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By: F. Jaffar, M.A., M.D.
Professor, Oakland University William Beaumont School of Medicine
Determining the cause of acute liver failure is important for 2 reasons: 1) specific therapy may be available treatment 4s syndrome buy generic lariam on line, as for acetaminophen hepatotoxicity or herpes hepatitis medications nursing discount lariam express, and 2) the prognosis differs depending on the cause medicine 0636 order 250 mg lariam amex. For instance medicine for high blood pressure buy lariam no prescription, the spontaneous recovery rate for patients with acute liver failure due to acetaminophen or hepatitis A is more than 50%; consequently, a more cautious approach would be advised before proceeding with liver transplant. Liver increase in the serum level of ammonia, although alterations in unidentified neurotransmitters likely are involved in causing mental status changes. Cerebral edema is estimated to cause about 20% of the deaths of patients with acute liver failure. Patients with acute liver failure are predisposed to infections likely due to severe illness and the need for numerous interventions and monitoring. The clinical features typical of infection, such as fever and leukocytosis, may not occur in patients with acute liver failure, so a high level of awareness for infection needs to be maintained. Any clinical deterioration should mandate a search for infection, and the threshold for antimicrobial therapy should be low. It is likely due to both inadequate degradation of insulin and diminished production of glucose by the diseased liver. A hyperdynamic circulation and a decrease in systemic vascular resistance are seen in patients with acute liver failure. These features may be well tolerated by patients, but occasionally hemodynamic compromise can develop. Fluid resuscitation usually is necessary, although caution is advised because the administration of excessive fluid may worsen intracranial pressure. Renal and electrolyte abnormalities occur because of underlying disease such as Wilson disease, functional renal failure due to sepsis or hepatorenal syndrome, or acute tubular necrosis. Renal dysfunction is particularly common in acetaminophen-induced acute liver failure. Monitoring of electrolytes, including sodium, potassium, bicarbonate, magnesium, and phosphorus, is important, and the presence of acidosis is a risk factor for poor outcome in acute liver failure and has been incorporated into prognostic models. Management the appearance of encephalopathy precedes cerebral edema; therefore, patients with acute hepatitis and evidence of liver failure need to be monitored carefully for mental status changes. Patients with encephalopathy should receive lactulose, although this agent is not as effective in acute liver failure as in chronic liver disease and may not prevent cerebral edema from developing later. Computed tomography of the head is performed to exclude an alternative cause of mental status changes. Endotracheal intubation and mechanical ventilation usually precede placement of the intracranial pressure monitor. Various monitors are used, but infection and bleeding can complicate any monitoring. The goal of intracranial pressure monitoring is to allow treatment of high pressure and to identify which patients are too ill for liver transplant because of a prolonged period of excessively high intracranial pressure. Generally, the goal is to maintain intracranial pressure less than 40 mm Hg and cerebral perfusion pressure (the difference between mean arterial pressure and intracranial pressure) between 60 and 100 mm Hg. Excessively high cerebral perfusion pressures (>120 mm Hg) can increase cerebral edema. Maneuvers that cause straining, including endotracheal suctioning, should be avoided or limited. Paralyzing agents and sedatives may be necessary, although they may limit further assessment of neurologic status. A prolonged increase in intracranial pressure above mean arterial pressure may signify brain death and generally is a contraindication to liver transplant. In patients with acute liver failure, the prolonged prothrombin time is a simple noninvasive measure to follow, and coagulopathy is not corrected unless there is bleeding or an intervention is planned (eg, placement of a monitoring device). Continuous infusion of 5% or 10% dextrose is used to keep the plasma glucose level between 100 and 200 mg/dL. Both bacteremia and fungemia are sufficiently frequent that periodic blood cultures are advised and prophylaxis with antimicrobials may be initiated, although this practice has not been shown to affect survival. One recent randomized trial suggested that administration of N-acetylcysteine may be beneficial in some patients who have acute liver failure even when acetaminophen hepatotoxicity has been excluded. Patients with early-stage encephalopathy treated with N-acetylcysteine had better transplant-free survival than untreated patients. Models to predict the outcome of acute liver failure have been developed to facilitate the optimal timing of liver transplant before the patient becomes so ill that transplant is contraindicated yet still allow time for spontaneous recovery. Acute liver failure is the indication for 6% of liver transplants in the United States. Diagnostic and predictive factors of significant liver fibrosis and minimal lesions in patients with persistent unexplained elevated transaminases: a prospective multicenter study. Acetaminophen-induced acute liver failure: results of a United States multicenter, prospective study. Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States. The 5 primary hepatitis viruses that have been identified are A, B, C, D (or delta), and E. Other viruses, such as cytomegalovirus and Epstein-Barr virus, also can result in hepatitis as part of a systemic infection. In addition, medications, toxins, autoimmune hepatitis, or Wilson disease may cause acute or chronic hepatitis. Acute hepatitis can last from a few weeks to 6 months and is often accompanied by jaundice. Symptoms of acute hepatitis tend to be similar regardless of cause and include anorexia, malaise, dark urine, fever, and mild abdominal pain.
