Traumatic brain injury complications [Neurosurgery Wiki]

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====== Traumatic brain injury complications ======

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1. ≈ 75% will exhibit an [[traumatic intracranial hematoma]]

a) may be present on initial evaluation and can then worsen

b) may develop in a delayed fashion

delayed [[epidural hematoma]] (EDH) 

delayed [[subdural hematoma]] (SDH)

delayed traumatic [[contusion]]s. see [[Traumatic intracerebral hemorrhage]]

Posttraumatic diffuse cerebral edema 

Tension pneumocephalus

Hyponatremia

Hypoxia: etiologies include pneumothorax, MI, CHF...

Hepatic encephalopathy

Hypoglycemia: including insulin reaction

Adrenal insufficiency

Drug or alcohol withdrawal

[[Dural sinus thrombosis]] 

[[Carotid  artery dissection]] (or rarely, vertebral)

c) [[SAH]]: due to rupture of [[aneurysm]] (spontaneous or posttraumatic) or [[carotid cavernous fistula]]
(CCF) 

Cerebral embolism: including [[fat embolism syndrome]] 

[[Hypotension]] (shock).

===== Alzheimer’s disease =====

Traumatic brain injury (TBI) is associated with increased [[dementia]] risk.

[[Alzheimer’s disease]].

===== Brain abscess =====
[[Traumatic brain abscess]].

===== Intracranial hypertension =====

see [[Intracranial hypertension after traumatic brain injury]]
===== Brain edema =====
[[Brain edema]] can result from a combination of several pathological mechanisms associated with primary and secondary injury patterns in [[traumatic brain injury]] (TBI).

As pressure within the [[skull]] increases, brain tissue displacement can lead to [[brain herniation]], resulting in disability or death.

see [[Anticoagulation in traumatic brain injury]].

Harris et al, suggest a link between head injury and Parkinson's disease and indicates further scrutiny of workplace incurred head injuries is warranted
((Harris MA, Shen H, Marion SA, Tsui JK, Teschke K. Head injuries and
Parkinson's disease in a case-control study. Occup Environ Med. 2013
Dec;70(12):839-44. doi: 10.1136/oemed-2013-101444. Epub 2013 Sep 18. PubMed PMID:
24142978.)).

===== Cerebral contusion =====
Cortical [[cerebral contusion]]s are one of the most common [[computed tomography]] (CT) findings in [[head injury]]
((Becker DP, Miller JD, Ward JD, Greenberg RP, Young HF, Sakalas R. The outcome 
from severe head injury with early diagnosis and intensive management. J
Neurosurg. 1977 Oct;47(4):491-502. PubMed PMID: 903803.
))
((Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW, Servadei F,
Walters BC, Wilberger J; Surgical Management of Traumatic Brain Injury Author
Group.. Surgical management of traumatic parenchymal lesions. Neurosurgery. 2006 
Mar;58(3 Suppl):S25-46; discussion Si-iv. Review. PubMed PMID: 16540746.)).

===== Cerebral Venous Sinus Thrombosis =====
[[Cerebral Venous Sinus Thrombosis]].

===== Cerebrospinal fluid fistula =====

see [[Traumatic cerebrospinal fluid fistula]].



===== Chronic traumatic encephalopathy =====

[[Chronic traumatic encephalopathy]].

===== Deep-Vein Thrombosis =====
[[Deep-Vein Thrombosis]].

===== Delayed deterioration =====
[[Delayed deterioration]].

===== Coagulopathy =====
The occurrence of coagulopathy in patients with traumatic brain injury (TBI) is related to severe complications. The authors performed the first systematic review to investigate whether biomarkers can predict the occurrence of hypocoagulopathy or progressive hemorrhagic injury in patients with TBI. Methods: The authors included studies that performed a receiver operating characteristics analysis for the biomarker and provided a clear value along with the respective sensitivity and specificity. Additionally, they attempted to classify each biomarker, taking into account its physiological role. Results: Twelve studies were included. All biomarkers were protein molecules, except in one study that examined the prognostic role of glucose. Copeptin had the highest sensitivity, and S100A12 had the highest specificity in predicting coagulopathy, while IL-33 had the highest sensitivity and GALECTIN-3 had the highest specificity in predicting progressive hemorrhagic injury. Conclusion: The study of the role of biomarkers in predicting the occurrence of coagulopathy in patients with TBI remains in its infancy
((Vlachos N, Lampros MG, Lianos GD, Voulgaris S, Alexiou GA. Blood biomarkers for predicting coagulopathy occurrence in patients with traumatic brain injury: a systematic review. Biomark Med. 2022 Jul 14. doi: 10.2217/bmm-2022-0294. Epub ahead of print. PMID: 35833883.)).

