clinical Anaesthesiology (2016), doi: 10.1016/
j.bpa.2016.01.002.
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Swann, Hoes, Aoun, McDonagh Postoperative Complications-Perioperative Management for Major Spine Surgery
Postoperative Complications (outline)
1. Anesthetic complications (pain management covered in another chapter)

a. PONV
b. Tongue injury
c. Airway complications
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i. Airway edema/obstruction
ii. Esophageal Injury & Dysphagia
2. Positioning complications
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a. Blindness (covered in another chapter)
b. Nerve injury
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c. Skin breakdown
3. Acute spinal cord injury (covered in another chapter)
4. Vascular Injury
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a. Vertebral Injury
b. Aorto-iliac injury
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5. Cardiovascular Events-
a. MACE, stroke
6. Pulmonary Complications
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a. Pulm emboli
b. Pulm edema
i. TRALI, transfusion related circulatory overload
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7. Acute kidney injury

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8. Ileus
9. Coagulopathy
10. Wound infection
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Postoperative Complications of Spine Surgery
Matthew C. Swann, MD1, Kathryn S. Hoes, MD2, Salah G. Aoun, MD2, David L. McDonagh,
MD2,3
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Departments of 1Orthopedic Surgery, 2Neurosurgery, and 3Anesthesiology & Pain
Management
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University of Texas Southwestern Medical Center, Dallas, Texas, USA 75209
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Conflicts of Interest: The authors have no conflicts of interest related to this material.
Corresponding Author:
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David McDonagh, MD
Professor & Vice Chair; Department of Anesthesiology & Pain Management

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David.mcdonagh@utsouthwestern.edu
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Abstract
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There are a variety of surgical approaches to the treatment of diseases of the spine.
Complications can arise intraoperatively, in the immediate postoperative period, or in a

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delayed fashion. These complications may lead to severe or even permanent morbidity if
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left unrecognized and untreated [1-4]. Here we review a range of complications in the early
postoperative period from more benign complications such as postoperative nausea and
vomiting (PONV), to more feared complications leading to permanent loss of neurological
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function or death [5]. Perioperative pain management is covered in a separate review
(Chapter 8).
COMPLICATIONS OF ANESTHETIC CARE
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Postoperative Nausea and Vomiting
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Intraoperatively, anesthetic and surgical factors contribute to PONV, with the
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anesthetic factors being most modifiable (although surgical length is contributory and
potentially modifiable). Postoperatively, while patient-controlled opioid analgesia has
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revolutionized pain control it often contributes to PONV [6]. Despite prophylactic
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pharmacotherapy PONV remains very common. Identifying the high risk patient is the first
step in managing PONV (Table 1)[7]. Current strategies focus on multimodal pharmacologic
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nausea prophylaxis; as well as multimodal analgesia to limit opioid administration (Table

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2)[7]. Avoidance of nitrous oxide, inhalational anesthetics, and neostigmine is

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recommended in high risk patients as long as medically appropriate (ie, neostigmine use to
reverse residual neuromuscular blockade supercedes an increased risk of PONV).

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Table 1[7]:
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Risk Factors Approach to Treatment**

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Non-smoker Low risk patient- 1 agent

Female Gender Medium risk patient- 2-3 agents of different
pharmacologic classes
PONV after previous surgeries High risk patient- 3+ agents (such as aprepitant,
dexamethasone, ondansetron, & scopolamine)
Susceptible to Motion Sickness
General anesthesia (nitrous **Breakthrough PONV- treat with an agent from a
oxide, inhalational anesthetics, different pharmacologic class
neostigmine)
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Table 2[7]:
Nausea Pharmacologic Example Multimodal Pharmacologic Example
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Pharmaco- Class Analgesia Class
prophylaxis
Corticosteroids Dexamethasone Opioids Fentanyl
Serotonin Ondansetron Local anesthetic Lidocaine
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antagonists infusions
Histamine Diphenhydramine Local anesthetic Bupivacaine
antagonists infiltration
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Dopamine Droperidol NMDA Ketamine
antagonists antagonists
Phenothiazines Promethazine Central alpha-2 Dexmedetomidine
agonist
Neurokinin Aprepitant Gabapentinoids Gabapentin
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Antagonists
Intravenous Propofol Muscle Relaxants Methocarbamol
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Anesthesia
Muscarinic Scopolamine Anti- Celecoxib
antagonist inflammatory
(COX-2 inhibitors)
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Opioid Naloxone (low Anti- Acetaminophen

antagonists dose infusion) inflammatory
Electro-acupoint Wrist band device Neuraxial Continuous
Stimulation Regional Epidural Analgesia
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Anesthesia
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Injuries to the Tongue

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Tongue injuries are generally uncommon and limited to minor intubation trauma with
modern airway management techniques. However, spine surgery poses a unique risk. In the
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prone position, the tongue can protrude between the incisors. Impaired venous and
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lymphatic outflow as well as mechanical/bite injury from the teeth can lead to swelling.
Severe tongue edema requiring a tracheostomy has been described [8]. A bite block must
be used to keep the tongue behind the incisors while avoiding intraoral compression injury
of the tongue (resulting in pressure necrosis- figure 1). During spine surgery in the prone,
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supine, or lateral position, the use of motor evoked potentials stimulates masseter
contraction and jaw closure/biting. The insufficiently protected tongue can sustain severe
lacerations and even tissue necrosis [9, 10]. Head elevation/reverse Trendelenburg
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positioning is useful in reducing orbital, oral, lingual, and pharyngeal edema. Careful bite
guard placement and frequent checks of the mouth/face/eyes are standard of care in
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anesthetic practice.
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Figure 1: Pressure necrosis injury to the tongue
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Injuries to the Hollow Organs of the Neck

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Airway Injuries
Airway compromise is one of the most feared complications of cervical spine surgery
[1, 3, 4]. Effective management requires prompt recognition and treatment (re-intubation,
neck incision to relieve the hematoma, or both). The incidence of airway obstruction has
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been reported to be as high as 6.1% after multilevel anterior cervical procedures [4, 11] with a
70% need for emergent re-intubation in one series of combined anterior/posterior cervical
cases [12]. Risk factors include medical comorbidities, the spinal levels involved in the
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procedure, and the nature of the procedure itself [11, 13-15]. Specific surgical factors shown
to be predictors of postoperative airway compromise include: the exposure of more than 3
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cervical levels especially if these include levels C2 to C4, blood loss of more than 300ml,
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operative time exceeding 5 hours, and a combined anterior and posterior approach [4, 11, 12,
16, 17]. Patient factors include: morbid obesity, a history of obstructive sleep apnea (OSA)
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or pulmonary disease, the presence of cervical myelopathy, history of previous cervical
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surgery, and the off label use of bone morphogenic protein [18-20]. Anesthetic risk factors
include the suboptimal visualization of the glottis with grade 3 or 4 views, and multiple
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intubation attempts [4].