Wire or cable fixed rods or loops represented an advance over prior techniques symptoms 7 days after conception discount lariam 250mg fast delivery, but such constructs only provided semirigid fixation medications rheumatoid arthritis cheap 250 mg lariam free shipping. Modern segmental screw-based constructs enable rigid shortsegment fixation and provide adequate stability to achieve successful fusion in over 90% of patients medicine education discount lariam 250 mg otc. Occipital plate fixation may limit the ability to place occipital screws along the midline medicine ubrania order lariam 250 mg free shipping, the thickest and strongest bone area in the occiput. Choice of Operative Approach A successful occipitocervical fusion can provide a favorable outcome in both acute and chronic types of craniocervical instability. These constructs are biomechanically superior to previous nonrigid fixation techniques and are very efficacious from a clinical perspective. Nevertheless, patients selection remains the key for successful outcome, and occipitocervical plating should be avoided in patients with irreducible symptomatic anterior compression and significant medical comorbidities precluding general anesthesia administration. Similarly, although atlantoaxial instability can be treated with occipitocervical fusion, it should primarily be treated with atlantoaxial fusion. Indications Occipitocervical instability can be acute, which is usually precipitated by trauma. The thickness of the bone in the suboccipital region varies depending on location, with anatomic studies demonstrating that the external occipital protuberance is the thickest in the midline and decreases laterally to inferiorly. Screw fixation is preferred below the level of the superior nuchal line to avoid a transverse sinus injury and along the dense midline ridge below the external occipital protuberance. Additionally, the soft tissue coverage above the nuchal line is very poor, and extending the instrumentation above this level places the patient at risk for exposure of the hardware due to scalp breakdown. The quality of and depth of the midline bone is optimal and this region is the ideal point for occiput screw fixation. For atlantoaxial instrumentation and fixation, multiple fixation methods may be used, including transarticular screws, C1 lateral mass screws, or C2 pedicle, pars, or translaminar screws. Generally, the presence of an irreducible C1-C2 subluxation, deficient C2 bony pars, or aberrant medialized vertebral artery excludes this option. The details of regional anatomy and specific instrumentation techniques involving the atlas, axis, and the subaxial cervical spine is discussed in Chapters 17 to 20, 31, and 38. These fixation points are precisely defined, whereas the occiput represents a relatively large target for screw implantation. For this reason the cervical screws should be placed prior to moving to the occiput. Surgical Technique Positioning and Preparation Patients are intubated in a carefully controlled manner, maintaining the alignment of the cervical spine at all times. Tong traction should not be used in patients with vertical displacement injuries to avoid further distraction. Caution should be exercised to keep the instrumentation below the level of the superior nuchal line to avoid a transverse sinus injury and along the dense midline ridge below the external occipital protuberance to obtain good fixation. This also provides good soft tissue coverage and avoids skin-related complication. Radiographic studies should be performed to confirm satisfactory anatomic alignment prior to starting the procedure. If such monitoring is employed, baseline studies with the patient in the supine position are necessary to compare with the potentials in the prone position. Occipital Plating and Occipital-Cervical Fusion 103 Exposure the incision is midline and extends from the inion to the lowest level to be incorporated into the fusion construct. Subperiosteal dissection with exposure of the suboccipital bone and dorsal elements of the cervical spine is performed using the Bovie electrocautery to minimize blood loss. Care is taken to note any aberrant vertebral artery loops on preoperative scans to avoid injury to these structures during the exposure. If a suboccipital decompression is performed the bone should be saved to use as autograft. The details relative to the exposure and fixation of the axis, atlas, and subaxial cervical spine are described in Chapters 17 to 20, 31, 38, and 39. Instrumentation Once adequate exposure is accomplished, decompression is performed if necessary, and ideally screw fixation of the caudal regions is accomplished. Currently, the most commonly used suboccipital fixation method is bicortical screw fixation into the midline suboccipital keel and paramedian cranium. The screws may be placed through a plate that is then connected to the longitudinal supporting members of the construct (most often rods), or the longitudinal rods can be secured to the skull with small connectors that each accommodate a single screw. The senior author prefers the latter because the technique offers the most flexibility in screw placement, usually enables fixation with six screws, and leaves more posterior occipital bone exposed for grafting. Bicortical holes are drilled though the apertures of the plate using a hand-held power drill. The angle to correctly place screws can be extreme, in which case angled instruments may be needed to obtain the appropriate trajectory. On occasion, a small amount of cerebrospinal fluid or slow venous bleeding may emanate from the pilot holes. It is possible to bend a straight rod into the proper configuration, but it is more efficient to use either a pre-bent rod or articulated rod. The rod is contoured to lie flat on the occiput and does not pass the superior nuchal line.
