Hypoxic ischaemic brain injury

Hypoxic ischaemic brain injury

Hypoxic ischaemic brain injury is common and usually due to cardiac arrest or profound hypotension. The clinical pattern and outcome depend on the severity of the initial insult, the effectiveness of immediate resuscitation and transfer, and the post-resuscitation management on the intensive care unit. Clinical assessment is difficult and so often these days compromised by sedationneuromuscular-blocking drugventilationhypothermia and inotropic management. Investigations can add valuable information, in particular brain MRI shows characteristic patterns depending on the severity of the injury and the timing of imaging. EEG patterns may also suggest the possibility of a good outcome. There is no entirely reliable algorithm of clinical signs or investigations which allow a definitive prognosis but the combination of careful repeated observations and appropriate ancillary investigations allows the neurologist to give an informed and accurate opinion of the likely outcome, and to advise on management. Overall, the prognosis is extremely poor and only a quarter of patients survive to hospital discharge, and often even then with severe neurological or cognitive deficits 1).


In eleven patients (median age of 47 [range 20-71], 8 male and 3 female). There was a linear relationship between ICP and non-invasive estimators of ICP (nICP) with optic nerve sheath diameter ultrasonography (ONSD) (R = 0.53 [p < 0.0001]), JVP (R = 0.38 [p < 0.001]) and transcranial Doppler ultrasonography (TCD) (R = 0.30 [p < 0.01]). The ability to predict intracranial hypertension was highest for ONSD and TCD (AUC = 0.96 [95% CI: 0.90-1.00] and AUC = 0.91 [95% CI: 0.83-1.00], respectively). Jugular venous bulb pressure (JVP). presented the weakest prediction ability (AUC = 0.75 [95% CI: 0.56-0.94]).

ONSD and TCD methods demonstrated agreement with invasively-monitored ICP, suggesting their potential roles in the detection of intracranial hypertension in hypoxic ischaemic brain injury (HIBI) after cardiac arrest 2).

References

1)

Howard RS, Holmes PA, Koutroumanidis MA. Hypoxic-ischaemic brain injury. Pract Neurol. 2011 Feb;11(1):4-18. doi: 10.1136/jnnp.2010.235218. Review. PubMed PMID: 21239649.
2)

Cardim D, Griesdale DE, Ainslie PN, Robba C, Calviello L, Czosnyka M, Smielewski P, Sekhon MS. A comparison of non-invasive versus invasive measures of intracranial pressure in hypoxic ischaemic brain injury after cardiac arrest. Resuscitation. 2019 Jan 7. pii: S0300-9572(18)30912-2. doi: 10.1016/j.resuscitation.2019.01.002. [Epub ahead of print] PubMed PMID: 30629992.

Neurologic Injury after Lateral Lumbar Interbody Fusion

Since the first description of LLIF in 2006, the indications for LLIF have expanded and the rate of LLIF procedures performed in the USA has increased. LLIF has several theoretical advantages compared to other approaches including the preservation of the anterior and posterior annular/ligamentous structures, insertion of wide cages resting on the dense apophyseal ring bilaterally, and augmentation of disc height with indirect decompression of neural elements. Favorable long-term outcomes and a reduced risk of visceral/vascular injuries, incidental dural tears, and perioperative infections have been reported. However, approach-related complications such as motor and sensory deficits remain a concern. In well-indicated patients, LLIF can be a safe procedure used for a variety of indications 1).

Hijji et al. published a systematic review analyzing the complication profile of LLIF. Their study included a total of 63 articles and 6819 patients. The most commonly reported complications were transient neurologic injury (36.07%). The clinical significance of those transient findings, however, is unclear since the rate of persistent neurologic complications was much lower (3.98%) 2)

The risk of lumbar plexus injury is particularly concerning at the L4-5 disc space. Although LLIF is associated with an increased prevalence of anterior thigh/groin pain as well as motor and sensory deficits immediately after surgery, our results support that pain and neurologic deficits decrease over time. The level treated appears to be a risk factor for lumbosacral plexus injury 3).

Interestingly, the use of rhBMP-2 was associated with higher rates of persistent motor deficits, which might be explained by a direct deleterious effect of this agent on the lumbosacral plexus 4).

In a retrospective chart review of 118 patients, Cahill et al. determined the incidence of femoral nerve injury, which is considered one of the worst neurological complications after LLIF. The authors reported an approximate 5% femoral nerve injury rate of all the LLIF procedures performed at L4-5. There were no femoral nerve injuries at any other levels 5).

During a 6-year time period of performing LLIF Aichmair et al., noted a learning curve with a decreasing proportional trend for anterior thigh pain, sensory as well as motor deficits 6)

Le et al. also observed a learning curve with a significant reduction in the incidence of postoperative thigh numbness during a 3-year period (from 26.1 to 10.7%) 7).

Levi AD from the University of Miami Hospital, adopted an exclusive mini-open muscle-splitting approach in LLIF with first-look inspection of the lumbosacral plexus nerve elements taht may improve motor and sensory outcomes in general and the incidence of postoperative groin/thighsensory dysfunction and psoas-pattern weakness in particular 8).