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The time frame of the airway compromise can be an indicator of the etiology.
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Wound hematomas usually occur early, manifesting within the first 12h after surgery.
Pharyngeal and prevertebral soft tissue edema, which is often the most common cause of
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airway obstruction, is usually slightly delayed and manifests at ~12-72 hours. Trials of
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preventive corticosteroid administration have failed to show benefit even at high doses [21,
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22]. Finally, airway obstruction that occurs later than 72 hours is usually indicative of abscess
formation, cerebrospinal fluid leak or construct failure[4]. Delayed extubation for hours to
days should be considered in certain cases based on patient and surgical factors in order to
allow resolution of head and neck edema, and minimize the risk for emergent and possibly
difficult/ morbid reintubation.
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Esophageal Injury
The location and shape of the esophagus make it vulnerable to injury during anterior
cervical spine procedures. For example, Lanniers triangle, an area bordered by the
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constrictor pharyngeous and cricopharyngeous muscles at the C5-C6 junction has mucosa
that is only protected by a thin fascial layer and is prone to injury, especially with the use of
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instrumentation [2, 23]. The reported incidence of esophageal injuries is relatively low, and
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may range from 0.3% in isolated discectomies, to 1.6% for cervical corpectomies [2, 24, 25].
Similar to airway injuries, esophageal injuries can present with variable timing and symptoms
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depending on the causal etiology. Acute damage can be due to sharp surgical dissection,
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excessive blunt retraction, direct surgical trauma, or traumatic endotracheal intubation.
Unrecognized perforation can lead to pharyngeal or cervical abscess or even life threatening
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mediastinitis. If the perforation is recognized early, patients tend to do uniformly well [26-
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29]. For immediately recognized injuries, direct repair with a resorbable suture is
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appropriate. An operative drain is placed, often along with a nasogastric tube and broad
spectrum antibiotics. If the discectomy or corpectomy procedure has not been initiated, it is
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typically aborted and postponed. While there is substantial variability in patient

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management, oral feedings are generally withheld until a radiographic study (such as barium
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swallow) shows no evidence of leakage through the mucosa.
Delayed perforations can either be early injuries that have gone unrecognized, or
injuries due to the instrumentation system a result of direct erosion from plates or migration
of screws [30-32]. Acute surgical injuries that are missed can present with dysphagia,
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odynophagia, subcutaneous emphysema, swelling, fever, and dyspnea. Later presentations
include abscess formation, sepsis, repeated pneumonias, and/or chronic neck pain. Even the
rectal passage of spinal instrumentation after transmural esophageal migration has been
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reported [2, 25]. Diagnostic studies include barium swallow radiography, neck CT, and
endoscopy. These delayed injuries may require more extensive repairs, and can lead to
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prolonged hospitalization and mortality rates as high as 50% [13, 14, 33].
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Dysphagia and Dysphonia
Dysphagia is one of the most common complaints after anterior cervical spine
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surgery. The incidence can reach 57% in the immediate postoperative phase, although a very
small percentage of patients (1.3% in a large series) can remain severely symptomatic at 2
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years [34]. Risk factors include age >60y, female sex, involvement of 2 or more cervical
levels, revision surgery, and the use of older and thicker anterior plating systems [34].
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Dysphagia can be multifactorial in etiology. Esophageal nerves can be injured by direct

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surgical manipulation or soft tissue swelling. The superior laryngeal nerves and the
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pharyngeal plexus can be injured in procedures involving C2 to C5 spinal levels. Dissection
above C3 can compromise the hypoglossal nerve which plays a role in the oral and
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pharyngeal phases of swallowing. Finally access to levels lower than C5 could potentially
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damage the recurrent laryngeal nerve. This type of injury typically causes milder dysphagia
mostly noticeable when swallowing liquids [34-37].
Hoarseness after cervical spine procedures is common and vocal cord paresis is
reported in up to 24% of cases in some series [38]. Causes include direct compression of the
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vocal cords, neurapraxia, and denervation injury. The recurrent laryngeal is most commonly
implicated with reported rates of injury ranging between 0.33-2.5% [39, 40]. Most injuries
heal without significant sequelae although a minority of cases will need referral to specialist
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services such as otolaryngology. Endotracheal tube cuff deflation, and gentle re-inflation
after retractor placement, has been advocated to reduce pressure injury on tissue between
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the cuff and retractor (which includes the recurrent laryngeal nerve), as well as to avoid
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direct injury to the nerve just below the vocal cords from a high-riding cuff or overinflated
cuff displaced superiorly by surgical retractors. However, prospective randomized studies
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have failed to show a significant reduction in the incidence of vocal cord paralysis with this
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practice [41].
POSITIONING COMPLICATIONS
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Postoperative Visual Loss (POVL).

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POVL is one of the rarest but most feared complications of spine surgery and can be
the result of hypotensive ischemia, direct orbital compression, orbital edema with
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compromise of small arterioles or veins, or a combination of these factors. Modifiable
intraoperative factors to minimize the risk of POVL include: head elevation (reverse
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Trendelenburg), avoidance hypotension and anemia, avoidance of direct orbital