Amino acid supplementation probably does not improve survival sufficiently for the added cost medicine 10 day 2 times a day chart order lariam. Corticosteroids Corticosteroids have been studied extensively for the treatment of alcoholic hepatitis medicine while breastfeeding generic lariam 250 mg line. Although many of the initial controlled trials did not show a benefit medicine rheumatoid arthritis purchase genuine lariam on line, further analysis suggested that patients with encephalopathy and more severe disease may benefit chapter 7 medications and older adults cheap 250 mg lariam amex. Therefore, follow-up studies focused on the role of corticosteroids in the treatment of patients who had a Maddrey discriminant function greater than 32 or hepatic encephalopathy (or both) but not renal failure, infection, gastrointestinal tract bleeding, or, in some studies, severe diabetes mellitus. Some studies and meta-analyses that used these criteria showed that corticosteroid therapy provided a survival benefit for patients with a Maddrey discriminant function greater than 32 or hepatic encephalopathy (or both). Currently, the use of corticosteroid therapy for alcoholic hepatitis varies among experienced hepatologists. Pentoxifylline Prognosis and Treatment Abstinence Abstinence is the most important factor in both short- and long-term survival of patients with alcoholic hepatitis. For patients who recover and remain abstinent, the disease may continue to improve (ie, clinical sequelae and laboratory variables improve) for as long as 6 months. Although the condition of some patients continues to deteriorate even with abstinence, the 5-year survival rate for this group is more than 60%. However, for patients who continue to drink, the 5-year survival rate is less than 30%. While medications to reduce alcohol cravings, such as acamprosate or baclofen, are attractive options, their use has not been studied well, and they should be considered only in conjunction with an experienced addiction specialist. Some suggest that the beneficial effects of pentoxifylline may relate to renal protection as opposed to direct liver effects. Nonetheless, because the toxicity profile of pentoxifylline is low, its use for alcoholic hepatitis is prevalent; however, confirmatory studies are needed. Other Pharmacotherapies Being Studied Malnutrition is almost universal among patients with alcoholic hepatitis because of concomitant poor dietary habits, anorexia, and encephalopathy. Although malnutrition was once thought to cause alcoholic liver disease, it is no longer considered to have a major role in the pathogenesis of the disease. However, Alcohol induces oxidative stress in the liver, resulting in an imbalance between oxidants and antioxidants. Looking for a way to decrease oxygen consumption by the liver, investigators have studied the role of propylthiouracil in treating alcoholic hepatitis, but the results have been inconclusive. Colchicine has also been evaluated for treating alcoholic hepatitis, but no clinical benefit has been found. Other hepatoprotective compounds, such as S-adenosyl-l-methionine, phosphatidylcholine, milk thistle, and N-acetylcysteine have been evaluated but are not widely accepted. Alcoholic Liver Disease Management of Portal Hypertension 271 History and Physical Examination Among persons with a clinical history of marked and prolonged alcohol abuse, liver cirrhosis eventually develops in only about 20%. The presence or absence of symptoms is due largely to the presence or absence of liver decompensation. The symptoms of patients with liver decompensation reflect the severity of portal hypertension, malnutrition, and degree of synthetic liver dysfunction and include nonspecific fatigue, weakness, and anorexia. More specific symptoms are related to the presence of specific complications of cirrhosis and portal hypertension, including gastrointestinal tract bleeding, ascites, encephalopathy, renal failure, and hepatocellular carcinoma. Physical examination findings may include stigmata of chronic liver disease (spider angiomas and palmar erythema), complications of portal hypertension (ascites, splenomegaly, asterixis, and pedal edema), signs of excess estrogen (gynecomastia and hypogonadism), and signs of systemic alcohol toxicity (peripheral