References

1)

Salzmann SN, Shue J, Hughes AP. Lateral Lumbar Interbody Fusion-Outcomes and Complications. Curr Rev Musculoskelet Med. 2017 Dec;10(4):539-546. doi: 10.1007/s12178-017-9444-1. Review. PubMed PMID: 29038952; PubMed Central PMCID: PMC5685966.
2)

Hijji FY, Narain AS, Bohl DD, Ahn J, Long WW, DiBattista JV, Kudaravalli KT, Singh K. Lateral lumbar interbody fusion: a systematic review of complication rates. Spine J. 2017 Oct;17(10):1412-1419. doi: 10.1016/j.spinee.2017.04.022. Epub 2017 Apr 26. Review. PubMed PMID: 28456671.
3)

Lykissas MG, Aichmair A, Hughes AP, Sama AA, Lebl DR, Taher F, Du JY, Cammisa FP, Girardi FP. Nerve injury after lateral lumbar interbody fusion: a review of 919 treated levels with identification of risk factors. Spine J. 2014 May 1;14(5):749-58. doi: 10.1016/j.spinee.2013.06.066. Epub 2013 Sep 5. PubMed PMID: 24012428.
4)

Lykissas MG, Aichmair A, Hughes AP, Sama AA, Lebl DR, Taher F, Du JY, Cammisa FP, Girardi FP. Nerve injury after lateral lumbar interbody fusion: a review of 919 treated levels with identification of risk factors. Spine J. 2014 May 1;14(5):749-58. doi: 10.1016/j.spinee.2013.06.066. Epub 2013 Sep 5. PubMed PMID: 24012428.
5)

Cahill KS, Martinez JL, Wang MY, Vanni S, Levi AD. Motor nerve injuries following the minimally invasive lateral transpsoas approach. J Neurosurg Spine. 2012 Sep;17(3):227-31. doi: 10.3171/2012.5.SPINE1288. Epub 2012 Jun 29. PubMed PMID: 22746272.
6)

Aichmair A, Lykissas MG, Girardi FP, Sama AA, Lebl DR, Taher F, Cammisa FP, Hughes AP. An institutional six-year trend analysis of the neurological outcome after lateral lumbar interbody fusion: a 6-year trend analysis of a single institution. Spine (Phila Pa 1976). 2013 Nov 1;38(23):E1483-90. doi: 10.1097/BRS.0b013e3182a3d1b4. PubMed PMID: 23873231.
7)

Le TV, Burkett CJ, Deukmedjian AR, Uribe JS. Postoperative lumbar plexus injury after lumbar retroperitoneal transpsoas minimally invasive lateral interbody fusion. Spine (Phila Pa 1976). 2013 Jan 1;38(1):E13-20. doi: 10.1097/BRS.0b013e318278417c. PubMed PMID: 23073358.
8)

Sellin JN, Brusko GD, Levi AD. Lateral Lumbar Interbody Fusion Revisited: Complication Avoidance and Outcomes with the Mini-Open Approach. World Neurosurg. 2019 Jan;121:e647-e653. doi: 10.1016/j.wneu.2018.09.180. Epub 2018 Oct 3. PubMed PMID: 30292030.

Traumatic spinal cord injury treatment

Early decompression surgery post-SCI can enhance patient outcomes, but does not directly facilitate neural repair and regeneration. Currently, there are no U.S. Food and Drug Administration-approved pharmacological therapies to augment motor function and functional recovery in individuals with traumatic SCI.

Acute traumatic spinal cord injury (SCI) is a devastating event with far-reaching physical, emotional, and economic consequences for patients, families, and society at large. Timely delivery of specialized care has reduced mortality; however, long-term neurological recovery continues to be limited. In recent years, a number of exciting neuroprotective and regenerative strategies have emerged and have come under active investigation in clinical trials, and several more are coming down the translational pipeline. Among ongoing trials are RISCIS (riluzole), INSPIRE study (Neuro-Spinal Scaffold), MASC (minocycline), and SPRING (VX-210). Microstructural MRI techniques have improved our ability to image the injured spinal cord at high resolution. This innovation, combined with serum and cerebrospinal fluid (CSF) analysis, holds the promise of providing a quantitative biomarker readout of spinal cord neural tissue injury, which may improve prognostication and facilitate stratification of patients for enrollment into clinical trials. Given evidence of the effectiveness of early surgical decompression and growing recognition of the concept that “time is spine,” infrastructural changes at a systems level are being implemented in many regions around the world to provide a streamlined process for transfer of patients with acute SCI to a specialized unit. With the continued aging of the population, central cord syndrome is soon expected to become the most common form of acute traumatic SCI; characterization of the pathophysiologynatural history, and optimal treatment of these injuries is hence a key public health priority. Collaborative international efforts have led to the development of clinical practice guidelines for traumatic SCI based on robust evaluation of current evidence 1).

1)

Badhiwala JH, Ahuja CS, Fehlings MG. Time is spine: a review of translational advances in spinal cord injury. J Neurosurg Spine. 2018 Dec 20;30(1):1-18. doi: 10.3171/2018.9.SPINE18682. Review. PubMed PMID: 30611186.
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