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compression, limiting crystalloid use in favor of colloids, and limiting surgical duration [42,
43]. This topic is discussed in detail in a separate review.
Peripheral Nerve Injury
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Perioperative nerve injury is uncommon after spine surgery, with an incidence
ranging from 0.03% to 0.1 [44]. However, it can lead to significant loss of function, and can
be potentially litigious. Ulnar nerve injury is the most common (28%), followed by brachial
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plexus injury (20%) and median nerve injury (4%)[44]. A single culprit is seldom identified as
the cause is often multifactorial and the injury not fully explained by direct compression.
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Increases in intraneural and extraneural pressures along with reduction of perfusion
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pressure in the vasa-nervorum may lead to neural ischemia. This can disrupt axonal transport
and nerve conduction. Stretch injury can occur- as elongation of a nerve of more than 5-15%
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of its resting length increases intraneural pressure and compresses small arterioles and veins
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[45-47]. Finally some studies have shown that systemic inflammatory mechanisms
associated with surgery can lead to lasting postoperative neuropathy, with diffuse
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microneuritis identified as pathological evidence of this phenomenon [48]. The role, if any,
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of perioperative steroids in preventing this process has not been fully elucidated.
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Risk factors for postoperative peripheral neuropathy include pre-existing
hypertension, diabetes, advanced age, and tobacco use. General anesthesia prevents muscle
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contraction in response to overstretch injury, so the utmost vigilance must be used during
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patient positioning [49, 50]. Neurosurgical and orthopedic procedures have been identified
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as independent risk factors for nerve injury, likely due to complexity of patient positioning
[50]. Intraoperative monitoring with somatosensory evoked potentials (SSEPs) and motor
evoked potentials has been increasingly used in spinal procedures to assist with initial
positioning. In a retrospective review of 1000 consecutive spine cases, simple station
modification consisting of correcting extreme limb positions allowed the resolution of 92%
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of SSEP changes [51]. Changes in SSEP or MEP signals intraoperatively should prompt a re-
assessment of limb positioning/padding/stretch in addition to an evaluation of the surgical
site itself [50-52].
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Skin Breakdown
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Multiple practices have been established to prevent skin ulcers due to prolonged
immobility during surgical procedures [53]. Surgical time exceeding 3 hours and obesity are
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known risk factors. Selection of the surgical frame should be made carefully on a case by
case basis with consideration of risk for soft tissue pressure injury [53]. Some framing
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systems such as the Relton-Hall frame can produce excessive pressure at select body resting
points while others such as the Wilson, Andrews, and Jackson frames can provide
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appropriate thoracolumbar exposure while minimizing focal pressure injury. Breasts, male
genitalia, bony prominences, superficial nerves (ulnar, superficial peroneal) and axillae
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should be padded carefully and rechecked periodically throughout the case. In the event of
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wound breakdown or the persistence of non-blanching erythema postoperatively,

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dermatology/wound care consultation should be considered [54].
Acute Spinal Cord Injury:

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This is covered fully in a separate chapter. Intraoperative and postoperative prevention
focuses on maintenance of adequate spinal cord perfusion pressure and frequent
assessment of neurologic function (evoked potentials intraoperatively and clinical
neurologic examination postoperatively). New onset postoperative neurologic symptoms
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referable to the spinal cord should prompt emergent imaging (CT or MRI) to rule out a
compressive hematoma, hardware, etc.
Vascular Injury:
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Certain patients have carotid or vertebral anatomic variants that place them at particular risk
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for vascular injury during cervical spine surgery[55]. Injury to the major vessels of the neck
during cervical spine surgery is generally recognized intraoperatively. However, injury to a
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vessel causing intimal dissection is possible without perforation/hemorrhage and thus may
not become apparent until the postoperative period [56]. Acute postoperative stroke
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syndromes in either the anterior (due to carotid injury) or posterior (due to vertebral injury)
circulation should be investigated emergently with angiographic imaging (CT, MR, or

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conventional angiography). Endovascular thrombectomy should be considered in the
presence of large vessel occlusion (discussed further below).

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Thoracolumbar spine surgery can cause inadvertent injury to the aorta, vena cava, or
iliac vessels [57]. Occult injury should be suspected in the presence of severe or persistent
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postoperative hypotension and/or anemia. Investigation is with emergent CT and CT
angiography.
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Cardiovascular Events
Cardiovascular complications in the postoperative period include myocardial infarction,
cardiac arrhythmias, and cardiac arrest. Collectively, such complications are referred to as
Major Adverse Cardiac Events (MACE). Massive intraoperative hemorrhage and stroke also
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fall under the umbrella of cardiovascular complications. Though rare, such complications can
carry high morbidity and mortality [58].
In order to prevent such complications, it is incumbent upon the surgical, medical and
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anesthesia teams to communicate before and during the procedure so that hemodynamics,
hemostasis, and resuscitation can be managed effectively. The establishment of appropriate
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preoperative protocols for high risk patients can reduce the incidence of MACE and
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associated medical costs. Since 1980, the American College of Cardiology (ACC) and the
American Heart Association (AHA) have compiled up-to-date literature and distilled it into
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guidelines that can facilitate an appropriate preoperative workup for non-cardiac surgery
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[59]. Procedures are placed into two major categories: low and elevated risk. These
classifications take into consideration both the patients health profile and the
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magnitude/risk of the procedure itself. According to the ACA/AHA 2014 guidelines:[59]

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A low risk procedure is one in which the combined surgical and patient characteristics
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predict a risk of MACE, of death, or myocardial infarction (MI) of <1%... Procedures with a risk
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of MACE 1% are considered elevated risk[59]
These guidelines are readily available on the AHA website

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(http://circ.ahajournals.org/content/130/24/2215.extract) and provide a comprehensive

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approach to categorizing patients in this manner. Also available is the convenient American
College of Surgeons National Surgical Quality Improvement Program (NSQIP) risk calculator,
which can be found at http://www.riskcalculator.facs.org/PatientInfo/PatientInfo. This can
be used to estimate the perioperative risk of MACE based on the aforementioned criteria.
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Another tool used by the ACC/AHA for perioperative risk stratification in non-cardiac surgery
is the Revised Cardiac Risk Index (RCRI), which has been validated for orthopedic surgical
procedures.[60] This index identifies six major risk factors associated with MACE in non-
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cardiac surgical procedures: high-risk surgery, ischemic heart disease, congestive heart
failure, cerebrovascular disease, preoperative treatment with insulin, and preoperative
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serum creatinine >2.0 mg/dL. [61] However, there is some evidence that this model may
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underrepresent the true risk of MACE in patients undergoing spinal fusion surgery. [62]
Spine surgeries encompass a variegated spectrum of procedures that range from minimally
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invasive outpatient procedures to highly invasive procedures associated with prolonged
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operative times and intraoperative blood loss. Procedures on both ends of this spectrum are
performed in younger healthier patients as well as fragile elderly patients. Therefore,

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establishing an individualized risk profile as part of the preoperative assessment is critical.

