Tuberculous vertebral osteomyelitis

Tuberculous vertebral osteomyelitis

Epidemiology

Tuberculosis of the central nervous system accounts for approximately 1% of all cases of tuberculosis and 50% of these involve the spine.

Spinal tuberculosis is more common in children and young adults. The incidence of spinal tuberculosis is increasing in developed nations. Genetic susceptibility to spinal tuberculosis has been demonstrated.

Vertebral granulomatous infections are found in 10–20% of TB cases in developed nations and upwards of 20–41% in undeveloped nations 1).

The most common levels involved are the lower thoracic and upper lumbar levels. Has a predilection for the vertebral body, sparing the posterior elements. Psoas abscess is common (the psoas major muscle attaches to the bodies and intervertebral discs from T12-L5). Sclerosis of the involved vertebral body may occur.

Etiology

M. tuberculosis is the most common etiology of vertebral granulomatous infection.

Immunocompromise has been found to increase the incidence of musculoskeletal lesions. While 3–5% of patients with pulmonary TB develop musculoskeletal lesions, this number substantially rises to nearly 60% in patients with HIV 2).

Clinical features

Characteristically, there is destruction of the intervertebral disk space and the adjacent vertebral bodies, collapse of the spinal elements, and anterior wedging leading to kyphosis and gibbus formation. The thoracic region of vertebral column is most frequently affected. Formation of a ‘cold’ abscess around the lesion is another characteristic feature. The incidence of multi-level noncontiguous vertebral tuberculosis occurs more frequently than previously recognized. Common clinical manifestations include constitutional symptoms, back pain, spinal tenderness, paraplegia, and spinal deformities.

Typically symptomatic for many months.

Neurologic deficit develops in 10–47% of patients 3) , and may be due to medullary and radicular artery inflammation in most cases. The infection itself rarely extends into the spinal canal 4) , however, epidural granulation tissue or fibrosis or a kyphotic bony deformity may cause cord compression 5).

Diagnosis

For the diagnosis of spinal tuberculosis magnetic resonance imaging is more sensitive imaging technique than x-ray and more specific than computed tomography. Magnetic resonance imaging frequently demonstrates involvement of the vertebral bodies on either side of the disk, disk destruction, cold abscess, vertebral collapse, and presence of vertebral column deformities.

Neuroimaging-guided needle biopsy from the affected site in the center of the vertebral body is the gold standard technique for early histopathological diagnosis.


The available gadgetry of investigations, such as AFB smear, culture of Mycobacterium tuberculosis, and Uniplex PCR, suffers from a lack of adequate sensitivity and/or a lack of rapidity. Therefore, many times a diagnosis is made either very late in the disease process or sometimes empirical therapy has to be started because a definite diagnosis could not be made. All of these are not ideal situations for a clinician.

MPCR using IS6110, protein b, and MPB64 primers has a high sensitivity and specificity in rapid diagnosis of spinal tuberculosis. This is particularly useful for paucibacillary infections like spinal tuberculosis. However, further studies using large sample sizes are needed to confirm the practical applicability of this technique 6).

Treatment

Esposito et al., highlighted the importance of suspecting this disorder in children with both aspecific systemic and neurological symptoms, in order to reach a timely diagnosis for appropriate and targeted intervention, avoiding the risk of overtreatment and malpractice claims 7).

In the context of evidence-based medicine and the rational use of antibiotics, it is clear that antibiotics should be preferred according to the culture antibiogram results in the treatment of infectious diseases 8).

Surgery may be required in selected cases, e.g. large abscess formation, severe kyphosis, an evolving neurological deficit, or lack of response to medical treatment.

The role of surgical debridement and fusion with TB is controversial, and good results may be obtained with either medical treatment or surgery. Surgery may be more appropriate when definite cord compression is documented or for complications such as abscess or sinus formation 9) or spinal instability.

Outcome

Early diagnosis and prompt treatment is necessary to prevent permanent neurological disability and to minimize spinal deformity 10) 11).

Case series

Fifty-nine adult patients with thoracic and thoracolumbar spinal tuberculosis underwent single-stage transpedicular debridement, posterior instrumentation and fusion. These patients were followed for a minimum of 5 years. Patients were assigned to one of two groups according to the infected anatomic segment. In the thoracic spinal tuberculosis group, there were 28 cases (17 males, 11 females) with a mean age of 38.9 years; in the thoracolumbar spinal tuberculosis group, there were 31 cases (19 males, 12 females) with a mean age of 40.3 years. All cases were evaluated clinically using the visual analog scale (VAS), Kirkaldy Willis criteria and the ASIA impairment scale (ASIA). Radiographs were performed for measuring the angle of kyphosis and scoliosis. Complications related to surgery were recorded.

