Penetrating head injury outcome

Penetrating head injury outcome

Surgical intervention in penetrating head injury patients with GCS 3-5 results in improved mortality but comes at a cost of increased resource utilization in the form of longer LOS and higher infection rate. On the other hand, in patients with GCS ≥6, surgery does not provide significant benefits in patient survival. Future prospective studies providing insight as to the impact of surgery on the resource utilization and quality of survival would be beneficial in determining the need for surgical intervention in this population 1).


Reports from civilian cohorts are small because of the high reported mortality rates (as high as 90%). Data from military populations suggest a better prognosis for penetrating brain injury, but previous reports are hampered by analyses that exclude the point of injury.

The purpose of a study was to provide a description of the long-term functional outcomes of those who sustain a combat-related penetrating brain injury (from the initial point of injury to 24 months afterward).

This study is a retrospective review of cases of penetrating brain injury in patients who presented to the Role 3 Multinational Medical Unit at Kandahar Airfield, Afghanistan, from January 2010 to March 2013. The primary outcome of interest was Glasgow Outcome Scale (GOS) score at 6, 12, and 24 months from date of injury.

A total of 908 cases required neurosurgical consultation during the study period, and 80 of these cases involved US service members with penetrating brain injury. The mean admission Glasgow Coma Scale (GCS) score was 8.5 (SD 5.56), and the mean admission Injury Severity Score (ISS) was 26.6 (SD 10.2). The GOS score for the cohort trended toward improvement at each time point (3.6 at 6 months, 3.96 at 24 months, p > 0.05). In subgroup analysis, admission GCS score ≤ 5, gunshot wound as the injury mechanism, admission ISS ≥ 26, and brain herniation on admission CT head were all associated with worse GOS scores at all time points. Excluding those who died, functional improvement occurred regardless of admission GCS score (p < 0.05). The overall mortality rate for the cohort was 21%.

Good functional outcomes were achieved in this population of severe penetrating brain injury in those who survived their initial resuscitation. The mortality rate was lower than observed in civilian cohorts 2).


At the time of the Boer War in 1899 penetrating head injuries, which formed a large proportion of the battlefield casualties, resulted in almost 100% mortality. Since that time up to the present day, significant improvements in technique, equipment and organisation have reduced the mortality to about 10% 3).

References

1)

D’Agostino R, Kursinskis A, Parikh P, Letarte P, Harmon L, Semon G. Management of Penetrating Traumatic Brain Injury: Operative versus Non-Operative Intervention [published online ahead of print, 2020 Aug 17]. J Surg Res. 2020;257:101-106. doi:10.1016/j.jss.2020.07.046
2)

Two-year mortality and functional outcomes in combat-related penetrating brain injury: battlefield through rehabilitation. Neurosurg Focus. 2018 Dec 1;45(6):E4. doi: 10.3171/2018.9.FOCUS18359. PubMed PMID: 30544304.
3)

Stanworth PA. A century of British military neurosurgery. J R Army Med Corps. 2015 Aug 4. pii: jramc-2015-000477. doi: 10.1136/jramc-2015-000477. [Epub ahead of print] Review. PubMed PMID: 26243803.

Iatrogenic peripheral nerve injury

Iatrogenic peripheral nerve injury

Treatment

Iatrogenic peripheral nerve injury is a considerable social and economic concern and the majority of cases are preventable. Complications should be referred to and dealt with promptly by experienced surgeons, to ensure the best chances for optimal functional recovery. Their prevention should be emphasized. Their management should include ensuring early diagnosis, administering an appropriate treatment with rehabilitation, rendering psychological support, and providing control of pain 1).


The combination of morphological assessment (neurosonography) with functional assessment (nerve conduction studies) is of paramount importance in the management of traumatic peripheral nerve injuries. If on sonography, the nerve appears intact, then intraoperative nerve conduction studies the functionality of the nerve. If conduction is impaired (signifying the presence of a neuroma-in-continuity), then nerve grafting is done. If the conduction is somewhat preserved, neurolysis is performed 2).


If it is noted during an operation that a nerve has been severed, it should be repaired immediately during the same operation (primary repair) or within 2–3 weeks (early secondary repair) 3).

The same is true when the nerve is torn or damaged but not cleanly cut. The same operative approach is used as for any other nerve injury. The repair ideally is done with microsurgical tools and magnifying devices, insuring maximal visualization for the repair.