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Myocardial infarction
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Myocardial infarction (MI) (defined as elevated troponin levels or EKG changes consistent
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with MI post operatively) has a reported incidence of 1-2% after spine surgery.[62-64] MI
after spine surgery is, on average, diagnosed on post-operative day two.[65] While there is
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high level evidence to support the myocardial protectant effects of perioperative beta-
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blockade, there is a simultaneous increase in perioperative stroke and mortality.[66]
Therefore current practice is to continue long-term beta blocker therapy but not to initiate
beta blocker therapy in the immediate preoperative period. [67]
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There is some evidence that patients who sustain a spinal cord injury or have a neurologic
deficit preoperatively are at increased risk of developing an acute MI.[64] In addition to this,
spinal cord injury at the thoracic level carries an increased risk compared to injury in the
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cervical or lumbar spine.[68] Prone positioning can alter normal hemodynamics in a
number of ways and possibly predispose patients with poor cardiovascular reserve to
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myocardial infarction. A study that compared five different prone positioning systems
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demonstrated that the Jackson spine table produces the least effect on cardiac
function.[54]
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Perioperative myocardial injury has long lasting implications. Independent of preoperative
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risk factors, serum markers of MI are associated with future adverse events. Elevated
troponin levels (ie, asymptomatic enzyme leaks; troponin 0.03 ng/ml) in the perioperative
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period, termed Myocardial Injury after Noncardiac Surgery (MINS) are associated with
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future cardiac complications including cardiac death.[69] Coupled with elevated serum CK-
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MB, elevated troponin levels after non-cardiac surgery are associated with a four-fold
increase in post-operative mortality,[70] even months to years after the index surgery.
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Manifestations of postoperative myocardial infarction may include chest pain, dyspnea, EKG
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changes, and dysrhythmias. Diagnosis of acute MI is based on EKG evidence of ischemia (ST
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elevation [STEMI] vs. Non-ST elevation [NSTEMI]) and serum troponin/CK-MB levels.
Emergent percutaneous coronary intervention must be considered in the setting of a STEMI;
and a risk:benefit decision must be made by the treating physicians given that the
intervention will require some degree of anti-platelet and/or thrombotic therapy.[71]
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Similarly, acute NSTEMI therapy involves anticoagulation.[72] General measures for
treatment of an acute postoperative MI consist of morphine analgesia, oxygen therapy,
beta-blockade, chewed aspirin and sublingual or IV nitrates. Echocardiography can identify
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regional wall motion abnormalities and evidence of pump failure. [73]
Hemorrhage
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Some spine surgeries can generate a large volume of intraoperative blood loss. Blood loss of
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greater than 3L has been reported to have an incidence of ~3% [63]. Major intraoperative
hemorrhage (defined as blood loss requiring transfusion of >4 units of packed red blood cell
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or whole blood) can generate MACE, independent of preoperative risk factors. For example,
major intraoperative hemorrhage has been shown to be an independent predictor of

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subsequent stroke and MI [74], as well as post-operative coagulopathies. [75]

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Stroke
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The reported rate of stroke after spine surgery is between 0.014-0.20%. [58, 74] Though rare,
perioperative stroke is associated with a high mortality rate. In one large study,
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perioperative stroke afforded an 8-fold increase in 30-day post-operative mortality. [76]

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Another study found that 16% of patients who suffered a perioperative stroke died before
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discharge from the hospital.[77] In terms of patient characteristics, independent risk factors
for perioperative stroke include older age, history of MI within 6 months of the surgery,
renal failure, atrial fibrillation, history of stroke, dialysis, hypertension, history of TIA, COPD,
and current tobacco use.[76, 77] In patients with pre-existing cardiovascular disease, current
literature has demonstrated decreased rates of cardiovascular death and non-fatal MI with
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use of perioperative beta blockade.[66] However, there is also evidence that perioperative
beta-blockade can more than double the risk of perioperative stroke.[67, 78] Moreover,
retrospective data suggests that intraoperative administration of metoprolol may carry a
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higher risk of stroke as compared to esmolol or labetalol.[67] Current anesthetic practice is
to titrate beta blockade, if used at all, to specific hemodynamic targets rather than
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empirically administer to all patients.
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As mentioned previously, iatrogenic vertebral and carotid artery injury can occur during
cervical spine surgery.[79-81] In the anterior approach to the cervical spine, retraction on the
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common carotid artery can significantly alter blood flow through it. With initial placement of
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a self-retaining retractor, the vessel cross-sectional area can decrease by 14%; because of
vessel compliance, the cross sectional area can diminish to 70% as the case progresses.[82]
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Gentle retraction and frequent adjustment of the retractor can reduce this effect. Iatrogenic
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injury through hardware penetration of the vertebral or carotid arteries has also been
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reported. The use of lateral mass screws in C1 and pedicle screws in C2 has a known
association with vertebral artery injury. In a large retrospective study, iatrogenic injury to the
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vertebral artery in these procedures occurred at a reported rate of 2.4%; however, of

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patients with a known or suspected vertebral artery injury, only 3.7% developed subsequent
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neurologic deficits.[83] Although infrequently used in spine surgery, intraoperative duplex
monitoring of the carotid artery, cerebral oximetry, and the bispectral index have been used
to monitor for and diagnose cerebral ischemia.[84-86] Despite the availability of these
systems, the clinical value and role in spine surgery is unclear.
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Three other issues must be considered in the perioperative management of the spine
surgery patient:
1. Timing of elective spine surgery after stroke - Best evidence to date demonstrates a
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significant drop in recurrent stroke risk at three months (after the initial stroke) for
patients with prior ischemic stroke having elective non-cardiac surgery.[87] The risk
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for recurrent stroke plateaus at its lowest level 9 months after the initial stroke.
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Therefore, for patients in need of purely elective non-cardiac surgery, the safest
approach is to wait 9 months to perform surgery.[87]
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2. Should aspirin be continued throughout the perioperative period? - The POISE-2 trial
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randomized over 10,000 patients at risk for vascular complications and undergoing
non-cardiac surgery to aspirin or placebo and found no difference in death or

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nonfatal MI between the groups.[88] Aspirin continuation did, however, increase

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bleeding. Therefore, there is no indication to continue - or initiate - aspirin therapy

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preoperatively in most patients at risk for vascular complications. The exception is
patients with intra-arterial (e.g. coronary, cerebral, etc) stents, where aspirin
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continuation perioperatively may be necessary based on the type of stent (bare

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metal or drug-eluting) and length of time since stent placement relative to the spine
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surgery. This should be a decision by the surgeon and cardiologist based on risk of
operative hemorrhage and MACE in the individual patient.
3. Management of acute stroke in the post-operative period - Intravenous alteplase
(rTPA) is standard of care for acute ischemic stroke up to 4.5 hours post-ictus.
However, systemic thrombolysis is contraindicated post-operatively after spine
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sugery. Acute endovascular thrombectomy should be considered in any patient with
an acute postoperative stroke (generally up to 6 hrs after stroke onset in the anterior
circulation and up to 12hrs in the vertebrobasilar circulation).[89] Initial evaluation is
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with emergent head CT and CT angiography, maintenance of cerebral perfusion
pressure, and stroke neurology consultation.
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Respiratory & Pulmonary Complications
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The most common respiratory complication after spine surgery is likely opioid-
induced respiratory depression. Patients with obesity and/or OSA are at particularly high
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risk. The STOP-BANG scoring system (http://www.stopbang.ca/screen.php) is commonly
used to assess risk preoperatively in patients without a definitive diagnosis of OSA.