All patients successfully resolved their infections, experienced one or more ASIA grades of improvement, and improved in their VAS pain scores at final follow-up. In both groups, patient-reported outcomes reached over 90% excellent or good results using Kirkaldy-Willis criteria. The loss of kyphotic angle correction was 2.6° in the thoracic spinal tuberculosis group and 3.2° in the thoracolumbar spinal tuberculosis group. No scoliosis was observed in either group. Fifty-eight (98.3%) cases achieved solid bony fusion. In the thoracolumbar spinal tuberculosis group, one patient experienced screw loosening, and another patient with nonunion and rod breakage underwent revision surgery.

The technique of single-stage transpedicular debridement, posterior instrumentation and fusion is an effective method for the treatment of thoracic and thoracolumbar spinal tuberculosis in adults. Long-term postoperative clinical and radiological outcomes were satisfactory 12).


Kim et al., performed a retrospective review of the medical records of patients with culture negative pyogenic spondylitis (CNPS) and tuberculous spondylitis (TS). They compared the characteristics of 71 patients with CNPS with those of 94 patients with TS.

Patients with TS had more previous histories of tuberculosis (9.9 vs 22.3 %, p = 0.034), simultaneous tuberculosis other than of the spine (0 vs 47.9 %, p < 0.001), and positive results in the interferon-gamma release assay (27.6 vs 79.2 %, p < 0.001). Fever (15.5 vs. 31.8 %, p = 0.018), psoas abscesses (15.5 vs 33.0 %, p = 0.011), and paravertebral abscesses (49.3 vs. 74.5 %, p = 0.011) were also more prevalent in TS than CNPS.

Different from or contrary to the previous comparisons between CPPS and TS, fever, psoas abscesses, and paravertebral abscesses are more common in patients with TS than in those with CNPS 13).


Many previous studies in Korea usually reported that tuberculous spondylitis is the predominant infection. However, in the study of Jeong et al., the number of pyogenic infection was 3 times greater than that of tuberculous spinal disease. Etiological agents were identified in a half of all infectious spinal disease. For better outcomes, we should try to identify the causative microorganism before antibiotic therapy and make every effort to improve the result of culture and biopsy 14).

Case reports

References

1)

Wu M, Su J, Yan F, Cai L, Deng Z. Skipped multifocal extensive spinal tuberculosis involving the whole spine: A case report and literature review. Medicine (Baltimore). 2018 Jan;97(3):e9692. doi: 10.1097/MD.0000000000009692. Review. PubMed PMID: 29505022; PubMed Central PMCID: PMC5779791.
2)

Rajasekaran S, Khandelwal G. Drug therapy in spinal tuberculosis. Eur Spine J. 2013 Jun;22 Suppl 4:587-93. doi: 10.1007/s00586-012-2337-5. Epub 2012 May 12. Review. PubMed PMID: 22581190; PubMed Central PMCID: PMC3691408.
3) , 5)

Rothman RH, Simeone FA. The Spine. Philadelphia
4)

Kinnier WSA. In: Tuberculosis of the Skull and Spine. Neurology. London: Edward Arnold; 1940:575–583
6)

Sharma K, Meena RK, Aggarwal A, Chhabra R. Multiplex PCR as a novel method in the diagnosis of spinal tuberculosis-a pilot study. Acta Neurochir (Wien). 2017 Jan 21. doi: 10.1007/s00701-016-3065-0. [Epub ahead of print] PubMed PMID: 28110400.
7)

Esposito S, Moscatelli M, Schiariti MP, Viganò I, Pantaleoni C, Marucci G. Pott’s Disease: An Emerging Source of Potentially Inappropriate Treatment. Neuropediatrics. 2019 May 29. doi: 10.1055/s-0039-1691833. [Epub ahead of print] PubMed PMID: 31141827.
8)

Dogan M, Simsek AT, Yilmaz I, Karaarslan N. Evaluation of Empirical Antibiotic Treatment in Culture Negative Pyogenic Vertebral Osteomyelitis. Turk Neurosurg. 2019 Jan 2. doi: 10.5137/1019-5149.JTN.25018-18.2. [Epub ahead of print] PubMed PMID: 31049918.
9)