===== Disseminated intravascular coagulation =====
[[Disseminated intravascular coagulation]].  

===== Empty sella syndrome =====
[[Empty sella syndrome]].

===== Growing skull fracture =====
[[Growing skull fracture]].

===== Nerve palsy =====

[[Abducens nerve palsy]].

[[Oculomotor nerve palsy]].

===== Olfactory loss =====
Olfactory loss due to [[head trauma]] is a frequent finding. It is attributed to the tearing or severing of the olfactory fibers at the [[cribriform plate]]. In contrast, posttraumatic gustatory loss is observed and reported rarely and the underlying mechanism is less understood. Rahban et al. present a case of a concomitant post-traumatic anosmia and [[ageusia]]. Imaging showed a considerable frontobasal brain damage and it is speculated that the gustatory impairment is due to a central injury of the secondary taste cortex. Based on this observation, Rahban et al.we believe that this clinical presentation might be much more frequent than previously reported
((Rahban C, Ailianou A, Jacot E, Landis BN. [Concomitant anosmia and ageusia: a 
case report]. Rev Med Suisse. 2015 Sep 30;11(488):1787-90. French. PubMed PMID:
26619700.)).

[[Autonomic impairment]] after acute [[traumatic brain injury]] has been associated independently with both increased [[morbidity]] and [[mortality]]. Links between autonomic impairment and [[increased intracranial pressure]] or impaired cerebral autoregulation have been described as well. However, relationships between autonomic impairment, intracranial pressure, impaired cerebral autoregulation, and outcome remain poorly explored. 

===== Osteomyelitis of the skull =====

[[Skull Osteomyelitis]]. 

===== Pituitary dysfunction =====
[[Diabetes insipidus]].

see [[Posttraumatic hypopituitarism]]

hypogonadotropic hypogonadism

===== Pneumonia =====
[[Pneumonia in traumatic brain injury]]


===== Postconcussive syndrome =====
[[Postconcussive syndrome]]

===== Posttraumatic epilepsy =====
see [[Posttraumatic epilepsy]].

===== Posttraumatic hydrocephalus =====

[[Posttraumatic hydrocephalus]].

===== Posttraumatic meningitis =====
[[Posttraumatic meningitis]].

===== Posttraumatic stress disorder =====
[[Posttraumatic stress disorder]].

===== Pulmonary embolism =====

[[Pulmonary embolism]].

===== Secondary Parkinsonism =====
[[Secondary parkinsonism]]

===== SIADH =====

[[SIADH]].

===== Subdural empyema =====

[[Subdural empyema]].

===== Traumatic intracranial hemorrhage =====

[[Traumatic intracranial hemorrhage]].

===== Post-traumatic hearing loss =====
[[Post-traumatic hearing loss]]

===== Spasticity =====
Findings advocate for a person-centered approach in spasticity management, emphasizing the integration of sensory impairment strategies into rehabilitation to enhance functional outcomes and quality of life. Such an approach aims to improve functional outcomes and enhance the quality of life for individuals experiencing spasticity post-stroke or TBI. Future directions include targeted interventions to alleviate these sensations, support better rehabilitation results and improve patient experiences
((Facciorusso S, Spina S, Picelli A, Baricich A, Molteni F, Santamato A. May Spasticity-Related Unpleasant Sensations Interfere with Daily Activities in People with Stroke and Traumatic Brain Injury? Secondary Analysis from the CORTOX Study. J Clin Med. 2024 Mar 16;13(6):1720. doi: 10.3390/jcm13061720. PMID: 38541945; PMCID: PMC10970961.)).
===== References =====