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Perioperative guidelines for management of this patient population have been published by
the American Society of Anesthesiologists [90]. The general approach is to identify high risk
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patients, minimize post-operative sedative agents, provide supplemental oxygen and

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continuous or bilevel positive airway pressure (CPAP/BIPAP), and monitor in an appropriate

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setting with pulse oximetry during the high risk period of recovery. The following URL leads
to a comprehensive document on current practice guidelines for managing OSA in the

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perioperative period:
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http://www.asahq.org/~/media/Sites/ASAHQ/Files/Public/Resources/standards-
guidelines/practice-guidelines-for-the-perioperative-management-of-patients-with-
obstructive-sleep-apnea.pdf
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Others pulmonary complications include pulmonary embolism, pneumonia,
pulmonary edema, aspiration, and acute respiratory distress syndrome (ARDS).[58]
Pulmonary complications are frequent after spine surgery, occurring at a rate of ~13%; with
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post-operative pneumonia representing the most common pulmonary adverse event.[63]
Assessment of pulmonary health and function is a fundamental element of the preoperative
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workup. Preoperative optimization with specialist consultation/guidance should be
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considered.
There are a number of patient related characteristics that are associated with an
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increased risk of developing pulmonary complications after surgery. Smoking confers a
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relative risk of 3.4 times the rate of complications compared to non-smokers.[91] Optimal
timing of preoperative smoking cessation remains controversial. As a general rule, patients

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should be encouraged to stop smoking at least 4 wks prior to their surgery in order to
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reduce pulmonary related complications,[92] reoperation from any cause,[93] and failure of
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bone fusion.[94, 95]

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Patients with COPD are clearly at an increased risk for pulmonary complications after
surgery.[96] The relative risk of complications is increased 2.7-4.7 times that of patients
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without COPD, depending on the operation.[91] Aggressive preoperative optimization of

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COPD prior to elective surgery is recommended. [91, 92, 96, 97] Intraoperatively and
postoperatively, lung-protective ventilation is used along with bronchodilator therapy.
Postoperative mobilization and aggressive respiratory therapy is essential.[98] An
individualized decision must be made by the surgeon and treating physicians regarding ICU
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admission and extubation to noninvasive positive pressure ventilation (BIPAP) in fragile
COPD patients.
Pulmonary Embolism
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Venous thromboembolism and subsequent pulmonary embolism (PE) have always
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been major drivers of postoperative morbidity. Based on two large retrospective studies,
PE, as identified by CT angiography, ventilation perfusion scan or conventional angiography
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occurs at a rate ranging from 0.3-1.4%,[63, 99] and it is fatal in 0.02-0.2% [58, 100] of patients
who undergo spine surgery. Randomized clinical trials have demonstrated a rate of VTE as
U
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high as 40-60% in medical and surgical patients who do not receive thromboprophylaxis.[101]
However, the routine use of both chemo- and mechano-thromboprophylaxis has greatly
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reduced the incidence of VTE and, more importantly, fatal PE.[101-105] Among spine
patients who did not receive prophylaxis, the rate of DVT and PE ranges from 0-18%, and
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from <0.1%-37.5%, respectively.[106-108] Older data on rates of VTE in spine patients who did
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not receive thromboprophylaxis are misleading because prolonged periods of recumbency

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were a standard practice at the time.[106, 107, 109]
Routine post-operative screening for DVT/PE is not recommended in current

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guidelines. The average time to diagnosis of a PE after spine surgery is 5 days.[65] Clinical
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manifestations of PE include tachycardia, desaturations/hypoxia, shortness of breath, cough
and chest pain all of which are nonspecific. Therefore, a diagnosis of PE is almost
exclusively confirmed with advanced imaging, typically CT angiography. The utility of D-
Dimer assay to assist with diagnosis of VTE is controversial; however, one study found that
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the assay was 100% sensitive and 80.7% specific using a cutoff value of 2.113 microgram/mL
from a sample on post-operative day 3 after spine surgery.[110] Based on a large literature
review, the rates of PE in post-operative spine patients using various modalities are as
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follows: No prophylaxis = 2.7%, Compression stockings (CS) = 2.7%, SCDs = 4.6%, SCDs and CS=
1.3%, chemical anticoagulation with SCD/CS = 0.6%.[99] The authors concluded that the use
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of SCDs and CS combined is an acceptable modality for VTE prophylaxis. [99]
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Epidural hematoma is always a concern in operative spine patients who receive
chemoprophylaxis but that concern may not be justified. A large retrospective literature
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review found that rates of symptomatic epidural hematoma in surgical spine patients who
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received VTE chemoprophylaxis range from 0-0.7%; this is compared to a rate of 0-1% overall
in the reviewed literature.[111] However, VTE chemoprophylaxis after spine surgery is often
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not routinely implemented[112]. The risk of developing a post-operative hematoma must be

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weighed against the risk of VTE and opinion varies amongst surgeons. There is a relative
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dearth of high level evidence to guide post-operative VTE chemoprophylaxis in spine surgery
patients.[99] Recent retrospective data suggests that initiating VTE prophylaxis following
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surgery for traumatic spine injury <48 hours postoperatively is likely safe.[113] Our standard
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practice includes intraoperative and post-operative lower extremity pneumatic compression

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devices, mobilization, and pharmacologic VTE prophylaxis starting as soon as the patient is
deemed hemostatic (typically 24-72 hours postoperatively).
Pulmonary Edema/ARDS/TRALI
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Pulmonary edema occurs in ~1.3% of patients after spine surgery. [58, 63] In more
complex procedures, such as combined anterior and posterior reconstructive spine surgery,
the rate of post-operative pulmonary edema may be as high as 14.5%.[114] Intraoperative
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goal directed fluid therapy is the first step in limiting both tissue edema including facial,
airway, and pharyngeal as well as pulmonary edema. More liberal use of colloid therapy
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intraoperatively is associated with less postoperative edema.
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Pulmonary edema and the related Acute Respiratory Distress Syndrome (ARDS) are
caused by many different factors associated with direct or indirect injury to the lungs.
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Extensive spine surgery can activate a global injury/inflammatory response similar to
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massive trauma.[115] In response to such an insult, the body initiates an inflammatory
cascade and releases mediators including tumor necrosis factor (TNF) and interleukins (e.g
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IL-1, IL-6).[116, 117] Although the mechanisms are unclear, in some patients this inflammatory
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cascade becomes poorly regulated and can lead to extravasation of interstitial fluid from
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leaky endothelial capillaries. There is limited data that suggests that fat emboli may also
play a role in respiratory injury after some spine procedures [118].