Medical Research Council Working Party on Tuber- culosis of the Spine. Controlled Trial of Short- Course Regimens of Chemotherapy in the Ambula- tory Treatment of Spinal Tuberculosis: Results at Three Years of a Study in Korea. J Bone Joint Surg. 1993; 75B:240–248
10)

Jain AK. Tuberculosis of the spine: a fresh look at an old disease. J Bone Joint Surg Br 2010;92(7):905–13
11)

Jain AK, Dhammi IK. Tuberculosis of the spine: a review. Clin Orthop Relat Res 2007;460(July):39–49
12)

Zhang P, Peng W, Wang X, Luo C, Xu Z, Zeng H, Liu Z, Zhang Y, Ge L. Minimum 5-year follow-up outcomes for single-stage transpedicular debridement, posterior instrumentation and fusion in the management of thoracic and thoracolumbar spinal tuberculosis in adults. Br J Neurosurg. 2016 Jul 8:1-6. [Epub ahead of print] PubMed PMID: 27387195.
13)

Kim CJ, Kim EJ, Song KH, Choe PG, Park WB, Bang JH, Kim ES, Park SW, Kim HB, Oh MD, Kim NJ. Comparison of characteristics of culture-negative pyogenic spondylitis and tuberculous spondylitis: a retrospective study. BMC Infect Dis. 2016 Oct 12;16(1):560. PubMed PMID: 27733126.
14)

Jeong SJ, Choi SW, Youm JY, Kim HW, Ha HG, Yi JS. Microbiology and epidemiology of infectious spinal disease. J Korean Neurosurg Soc. 2014 Jul;56(1):21-7. doi: 10.3340/jkns.2014.56.1.21. Epub 2014 Jul 31. PubMed PMID: 25289121; PubMed Central PMCID: PMC4185315.

Plexiform neurofibroma treatment

Plexiform neurofibroma treatment

Since plexiform neurofibromas are a major cause of the burden of disease and may also progress to malignancy, many efforts have been undertaken to find a cure for these tumors. However, neither surgery nor medication has so far produced a breakthrough therapeutic success.

Plexiform neurofibromas with sizable intraspinal extensions and resultant spinal cord compromise pose challenging management problems, because these lesions may involve multiple nerves and engulf adjacent vascular and visceral structures 1).

Decisions about surgical treatment and frequency of follow-up must be made judiciously and individualized for each patient 2).

Plexiform neurofibromas arising in the orbito-temporal area pose a greater challenge due to its critical function and cosmetic importance of the face. Such plexiform neurofibromas, separately designated as orbito-temporal plexiform neurofibromas, show complex symptoms such as severe ptosis, ectropion, lacrimal gland dysfunction, and even vision loss 3).


A clinical phase I study reported significant shrinkage of plexiform neurofibromas following treatment with the MEK inhibitor selumetinib.

Vaassen et al., reported an 11-year-old NF1 patient with a large plexiform neurofibroma of the neck that had led to a sharp-angled kinking of the cervical spine and subsequent myelopathy. Although surgical stabilization of the cervical vertebral column was urgently recommended, the vertebral column was inaccessible due to extensive tumor growth. In this situation, treatment with the MEK inhibitor trametinib was initiated which resulted in a 22% reduction in tumor volume after 6 months of therapy and finally enabled surgery. These data show that MEK inhibitors may not lead to complete disappearance of NF1-associated plexiform neurofibromas but can be an essential step in a multimodal therapeutic approach for these tumors. The course of our patient suggests that MEK inhibitors are likely to play a significant role in providing a cure for one of the most devastating manifestations of NF1 4).

References

1)

Pollack IF, Colak A, Fitz C, Wiener E, Moreland M, Mulvihill JJ. Surgical management of spinal cord compression from plexiform neurofibromas in patients with neurofibromatosis 1. Neurosurgery. 1998 Aug;43(2):248-55; discussion 255-6. PubMed PMID: 9696077.
2)

Gutmann DH, Aylsworth A, Carey JC, Korf B, Marks J, Pyeritz RE, Rubenstein A, Viskochil D. The diagnostic evaluation and multidisciplinary management of neurofibromatosis 1 and neurofibromatosis 2. JAMA. 1997 Jul 2;278(1):51-7. Review. PubMed PMID: 9207339.
3)

Choi J, Choi HJ, Kang KJ, Kwon H, Shin J. Simultaneous Forehead Lift and Blepharoplasty Techniques in Management of Orbito-Temporal Plexiform Neurofibroma. J Craniofac Surg. 2019 Mar 14. doi: 10.1097/SCS.0000000000005448. [Epub ahead of print] PubMed PMID: 30889063.
4)

Vaassen P, Dürr N, Röhrig A, Willing R, Rosenbaum T. Trametinib Induces Neurofibroma Shrinkage and Enables Surgery. Neuropediatrics. 2019 May 29. doi: 10.1055/s-0039-1691830. [Epub ahead of print] PubMed PMID: 31141829.