Once again, this ideal situation with the immediate repair is seldom achieved. Usually, the cause of the damage is unknown. In our experience, the operative report rarely provides useful information. When the mechanism for the damage is unknown but there is reason to think that the nerve may regenerate itself, we prefer to wait 3 months with monthly neurological examinations. If at this time, the deficit has not changed or only minimally improved, the nerve should be surgically explored in the next month. If the neurosonographic examination after exposure of the nerve identifies a neuroma, one should not delay. The operation should ideally occur within 3 weeks 4).

A severed nerve should be reconstructed, if possible. Usually, this requires nerve grafting. The sural nerve on the lateral calf is usually used as a source. Other cutaneous nerves such as the saphenous nerve and the medial antebrachial cutaneous nerve can also be used 5). If the nerve appears to be intact, then intraoperative nerve conduction studies help assess how functional it is in the area of damage. If conductivity is impaired, then the affected segment of the nerve surrounded by scar tissue—usually thickened and diagnosed as a neuroma in continuity—is excised and replaced by a transplant. In other cases, when conductivity studies are more promising, it suffices to free the nerve up from the surrounding reactive tissues (neurolysis). In recent years intraoperative neuro sonography has been employed, facilitating the evaluation of individual nerve fascicles, helping distinguish between a complete neuroma in continuity without any residual fascicles and a partial lesion still containing functioning fascicles 6).

The combination of the functional evaluation (nerve conduction studies) and the morphologic assessment (neuro sonography) is very helpful in the surgical management of traumatic injuries in peripheral nerve surgery. The exact approach is documented in the interdisciplinary guidelines of the AWMF “Versorgung peripherer Nervenverletzungen” 7).

A key factor in improving the prognosis is physical therapy, both after the deficit is identified and then post-operatively until re-innervation of the affected muscles has occurred. Electric stimulation therapy is also worthwhile in our option. In this way, the muscle structures can be better maintained until nerve regeneration has occurred.

Case series

Dubuisson et al. analyzed the management of iatrogenic peripheral nerve injury (iNI) in 42 patients.

The iNI occurred mostly during a surgical procedure (n = 39), either on a nerve or plexus (n = 13), on bone, joint, vessel, or soft tissue (n = 24) or because of malpositioning (n = 2). The most commonly injured nerves were the brachial plexusradial nervesciatic nervefemoral nerve, or peroneal nerves. 42.9% of the patients were referred to later than 6 months. A neurological deficit was present in 37 patients and neuropathic pain in 17. Two patients were lost to follow-up. Conservative treatment was applied in 23 patients because of good spontaneous recovery or compensation or because of expected bad prognosis whatever the treatment. Surgical treatment was performed in 17 patients because of known nerve section (n = 2), persistent neurological deficit (n = 12) or invalidating neuropathic pain (n = 3); nerve reconstruction with grafts (n = 8) and neurolysis (n = 8) were the most common procedures. The outcome was satisfactory in 50%. Potential reasons for poor outcomes were a very proximal injury, placement of very long grafts, delayed referral, and predominance of neuropathic pain. According to the literature, delayed referral of iNI for treatment is frequent. They provides an illustrative case of a young girl operated on at 6.5 months for femoral nerve reconstruction with grafts while the nerve section was obvious from the operative note and pathological tissue analysis. Litigation claims (n = 10) resulted in malpractice (n = 2) or therapeutic area (n = 5) (3 unavailable conclusions).

NI can result in considerable disability, pain, and litigation. Optimal management is required 8).


Rasulić et al. describe and analyze iatrogenic nerve injuries in a total of 122 consecutive patients who received surgical treatment at there institution during a period of 10 years, from January 1, 2003, to December 31, 2013. The final outcome evaluation was performed 2 years after surgical treatment.

The most common causes of iatrogenic nerve injuries among patients in the study were the operations of bone fractures (23.9%), lymph node biopsy (19.7%), and carpal tunnel release (18%). The most affected nerves were median nerve (21.3%), accessory nerve (18%), radial nerve (15.6%), and peroneal nerve (11.5%). In 74 (60.7%) patients, surgery was performed 6 months after the injury, and in 48 (39.3%) surgery was performed within 6 months after the injury. In 80 (65.6%) patients, we found lesion in discontinuity, and in 42 (34.4%) patients lesion in continuity. The distribution of surgical procedures performed was as follows: autotransplantation (51.6%), neurolysis (23.8%), nerve transfer (13.9%), direct suture (8.2%), and resection of neuroma (2.5%). In total, we achieved satisfactory recovery in 91 (74.6%), whereas the result was dissatisfactory in 31 (25.4%) patients.