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As discussed earlier in the chapter, extensive spine surgery is associated with high
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rates of intraoperative transfusion.[119] Although blood transfusion can result in a number

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of adverse events, the leading cause of associated morbidity and mortality is transfusion-
related acute lung injury (TRALI).[120] A diagnosis of TRALI is made when a new acute lung
injury (ALI) is identified within 6 hours after a blood transfusion, in the absence of pre-
existing risk factors or other clinical cause (e.g. ABO incompatibility, volume overload,
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allergic reaction, etc.).[121, 122] Regardless of the cause, ALI is associated with increased
pulmonary capillary permeability and increased protein in the alveolar fluid.[121] Although
the exact mechanism is unknown, two prevailing theories on the etiology of TRALI exist, and
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are as follows: 1) Leukocyte antibodies in donor blood (often associated with blood donated
by multiparous women) activate neutrophils in the recipient lung tissue, initiating an
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unregulated inflammatory cascade; reducing the amount of WBCs in donated blood reduces
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the incidence of TRALI. [123, 124] 2) Biologically active cytokines and lipids in donated blood
activate neutrophils in recipient pulmonary tissue, sequestered there after an insult such as
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trauma or surgery.[122, 125, 126]
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Treatment of both pulmonary edema/ALI and TRALI are similar, and primarily consists
of supplemental oxygen and ventilatory support (e.g. non-invasive BIPAP or invasive

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ventilation) with PEEP. Maintenance of volume status with diuresis is much more critical in
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ARDS from other causes; as patients with TRALI are often euvolemic, whereas patients with
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ARDS may be hyper-or hypovolemic. Unlike ARDS, patients with TRALI recover relatively
quickly, usually within ~96 hours.[127]

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Acute Kidney Injury (AKI)

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Using older definitions of AKI as an acute serum creatinine (sCR) rise >2.0 mg/dL over
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baseline, the incidence of AKI after spine surgery is only 0.88%.[63] However, recent
guidelines suggest more sensitive criteria (i.e., serum creatinine rise 0.3mg/dl by 48h or
increase to 1.5 times baseline). [128] The newer RIFLE classification for acute renal failure
(Risk of renal dysfunction, Injury to the kidney, Failure of kidney function, Loss of kidney
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function and End-stage renal disease) assesses glomerular filtration rate, creatinine and
urine output. Based on these criteria, patients are placed into three separate categories, in
order of severity: risk, injury, and failure[129] Using this method, the overall reported
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incidence of AKI after spine surgery is 3.9%. [130]
The etiology is likely multifactorial and due to factors including renal hypoperfusion,
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intravascular hypovolemia, nephrotoxic drugs and/or contrast agents, and inflammatory
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responses. Post-operative AKI can have long lasting implications and has been shown to be
an independent predictor of increased mortality in the long term, despite the vast majority
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of patients having a complete or partial resolution of the AKI at time of discharge.[129, 131]
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For example, patients with complete recovery of AKI at time of discharge still had a 20%
increase in risk of death at 10 years, after adjusting for other postoperative

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complications.[131] When AKI is identified in the postoperative setting, avoiding a second

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hit phenomenon to the kidneys is imperative.

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Ileus
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Post-operative paralytic ileus (POI) after spine surgery causes patient discomfort and
decreased mobility with associated prolonged hospital stays and increased costs.[132, 133]
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Moreover, patients who develop POI are at higher risk of developing other, more severe
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complications, such as pulmonary embolus (nearly 20-fold in one study).[134] Defined as
abdominal distention and no passage of stool or flatus by post-operative day 3, ileus after
spine surgery occurs at a rate of 2.3%. [63] The incidence of ileus and other GI complications
is related to the type of spine procedure performed. Procedures on the lumbar spine have
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increased rates of POI compared to cervical procedures.[135-137] Indeed, there is a stepwise
increased of ileus in patients who undergo lumbar fusion though a posterior approach
(2.6%), anterior approach (7.5%) and circumferential (anterior/posterior) approach
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(8.4%).[133] Patient characteristics associated with increased risk of POI in spine patients
include male gender, increased age, and African American ethnicity.[133]
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There are multiple perioperative strategies that have been implemented to prevent
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POI. These include, but are not limited to, preoperative probiotics, preoperative
carbohydrate loading, preoperative COX-2 inhibitors, gum chewing, early enteral feeding,
minimizing intraoperative and

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postoperative opioids, aggressive use of stool
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softeners/laxatives, goal directed IV fluid administration, and early postoperative
mobilization.[138] However, many of these fall under the probably beneficial category,
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and may not be independently beneficial.[139] The use of thoracic epidural anesthesia has
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been shown to reduce the rate and duration of POI.[140-142] This is thought to work by
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blocking inhibitory reflexes in the gastrointestinal tract which are triggered by manipulation
of the bowel and systemic inflammation; sympathetic blockade also leads to increased
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splanchnic blood flow.[139] The pain relief provided by the epidural anesthetic can also
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reduce the need for opioid analgesia, which in turn improves bowel motility.[143] There is
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limited data regarding its use in spine surgery.[144]
Treatment of POI begins with reducing or eliminating the administration of opioid
analgesia and increasing mobilization. Many spine patients are on some form of opioid
based pain control before they undergo surgery.[145] Although tolerance to the analgesic
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properties of opioid medication is readily acquired, resistance to the GI effects is not.[139]
Novel approaches to POI include neostigmine which has been used to treat POI in spine
patients, and has been shown to reduce abdominal distention both clinically and
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radiographically.[146] Methylnaltrexone and alvimopan are peripherally acting mu-opioid
antagonists FDA approved to treat opioid induced ileus and postoperative ileus,
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respectively.[147] Efficacy in postoperative ileus after spine surgery is undefined.[147]
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Coagulopathy
Large spine surgeries, such as extensive fusion and deformity correction, can
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generate high volumes of intraoperative blood loss. Average estimates of blood loss in these
procedures range from 1000-3000mL, with an attendant high rate of perioperative

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transfusions.[63, 75, 119, 148, 149] Among all spine surgeries, the rate of post-operative
coagulopathy as defined by INR >2, platelets <50 or fibrinogen <100, is 0.82%.[63] Among
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procedures with high volumes of blood loss (~3L), and therefore increased requirements for
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blood transfusion, the rate of post-operative coagulopathy is as high as 53%.[75] Most of the
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data available on hemorrhagic coagulopathy revolve around the acute trauma setting;
however, the massive blood loss inherent to some spine procedures can trigger analogous
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homeostatic cascades and resuscitative efforts.