Cerebellar hemorrhage surgery

Cerebellar hemorrhage surgery

In 1906, Ballance first reported a surgical approach to treatment of cerebellar hemorrhage1) 2).

Since then, surgical treatment has become the general option for treatment 3).

Recommendations from Kobayashi et al in 1994 4)

1. patients with a Glasgow Coma Scale (GCS) score ≥14 and hematoma <4 cm diameter: treat conservatively

2. patients with GCS≤13 or with a hematoma ≥4 cm: surgical evacuation.

3. patients with absent brain stem reflexes and flaccid quadriplegia: intensive therapy is not indi- cated. Note: some authors contend that the loss of brain stem reflexes from direct compression may not be irreversible, 5) and that cerebellar hemorrhage represents a surgical emergency (and that the above criteria would thus deny potentially helpful surgery to some, see discussion of cerebellar infarction and decompression.

4. patients with hydrocephalus: ventricular catheter (if no coagulopathy). Caution: do not overdrain to avoid upward cerebellar herniation. Most cases with hydrocephalus also require evacuation of the clot

Criteria

Surgical treatment of cerebellar ICH can be life-saving but often leads to a poor functional outcome. New studies are needed on long-term functional outcome after a cerebellar ICH 6).

Since the 1970s, there has been a wide mutual consensus in the neurological and neurosurgical community that cerebellar ICHs should be operated on. However, the scientific proof is mainly based on small retrospective series with conflicting results 7).

To relieve brainstem compression and hydrocephalus, surgeons tend to favor occipital craniectomy or occipital craniotomy with hematoma evacuation in patients with a declining level of consciousness 8). Some regard this counterintuitive as long-term outcomes after surgical treatment of cerebellar ICH are generally pessimistic 9).


Since the report by Little et al., 10) the hematoma diameter has been considered a significant factor in the decision-making process for optimal treatment.

The criteria for surgery remain controversial, and many researchers have determined that a hematoma larger than 3 cm, obstruction of the quadrigeminal cistern, and compression of the fourth ventricle are surgical criteria 11) 12) 13).

Cohen et al. 14) used a maximal hematoma diameter greater than 3 cm as the surgical criterion, however, some patients with a hematoma larger than 3 cm who underwent conservative treatment had a good prognosis as well. In addition, a hematoma volume greater than 15 mL, being equivalent with a hematoma with a maximal diameter greater than 3 cm, has also been used as a criterion in some cases 15).


The criteria of Kobayashi et al., are as follows:

1) patients with Glasgow Coma Scale scores of 14 or 15 and with a hematoma of less than 40 mm in maximum diameter are treated conservatively

2) for the patients with Glasgow Coma Scale scores of 13 or less at admission or with a hematoma measuring 40 mm or more, hematoma evacuation with decompressive suboccipital craniectomy should be a treatment of choice

3) for the patient whose brain stem reflexes are entirely lost with flaccid tetraplegia or whose general condition is poor, intensive therapy is not indicated. The validity of these criteria was tested and confirmed in 49 cases 16).

Technique

Position

Lateral oblique position with the involved side up.

If rapidity is crucial a suboccipital midline skin incision is preferred because it can be taken down quickly with little fear of encountering a vertebral artery.

Suboccipital craniectomy is preferred over suboccipital craniotomy to accomodate postoperative swelling.

A prophylactically ventriculostomy at Frazier’s point is recommended to allow rapid treatment of postoperative hydrocephalus or intracranial pressure monitoring.

In cases where there has been rupture into the ventricular system, the surgical microscope should be used to follow the clot to the fourth ventriclewhich is then cleared of clot.

External ventricular drainage (EVD) combined with intraventricular thrombolysis (IVF) is rarely used in severe spontaneous cerebellar hemorrhage(SCH) with intraventricular hemorrhage (IVH).