Patients with iatrogenic nerve injuries should be examined as soon as possible by experts with experience in traumatic nerve injuries so that the correct diagnosis can be reached and the appropriate therapy planned. The timing of reconstructive surgery and the technique used are the crucial factors for functional recover 9).


340 patients underwent surgery for iatrogenic nerve injuries over a 23-year period in the District Hospital of Günzburg (Neurosurgical Department of the University of Ulm). In a study published by the authors in 2001, 17.4% of the traumatic nerve lesions treated were iatrogenic. 94% of iatrogenic nerve injuries occurred during surgical procedures 10).

References

1)

Kumar A, Shukla D, Bhat DI, Devi BI. Iatrogenic peripheral nerve injuries. Neurol India. 2019;67(Supplement):S135-S139. doi:10.4103/0028-3886.250700
2)

Sinha S. Management protocol in the case of iatrogenic peripheral nerve injuries. Neurol India. 2019;67(Supplement):S140-S141. doi:10.4103/0028-3886.250696
3) , 4) , 5) , 7)

Deutsche Gesellschaft für Handchirurgie (DGH), Deutsche Gesellschaft für Neurologie (DGN), Deutsche Gesellschaft für Neurochirurgie (DGNC), Deutsche Gesellschaft für Orthopädie und Orthopädische Chirurgie (DGOOC), Deutsche Gesellschaft der Plastischen, Rekonstruktiven und Ästhetischen Chirurgen (DGPRÄC), Deutsche Gesellschaft für Unfallchirurgie (DGU) Leitlinen: Versorgung peripherer Nervenverletzungen. http://www.awmf.org/leitlinien/detail/ll/005-010.html Stand 30.06.2013
6)

Koenig RW, Schmidt TE, Heinen CPG, et al. Intraoperative high-resolution ultrasound: a new technique in the management of peripheral nerve disorders. Clinical article Journal of Neurosurgery. 2011;114:514–521
8)

Dubuisson A, Kaschten B, Steinmetz M, et al. Iatrogenic nerve injuries: a potentially serious medical and medicolegal problem. About a series of 42 patients and review of the literature [published online ahead of print, 2020 Jul 11]. Acta Neurol Belg. 2020;10.1007/s13760-020-01424-0. doi:10.1007/s13760-020-01424-0
9)

Rasulić L, Savić A, Vitošević F, et al. Iatrogenic Peripheral Nerve Injuries-Surgical Treatment and Outcome: 10 Years’ Experience. World Neurosurg. 2017;103:841-851.e6. doi:10.1016/j.wneu.2017.04.099
10)

Antoniadis G, Kretschmer T, Pedro MT, König RW, Heinen CP, Richter HP. Iatrogenic nerve injuries: prevalence, diagnosis and treatment. Dtsch Arztebl Int. 2014;111(16):273-279. doi:10.3238/arztebl.2014.0273

Severe traumatic brain injury treatment

Severe traumatic brain injury treatment

There are currently no established treatments for the underlying pathophysiology in TBI and while neuro-rehabilitation efforts are promising, there are currently is a lack of consensus regarding rehabilitation following TBI of any severity 1).

see Severe traumatic brain injury guidelines.

see also Pediatric traumatic brain injury guidelines.

Severe traumatic brain injury (TBI) is currently managed in the intensive care unit with a combined medical-surgical approach. Treatment aims to prevent additional brain damage and to optimise conditions for brain recovery. TBI is typically considered and treated as one pathological entity, although in fact it is a syndrome comprising a range of lesions that can require different therapies and physiological goals. Owing to advances in monitoring and imaging, there is now the potential to identify specific mechanisms of brain damage and to better target treatment to individuals or subsets of patients. Targeted treatment is especially relevant for elderly people-who now represent an increasing proportion of patients with TBI-as preinjury comorbidities and their therapies demand tailored management strategies. Progress in monitoring and in understanding pathophysiological mechanisms of TBI could change current management in the intensive care unit, enabling targeted interventions that could ultimately improve outcomes 2).