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Two other important factors that can cause coagulopathy in the perioperative setting
are hypothermia and acidosis. Both of these decrease the rate of biochemical reactions that
facilitate coagulation. Lengthy spine procedures can lead to increased risk of hypothermia,
which has been found to be an independent predictor of increased blood loss.[150] This
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seems to be primarily caused by an effect on platelets; at 33C, platelet aggregation and
adhesion are significantly reduced, but coagulation enzyme activity (i.e. thrombin cascade
propagation) is not.[151, 152] On the other hand, acidosis seems to primarily effect the
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propagation phase of thrombin formation by inhibiting enzymatic activity. [152]
Many high volume complex spine centers have developed intraoperative transfusion
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protocols analogous to trauma transfusion protocols. In the postoperative setting, these
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should be continued until the patient is hemostatic, followed by gradual de-escalation.
Coagulation parameters including prothrombin time (PT), international normalized ratio
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(INR) and activated partial thromboplastin time (aPTT) are used to evaluate the coagulation
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system. The reported sensitivity for increased intraoperative hemorrhage (as determined by
the surgeon) for INR, PT and aPTT is 94, 90 and 85 percent, respectively; the reported
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specificity is 88, 64 and 64 percent, respectively.[148] Newer methods to analyze the

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coagulation process intraoperatively are the viscoelastic blood tests known as

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thromboelastography (TEG) and rotational thromboelastometry (ROTEM). These tests are
able to analyze all phases of the coagulation cascade, including fibrinolysis.[153] They can
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also be performed at the patients own body temperature, which can give insight into the
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effect on coagulation for a given core temperature milieu.[153] There is some evidence that
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these tests can reduce the administration of blood product transfusions,[154] as well as
standardize transfusion practice and identify hypofibrinogenemia in spine surgery.[155]
Further research is needed to define the role of these tests in spine surgery.
Surgical Site Infection
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Surgical site infections (SSIs) remain a common complication after spine surgery.
Although there are myriad studies reporting a wide incidence of SSI after spine procedures,
a rate of 2.0-2.5% is frequently cited.[156-158] SSIs can have a dramatic impact on patient
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outcomes, leading to return trips to the operating room, increased expenses, prolonged
disability and in some cases, death. Sepsis, though rare at a rate of 0.03%, is the third leading
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cause of mortality after major spine surgery in some reports.[58] The rate of SSI is highly
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dependent on the type of procedure performed. For example, patients undergoing
deformity correction and those in a trauma setting are at increased risk compared to those
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undergoing surgery for degenerative procedures.[156, 159] Minimally invasive techniques
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(defined as a procedure done through tubular retractors) can reduce the rate of SSIs for
certain procedures.[160]
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SSIs after spine surgery are diagnosed, on average, on post-operative day 17.[65]
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Thus the patient has usually been discharged prior to the recognition of a SSI. Most SSIs are
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indolent, and some deep infections may have no outward physical manifestations for a
prolonged period of time. Subtle signs and symptoms may not prompt a patient to seek
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treatment sooner. The surgeon must have a high index of suspicion for SSIs and be wary of
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outward signs such as swelling, tenderness to palpation, erythema, and symptoms such as
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persistent pain, nausea, loss of appetite, and fatigue.[158] Standard lab workup includes
serum erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and complete blood
count. Of note, post-operative CRP levels normally remain elevated for ~2 weeks, with a
peak at post-operative day 3; whereas ESR may require ~6 weeks to normalize.[161]
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Recognizing which patients are at increased risk for infection is an important part of
the diagnostic process. One study identified three groups with high risk for infection after
spine surgery: patients with an underlying neurologic disorder, patients who abuse drugs or
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alcohol, or have an underlying cardiac disorder other than hypertension.[157] In this study,
diabetes carried a lesser risk for SSI than the above factors;[157] but other reports identify
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up to 4-fold increases in SSI in diabetic patients.[162] The role of obesity and its impact on
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SSI after spine surgery is unclear there is data that has demonstrated both increased risk
and no difference in this subgroup.[163, 164] The distribution of fat among obese patients is
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highly variable, so body mass index may not be the best metric to assess risk.
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As with other post-operative complications, prevention of SSIs is the most efficient
method to reduce health care costs and improve patient outcomes. There is an abundance
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of literature on the prevention of SSIs in the perioperative setting. Screening patients for
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colonization with MRSA is an increasingly popular practice but no firm guidelines exist.
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Treating these patients with intranasal mupiricin has been shown to reduce the incidence of
SSIs in orthopedic patients.[165, 166] Perioperative glycemic control is consistently

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recommended to reduce SSIs in the diabetic population. A target hemoglobin A1c of <8.0
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preoperatively has been recommended in some reports, and intraoperative/postoperative

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maintenance of blood glucose below 180-200mg/dl based on extrapolation from other
surgical populations.[162, 166, 167] CHG bathing preoperatively is a common practice but
evidence of efficacy is limited.[168]
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The use of prophylactic antibiotics has been shown to reduce the incidence of SSIs
after spine surgery.[169, 170] Despite great variability among practitioners in terms of
antibiotic selection and duration, there is no evidence that utilizing broad spectrum
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antibiotics or additional post-operative doses improves outcomes, as long as one pre-
operative dose with gram positive coverage is administered.[169] Additionally, if a drain is
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used, there is no reported benefit for continuing antibiotics until the drain is removed
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compared to standard 24hour post-operative antibiotics.[171]
Though perioperative intravenous administration of antibiotics has been well
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established in spine surgery, a technique that has gained recent popularity is the use of
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intrasite vancomycin powder. Although there are no technical or dosing guidelines
available, there is evidence that utilizing this technique can reduce SSIs in spine patients
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without systemic adverse effects.[172, 173] At present, however, high quality evidence
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remains limited. Another intrasite adjunct to reduce SSIs is dilute betadine solution. In
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one randomized controlled trial, immersing the wound in 0.35% betadine solution followed
by irrigation with normal saline resulted in a significant reduction in both deep and
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superficial SSIs after spine surgery.[174]

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The impact of intraoperative thermoregulation on SSIs has also been studied.