It is a treatment option for elderly patients with severe SCH + IVH 17).

Video

References

1) , 15)

Cho SM, Hu C, Pyen JS, Whang K, Kim HJ, Han YP, et al. Predictors of outcome of spontaneous cerebellar hemorrhage. J Korean Neurosurg Soc. 1997 Oct;26(10):1395–1400.
2) , 3)

Dahdaleh NS, Dlouhy BJ, Viljoen SV, Capuano AW, Kung DK, Torner JC, Hasan DM, Howard MA 3rd. Clinical and radiographic predictors of neurological outcome following posterior fossa decompression for spontaneous cerebellar hemorrhage. J Clin Neurosci. 2012 Sep;19(9):1236-41. doi: 10.1016/j.jocn.2011.11.025. Epub 2012 Jun 20. PubMed PMID: 22721890.
4)

Kobayashi S, Sato A, Kageyama Y, et al. Treatment of Hypertensive Cerebellar Hemorrhage – Surgical or Conservative Management. Neurosurgery. 1994; 34:246–251
5)

Heros RC. Surgical Treatment of Cerebellar Infarc- tion. Stroke. 1992; 23:937–938
6)

Satopää J, Meretoja A, Koivunen RJ, Mustanoja S, Putaala J, Kaste M, Strbian D, Tatlisumak T, Niemelä MR. Treatment of intracerebellar haemorrhage: Poor outcome and high long-term mortality. Surg Neurol Int. 2017 Nov 9;8:272. doi: 10.4103/sni.sni_168_17. eCollection 2017. PubMed PMID: 29204307; PubMed Central PMCID: PMC5691556.
7)

Witsch J, Neugebauer H, Zweckberger K, Jüttler E. Primary cerebellar haemorrhage: complications, treatment and outcome. Clin Neurol Neurosurg. 2013 Jul;115(7):863-9. doi: 10.1016/j.clineuro.2013.04.009. Epub 2013 May 6. Review. PubMed PMID: 23659765.
8)

Wijdicks EF, St Louis EK, Atkinson JD, Li H. Clinician’s biases toward surgery in cerebellar hematomas: an analysis of decision-making in 94 patients. Cerebrovasc Dis. 2000 Mar-Apr;10(2):93-6. PubMed PMID: 10686446.
9)

Luney MS, English SW, Longworth A, Simpson J, Gudibande S, Matta B, Burnstein RM, Veenith T. Acute Posterior Cranial Fossa Hemorrhage-Is Surgical Decompression Better than Expectant Medical Management? Neurocrit Care. 2016 Dec;25(3):365-370. PubMed PMID: 27071924; PubMed Central PMCID: PMC5138260.
10)

Little JR, Tubman DE, Ethier R. Cerebellar hemorrhage in adults. Diagnosis by computerized tomography. J Neurosurg. 1978 Apr;48(4):575-9. PubMed PMID: 632882.
11) , 14)

Cohen ZR, Ram Z, Knoller N, Peles E, Hadani M. Management and outcome of non-traumatic cerebellar haemorrhage. Cerebrovasc Dis. 2002;14(3-4):207-13. PubMed PMID: 12403953.
12)

Kirollos RW, Tyagi AK, Ross SA, van Hille PT, Marks PV. Management of spontaneous cerebellar hematomas: a prospective treatment protocol. Neurosurgery. 2001 Dec;49(6):1378-86; discussion 1386-7. PubMed PMID: 11846937.
13)

Salvati M, Cervoni L, Raco A, Delfini R. Spontaneous cerebellar hemorrhage: clinical remarks on 50 cases. Surg Neurol. 2001 Mar;55(3):156-61; discussion 161. PubMed PMID: 11311913.
16)

Kobayashi S, Sato A, Kageyama Y, Nakamura H, Watanabe Y, Yamaura A. Treatment of hypertensive cerebellar hemorrhage–surgical or conservative management? Neurosurgery. 1994 Feb;34(2):246-50; discussion 250-1. PubMed PMID: 8177384.
17)

Zhang J, Wang L, Xiong Z, Han Q, Du Q, Sun S, Wang Y, You C, Chen J. A treatment option for severe cerebellar hemorrhage with ventricular extension in elderly patients: intraventricular fibrinolysis. J Neurol. 2014 Feb;261(2):324-9. doi: 10.1007/s00415-013-7198-2. Epub 2013 Dec 3. PubMed PMID: 24297364.
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