Monitoring

see Intracranial pressure monitoring for severe traumatic brain injury.

Hormonal replacement

Hormonal analysis should be considered in patients with moderate-to-severe traumatic brain injury, so that appropriate hormonal replacement can be done to optimize the clinical outcome 3).

Case series

Data from 729 severe traumatic brain injury patients admitted between 1996 and 2016 were used. Treatment was guided by controlling intracranial pressure and cerebral perfusion pressure according to a local protocol.

Cerebral perfusion pressurepressure reactivity index curves were fitted automatically using a previously published curve-fitting heuristic from the relationship between pressure reactivity index and cerebral perfusion pressure. The cerebral perfusion pressure values at which this “U-shaped curve” crossed the fixed threshold from intact to impaired pressure reactivity (pressure reactivity index = 0.3) were denoted automatically the “lower” and “upper” cerebral perfusion pressure limits of reactivity, respectively. The percentage of time with cerebral perfusion pressure below (%cerebral perfusion pressure < lower limit of reactivity), above (%cerebral perfusion pressure > upper limit of reactivity), or within these reactivity limits (%cerebral perfusion pressure within limits of reactivity) was calculated for each patient and compared across dichotomized Glasgow Outcome Scores. After adjusting for age, initial Glasgow Coma Scale, and mean intracranial pressure, percentage of time with cerebral perfusion pressure less than lower limit of reactivity was associated with unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity, 1.04; 95% CI, 1.02-1.06; p < 0.001) and mortality (odds ratio, 1.06; 95% CI, 1.04-1.08; p < 0.001).

Individualized autoregulation-guided cerebral perfusion pressure management may be a plausible alternative to fixed cerebral perfusion pressure threshold management in severe traumatic brain injury patients. Prospective randomized research will help define which autoregulation-guided method is beneficial, safe, and most practical 4).

Medicaments

Despite the incidence of these injuries and their substantial socioeconomic implications, no specific pharmacological intervention is available for clinical use.

see Progesterone for acute traumatic brain injury.

see 21-aminosteroids for severe traumatic brain injury.

Neuroprotection

see Neuroprotection in traumatic Brain Injury

see Decompressive craniectomy for severe traumatic brain injury.

Cell-based therapies

Cell-based therapies are currently being investigated in treating neurotrauma due to their ability to secrete neurotrophic factors and anti-inflammatory cytokines that can regulate the hostile milieu associated with chronic neuroinflammation found in TBI. In tandem, the stimulation and mobilization of endogenous stem/progenitor cells from the bone marrow through granulocyte colony stimulating factor (G-CSF) poses as an attractive therapeutic intervention for chronic TBI.

The potential of a combined therapy of human umbilical cord blood cells (hUCB) and G-CSF at the acute stage of TBI to counteract the progressive secondary effects of chronic TBI using the controlled cortical impact model.

Four different groups of adult Sprague Dawley rats were treated with saline alone, G-CSF+saline, hUCB+saline or hUCB+G-CSF, 7-days post CCI moderate TBI. Eight weeks after TBI, brains were harvested to analyze hippocampal cell loss, neuroinflammatory response, and neurogenesis by using immunohistochemical techniques. Results revealed that the rats exposed to TBI treated with saline exhibited widespread neuroinflammation, impaired endogenous neurogenesis in DG and SVZ, and severe hippocampal cell loss. hUCB monotherapy suppressed neuroinflammation, nearly normalized the neurogenesis, and reduced hippocampal cell loss compared to saline alone. G-CSF monotherapy produced partial and short-lived benefits characterized by low levels of neuroinflammation in striatum, DG, SVZ, and corpus callosum and fornix, a modest neurogenesis, and a moderate reduction of hippocampal cells loss. On the other hand, combined therapy of hUCB+G-CSF displayed synergistic effects that robustly dampened neuroinflammation, while enhancing endogenous neurogenesis and reducing hippocampal cell loss. Vigorous and long-lasting recovery of motor function accompanied the combined therapy, which was either moderately or short-lived in the monotherapy conditions. These results suggest that combined treatment rather than monotherapy appears optimal for abrogating histophalogical and motor impairments in chronic TBI 5).