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Although there is some limited evidence that mild hypothermia (~35.5 C) may be protective
of the neurological elements during spine surgery, [175] it has also been associated with
increased risk of SSI.[176, 177] Overall, the benefits of maintaining normothermia in spine
patients seem to outweigh any theoretical benefit of hypothermia.
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Practice Points:
Preventing postoperative complications in spine surgery patients is a multifaceted
endeavor encompassing careful individualized preoperative patient selection and
optimization, operative surgical and anesthetic planning, and preparation for
postoperative and rehabilitative care.
Anesthetic factors to be optimized include:
o Cardiopulmonary assessment.
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o Careful positioning to avoid injury.
o Nausea prophylaxis.
o Multimodal analgesic therapy.
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o Goal-directed fluid resuscitation therapy avoiding excessive crystalloid
administration (to reduce tissue edema and risk for POVL).
o Maintenance of adequate spinal cord perfusion pressure.
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Patients at risk for opioid-induced respiratory depression should be monitored
appropriately and given supplemental oxygen.
o Similarly, patients with OSA should be assessed for possible CPAP/BIPAP therapy
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Rapid assessment and treatment of acute postoperative complications including
coagulopathy, myocardial injury, acute stroke, VTE, ileus, and/or acute kidney injury can
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circumvent major morbidity or mortality.
o New onset neurologic deficits referable to the spine should prompt emergent
imaging to rule out spinal cord or nerve root compression from a hematoma
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o New onset neurologic deficits referable to the brain/brainstem should prompt

emergent CT (or MRI) and CT Angiography (or MR angiography) to look for large
vessel occlusion.
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Research Agenda:
Further research in spine surgery is needed regarding the:
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o Role and benefit of enhanced recovery pathways.

o Optimal use of colloid and transfusion therapy in the intraoperative and early
postoperative period.
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o Ideal perioperative analgesic techniques that minimize opioid usage (such as

neuraxial analgesia), maximize mobility, and reduce the incidence of chronic
pain.
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o Factors underlying the physiologic/inflammatory response to surgery and

inter-individual susceptibility to postoperative organ dysfunction (such as
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renal injury).
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37. Smith-Hammond, C.A., et al., Prospective analysis of incidence and risk factors of dysphagia in
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38. Tan, T.P., et al., Vocal cord palsy after anterior cervical spine surgery: a qualitative systematic
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40. Apfelbaum, R.I., M.D. Kriskovich, and J.R. Haller, On the incidence, cause, and prevention of
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Postoperative Complications of Spine Surgery

To appear in: Best Practice & Research Clinical Anaesthesiology

Received Date: 16 November 2015

Postoperative Complications (outline)

1. Anesthetic complications (pain management covered in another chapter)

7. Acute kidney injury

Postoperative Complications of Spine Surgery

Professor & Vice Chair; Department of Anesthesiology & Pain Management

Complications can arise intraoperatively, in the immediate postoperative period, or in a

vomiting (PONV), to more feared complications leading to permanent loss of neurological

function or death [5]. Perioperative pain management is covered in a separate review

COMPLICATIONS OF ANESTHETIC CARE

potentially modifiable). Postoperatively, while patient-controlled opioid analgesia has

nausea prophylaxis; as well as multimodal analgesia to limit opioid administration (Table

2)[7]. Avoidance of nitrous oxide, inhalational anesthetics, and neostigmine is

reverse residual neuromuscular blockade supercedes an increased risk of PONV).

Risk Factors Approach to Treatment**

Non-smoker Low risk patient- 1 agent

Nausea Pharmacologic Example Multimodal Pharmacologic Example

Opioid Naloxone (low Anti- Acetaminophen

Injuries to the Tongue

Injuries to the Hollow Organs of the Neck

to be predictors of postoperative airway compromise include: the exposure of more than 3

intubation attempts [4].

difficult/ morbid reintubation.

typically aborted and postponed. While there is substantial variability in patient

swallow) shows no evidence of leakage through the mucosa.

odynophagia, subcutaneous emphysema, swelling, fever, and dyspnea. Later presentations

Dysphagia can be multifactorial in etiology. Esophageal nerves can be injured by direct

pharyngeal plexus can be injured in procedures involving C2 to C5 spinal levels. Dissection

mostly noticeable when swallowing liquids [34-37].

cuff displaced superiorly by surgical retractors. However, prospective randomized studies

Postoperative Visual Loss (POVL).

compromise of small arterioles or veins, or a combination of these factors. Modifiable

Trendelenburg), avoidance hypotension and anemia, avoidance of direct orbital

43]. This topic is discussed in detail in a separate review.

Peripheral Nerve Injury

Perioperative nerve injury is uncommon after spine surgery, with an incidence

Risk factors for postoperative peripheral neuropathy include pre-existing

positioning. In a retrospective review of 1000 consecutive spine cases, simple station

assessment of limb positioning/padding/stretch in addition to an evaluation of the surgical

site itself [50-52].

wound breakdown or the persistence of non-blanching erythema postoperatively,

dermatology/wound care consultation should be considered [54].

Acute Spinal Cord Injury:

This is covered fully in a separate chapter. Intraoperative and postoperative prevention

focuses on maintenance of adequate spinal cord perfusion pressure and frequent

assessment of neurologic function (evoked potentials intraoperatively and clinical

neurologic examination postoperatively). New onset postoperative neurologic symptoms

compressive hematoma, hardware, etc.

during cervical spine surgery is generally recognized intraoperatively. However, injury to a

circulation should be investigated emergently with angiographic imaging (CT, MR, or

conventional angiography). Endovascular thrombectomy should be considered in the

presence of large vessel occlusion (discussed further below).

postoperative hypotension and/or anemia. Investigation is with emergent CT and CT

Cardiovascular complications in the postoperative period include myocardial infarction,

carry high morbidity and mortality [58].

hemostasis, and resuscitation can be managed effectively. The establishment of appropriate

magnitude/risk of the procedure itself. According to the ACA/AHA 2014 guidelines:[59]

of MACE 1% are considered elevated risk[59]

These guidelines are readily available on the AHA website

(http://circ.ahajournals.org/content/130/24/2215.extract) and provide a comprehensive

which can be found at http://www.riskcalculator.facs.org/PatientInfo/PatientInfo. This can