neuropathy, dementia, and Dupuytren contracture). Complications of portal hypertension may develop in patients with alcoholic hepatitis regardless of the presence or absence of underlying cirrhosis. This clinical observation is supported by studies showing that alcohol directly increases portal pressure, and it emphasizes the importance of the vascular component of intrahepatic resistance and portal hypertension. Hepatic encephalopathy, bleeding esophageal varices, ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome are complications of portal hypertension commonly encountered in patients with alcoholic hepatitis. Treatment of Infection Because of underlying malnutrition, liver cirrhosis, and iatrogenic complications, infection is one of the most common causes of death of patients with alcoholic hepatitis. The patients must be evaluated carefully for infections, including spontaneous bacterial peritonitis, aspiration pneumonia, and lower extremity cellulitis. However, fever and leukocytosis are common in patients with alcoholic hepatitis, even without infection. Liver Transplant Laboratory and Radiographic Features Prominent laboratory abnormalities include an increase in prothrombin time and bilirubin and a decrease in albumin, which are reflected in an increased Child-Turcotte-Pugh score. Imaging findings may be suggestive of cirrhosis and ensuing portal hypertension, as indicated by heterogeneous liver echotexture, splenomegaly, collateralization, and ascites on ultrasonography. Computed tomography may show changes in liver contour, splenomegaly, collateralization, or ascites. Patients with cirrhosis are at risk for hepatocellular carcinoma and should be evaluated biannually with ultrasonography with or without serum alpha-fetoprotein levels, as should patients who have had recent clinical decompensation. A recent trial demonstrated that early liver transplant improved survival among a highly selected group of patients not responding to medical therapy. While most patients with alcoholic hepatitis are not suitable candidates for liver transplant, less than 6 months of abstinence is not itself an absolute contraindication to liver transplant. Thus, patients not responding to medical therapy may warrant discussion with a liver transplant center team, although this is a highly controversial area with significant practice variation among transplant centers. The distinction is made best on the basis of the clinical history and the pattern of laboratory test results. Histologic Features Traditionally, alcoholic cirrhosis is classified as a micronodular cirrhosis (Figure 25. However, in many cases, larger nodules also develop, leading to mixed micro-macronodular cirrhosis.
The yield of these tests is low treatment 001 - b cheap lariam 250 mg mastercard, but they are useful for evaluating patients who have chronic diarrhea with increased stool volume treatment stye purchase discount lariam on-line. Treatment with high-dose loperamide (up to 16 mg daily) symptoms you are pregnant safe 250mg lariam, cholestyramine medicine just for cough cheap lariam 250 mg visa, clonidine, verapamil, or octreotide may be considered. The potential risk of ischemic colitis has led to a restricted prescription program for alosetron. A plain radiograph of the abdomen obtained during a time of severe pain may help to exclude obstruction. In academic medical centers, pseudo-obstruction or other motility disorders may be evaluated, but pain is not common in these conditions. Often, the next step is a course of treatment with a low dose of a tricyclic antidepressant. When formal psychiatric disorders are present, appropriate therapy directed toward treating the underlying disorder is mandatory. Initial treatment involves lifestyle and dietary modifications with symptomatic remedies. Patients with persistent gastrointestinal symptoms despite these initial measures should undergo tests to identify causative factors. Rifaximin therapy for patients with irritable bowel syndrome without constipation. Do the symptom-based, Rome criteria of irritable bowel syndrome lead to better diagnosis and treatment outcomes Cognitive-behavioral therapy versus education and desipramine versus placebo for moderate to severe functional bowel disorders. The colon absorbs all but 100 mL of