Research

Research in traumatic brain injury (TBI) is challenging for several reasons; in particular, the heterogeneity between patients regarding causes, pathophysiology, treatment, and outcome. Advances in basic science have failed to translate into successful clinical treatments, and the evidence underpinning guideline recommendations is weak. Because clinical research has been hampered by non-standardised data collection, restricted multidisciplinary collaboration, and the lack of sensitivity of classification and efficacy analyses, multidisciplinary collaborations are now being fostered. Approaches to deal with heterogeneity have been developed by the IMPACT study group. These approaches can increase statistical power in clinical trials by up to 50% and are also relevant to other heterogeneous neurological diseases, such as stroke and subarachnoid haemorrhage. Rather than trying to limit heterogeneity, we might also be able to exploit it by analysing differences in treatment and outcome between countries and centres in comparative effectiveness research. This approach has great potential to advance care in patients with TBI 6).

Anticoagulation Resumption after traumatic brain injury

Anticoagulation Resumption after traumatic brain injury.

Thromboprophylaxis

The early administration of venous thromboembolism (VTE) chemoprophylaxis within 24 h after admission in patients with severe TBI did not increase the risk of intracranial bleeding progression 7).

Transcutaneous Vagus Nerve Stimulation for Severe Traumatic Brain Injury

see Transcutaneous Vagus Nerve Stimulation for Severe Traumatic Brain Injury.

References

1)

Marklund N, Bellander BM, Godbolt A, Levin H, McCrory P, Thelin EP. Treatments and rehabilitation in the acute and chronic state of traumatic brain injury. J Intern Med. 2019 Mar 18. doi: 10.1111/joim.12900. [Epub ahead of print] PubMed PMID: 30883980.
2)

Stocchetti N, Carbonara M, Citerio G, Ercole A, Skrifvars MB, Smielewski P, Zoerle T, Menon DK. Severe traumatic brain injury: targeted management in the intensive care unit. Lancet Neurol. 2017 Jun;16(6):452-464. doi: 10.1016/S1474-4422(17)30118-7. Review. PubMed PMID: 28504109.
3)

Prasanna KL, Mittal RS, Gandhi A. Neuroendocrine dysfunction in acute phase of moderate-to-severe traumatic brain injury: A prospective study. Brain Inj. 2015;29(3):336-342. PubMed PMID: 25671810.
4)

Donnelly J, Czosnyka M, Adams H, Robba C, Steiner LA, Cardim D, Cabella B, Liu X, Ercole A, Hutchinson PJ, Menon DK, Aries MJH, Smielewski P. Individualizing Thresholds of Cerebral Perfusion Pressure Using Estimated Limits of Autoregulation. Crit Care Med. 2017 Sep;45(9):1464-1471. doi: 10.1097/CCM.0000000000002575. PubMed PMID: 28816837.
5)

Acosta SA, Tajiri N, Shinozuka K, Ishikawa H, Sanberg PR, Sanchez-Ramos J, Song S, Kaneko Y, Borlongan CV. Combination therapy of human umbilical cord blood cells and granulocyte colony stimulating factor reduces histopathological and motor impairments in an experimental model of chronic traumatic brain injury. PLoS One. 2014 Mar 12;9(3):e90953. doi: 10.1371/journal.pone.0090953. eCollection 2014. PubMed PMID: 24621603.
6)

Maas AI, Murray GD, Roozenbeek B, Lingsma HF, Butcher I, McHugh GS, Weir J, Lu J, Steyerberg EW; International Mission on Prognosis Analysis of Clinical Trials in Traumatic Brain Injury (IMPACT) Study Group. Advancing care for traumatic brain injury: findings from the IMPACT studies and perspectives on future research. Lancet Neurol. 2013 Dec;12(12):1200-10. doi: 10.1016/S1474-4422(13)70234-5. Epub 2013 Oct 17. PubMed PMID: 24139680; PubMed Central PMCID: PMC3895622.
7)

Störmann P, Osinloye W, Freiman TM, Seifert V, Marzi I, Lustenberger T. Early Chemical Thromboprophylaxis Does not Increase the Risk of Intracranial Hematoma Progression in Patients with Isolated Severe Traumatic Brain Injury. World J Surg. 2019 Jul 2. doi: 10.1007/s00268-019-05072-1. [Epub ahead of print] PubMed PMID: 31267142.
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