fluid and 1 mEq of sodium and chloride from approximately 1,500 mL of chyme received over 24 hours. Absorptive capacity can increase to 5 to 6 L of fluid and to 800 to 1,000 mEq of sodium and chloride daily. In healthy people, the average mouth-to-cecum transit time is approximately 6 hours, and average regional transit times through the right, left, and sigmoid colon are about 12 hours each, with an average total colonic transit time of 36 hours. The ileocolic sphincter regulates the intermittent transfer of ileal contents into the colon, a process that normalizes in response to augmented storage capacity in the residual transverse and descending colon within 6 months after right hemicolectomy. Motor Patterns Colonic motor activity is extremely irregular, ranging from being quiescent (particularly at night) to having isolated contractions, bursts of contractions, or propagated contractions. In contrast to the small intestine, the colon does not have rhythmic migrating motor complexes. Contractions are tonic or sustained, lasting several minutes to hours, and shorter or phasic. Propagated phasic contractions propel colonic contents over longer distances than nonpropagated phasic contractions. High-amplitude propagated contractions are more than 75 mm Hg in amplitude, occur about 6 times daily (frequently after awakening and after meals), are responsible for mass movement of colonic contents, and frequently precede defecation. Stimulant laxatives such as bisacodyl (Dulcolax) and glycerol induce high-amplitude propagated contractions. Regional Differences in Colonic Motor Function the right colon is a reservoir that mixes and stores contents and absorbs fluid and electrolytes. This response may explain postprandial urgency and abdominal discomfort in patients with irritable bowel syndrome. Colonic Relaxation Colonic relaxation resulting from sympathetic stimulation or opiates may cause acute colonic pseudo-obstruction, or Ogilvie syndrome. Stimulation of 2-adrenergic receptors decreases the release of acetylcholine from excitatory cholinergic terminals in the myenteric plexus, thereby inhibiting gastrointestinal motility. Conversely, reduced tonic inhibition of the sympathetic system impairs the net absorption of water and electrolytes and accelerates transit in patients who have diabetic neuropathy, thus resulting in diarrhea. Colocolonic Inhibitory Reflexes Peristalsis is a local reflex mediated by intrinsic nerve pathways and characterized by contraction proximal to the distended segment and relaxation distal to it. In addition, rectal or colonic distention can inhibit motor activity in the stomach, small intestine, or colon. These inhibitory reflexes are mediated by extrinsic reflex pathways with synapses in the prevertebral ganglia, independent of the central nervous system. They may account for delayed left colonic transit or small intestinal transit (or both) in patients with obstructive defecation. Assessment of Colonic Transit Colonic transit can be measured with commercially available radiopaque markers (Sitzmark capsule), scintigraphy, or a wireless pH-pressure capsule. These techniques entail counting the number of orally ingested markers that remain in the colon as seen on plain radiographs of the abdomen. Delayed colonic transit is manifested by 8 or more markers seen on plain films on day 3 or by 5 or more markers seen on day 5. With scintigraphy, the isotope (generally, technetium Tc 99m or indium In 111) is delivered into the colon by orocecal intubation or within a delayed-release capsule. The delayed-release capsule contains radiolabeled activated charcoal covered with a pH-sensitive polymer (methacrylate) designed to dissolve in the alkaline pH of the distal ileum. Gamma camera scans taken 4, 24, and, if necessary, 48 hours after ingestion of the isotope show the colonic distribution of isotope. Regions of interest are drawn around the ascending, transverse, descending, and sigmoid colon combined with the rectum; counts in these areas are weighted by factors of 1 through 4, respectively, and stool counts are weighted by a factor of 5. Thus, colonic transit may be summarized as an overall geometric center (Figure 20. The 4-hour scan identifies rapid colonic transit, and the 24-hour and 48-hour scans show slow colonic transit.
The inferior oblique muscles arise from the posterior tubercle of the axis and attach to the transverse process of the atlas medicine mountain scout ranch order lariam 250mg online. The superior oblique muscles span the transverse processes of the atlas and attach to the suboccipital bone medicine x ed cheap lariam 250 mg without a prescription. The suboccipital triangle consists of the inferior oblique muscle inferiorly walmart 9 medications buy generic lariam 250 mg on line, the superior oblique laterally treatment for bronchitis lariam 250 mg online, and the rectus major muscle superiorly. The suboccipital nerve and vertebral artery pass through the suboccipital triangle as they perforate the posterior atlanto-occipital membrane and are important references during surgical exposures. Atlantoaxial Wiring and Arthrodesis 115 Atlantoaxial Wiring and Arthrodesis If the C1 posterior arch is intact, then the use of cable fixation from C1 to C2 is a viable option. Three basic cable/wire fixation techniques-the Gallie, the Brooks, and the interspinous technique-are commonly used for C1-C2 fixation. Following exposure of the C1-C2 region, a meticulous sublaminar dissection at C1 and C2 is performed after removal of the occipitoatlantal membrane and ligamentum flavum. Ensuring free access of the wire between the lamina and dura minimizes the risk of dural tears. The graft is placed over the C2 spinous process and leaned against the posterior arch of C1. In this technique a single 20-gauge steel wire is passed underneath the C1 lamina from inferior to superior, which holds the graft in place and then wraps around the spinous process of C2. Passage of the sublaminar wire under the lamina of C2 is avoided to decrease the risk of neural or dural injury. These wires are tightened, compressing the bone graft over the arch of C1 and to the lamina of C2. The Gallie fusion provides good stabilization in flexion but very poor stabilization during extension and rotational maneuvers. Consequently, the rate of nonunion with the Gallie fusion has been reported to be as high as 25%. This technique has been almost completely replaced with other methods, but it is still found in the literature and so it is appropriate to understand the procedure. The BrooksJenkins fusion technique provides more rotational stability than does the Gallie technique, and it has stability in flexion and extension that is similar to that of the Gallie fusion technique. The rate of fusion after this technique has been reported to be as high as 93%, and achievement of the optimal rates requires postoperative halo immobilization. One disadvantage of the Brooks-Jenkins fusion technique is the need for passage of bilateral sublaminar cables beneath both C1 and C2. Interspinous C1-C2 Technique the Gallie technique was modified by Volker Sonntag in the early 1990s in such a manner that the rotational stability was improved without the need for bilateral sublaminar C1-C2 cables as in the Brooks-Jenkins technique. Fixation is accomplished by passing a sublaminar cable under the posterior C1 arch from inferior to superior. This requires a two-handed process, simultaneously feeding and pulling the wire to avoid anterior displacement of the wire and compression of the dorsal aspect of the spinal cord. This can be relatively easily passed by sliding the blunt end of the needle beneath the lamina. The suture is tied to the cable and is used to pull the cable under the C1 lamina from a superior to inferior direction. A notch is created at the spinolaminar junction bilaterally at C2 with a Kerrison rongeur, providing a slot for seating the wire at the C2 level. Next, a carefully cut autograft (iliac crest or rib) is placed between the dorsal elements of C1 and C2 after first decorticating the spinal regions that contact the graft. The cable is next looped over the autograft and placed into a notch created on the inferior aspect of the C2 spinous process, trapping the graft between C1 and C2. Biomechanically, this fixation technique is superior to that of the Gallie, but there is additional risk because it involves the passage of wire beneath two laminae. The superior portion of the C2 lamina is fashioned to receive the grafts on each side of the midline to minimize translation during compression of the wires. In the Brooks-Jenkins fusion technique, unlike the Gallie fusion technique, two separate iliac crest autografts are placed between C1 and C2. Each autologous iliac crest graft is beveled superiorly and inferiorly and wedged in between the C1 116 I Occipital-Cervical Junction a. These systems have a variable angle eyelet crimp at one end that allows passing the other end through it. Each system has a slightly different method of applying tension to the cable and fixing it in place. The maximum recommended tension for stainless steel cables is 60 pounds and for titanium alloy cables is generally 35 pounds. Once set to the appropriate tension, the cable is tightened and crimped, and this not only secures the spine but also places the graft under compression. It should be kept in mind that, in the spine, the cables can fail not by breaking but by cutting through bone. The patient should be followed clinically and radiographically until fusion has occurred. Although a rigid orthosis may be used instead of a halo, the fusion rate will suffer. In patients treated with only the interspinous technique and no other instrumentation, Sonntag recommended the use of a halo to immobilize patients for 3 months after surgery and the use of a rigid cervical collar for an additional 1 to 2 months after that, demonstrating a 97% fusion rate with the technique. Nonunion is a well-known complication of any arthrodesis procedure and may occur in up to 30% of cases. Other complications following atlantoaxial wiring are iatrogenic fracture of the posterior arch during wire tensioning, necessitating extension of the fusion construct; risk of dural tear; and neurologic injury while passing sublaminar wires. Even though the wiring techniques are not as rigid as screwbased techniques, they do offer higher rates of fusion when combined with halo immobilization.
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