Medical and neurologic complications determine the ultimate functional outcome, community reintegration, and employment potential after traumatic brain injury. Therefore, it is important to recognize the potential risks of these pathologies and follow evidence-based protocols to minimize Risk and extent of secondary complications.
Long-term somatic cognitive and behavioral complications are related both to direct injury to the brain and to central nervous system dysfunction and trauma to other organs and systems. Multiple complications can occur immediately or soon after traumatic brain injury But others may not be recognized until recovery. A serious injury increases the risk of more, more serious complications.
The presence of complications and injury-related injuries can affect the quality of life of patients with traumatic brain injury. These issues can cause frustration, conflict and misunderstanding for the person with TBI, as well as family or friends.  a Individuals may be at increased risk for suicide and for mood and anxiety disorders due to a combination of symptomatic and neuropsychiatric factors, which are often exacerbated by trauma.
Medical complications include:
Traumatic brain injury involving a skull fracture or penetrating injury can result in damage to the meninges. This can lead to a bacterial infection of the brain. If left untreated, infection of the meninges (meningitis) may spread to the rest of the nervous system.
Sepsis or multiorgan dysfunction are major causes of subsequent morbidity and mortality in traumatic brain injury. Elevated catecholamine levels following systemic insults directly affect the regulation of cytokine expression under conditions of acute stress disorder clinical setting and ultimately adverse outcome. Depression-induced elevated catecholamine levels affect internal organs and contribute to organ damage.  .
Spasticity is one of the upper motor disorders that progresses rapidly in some cases within a week after traumatic brain injury and often leads to orthopedic consequences.  Mild spasticity may have some benefits such as increasing muscle mass or increasing gait but it is moderate to severe increased muscle strength and weakness can significantly affect rehabilitation outcomes in terms of functional recovery and ability to participate in activities of daily living. Moderate to severe spasticity requires a management plan.
Impaired respiratory function is common after traumatic brain injury and depends on the severity of the injury. There is a correlation between lung function and brain function: the brain requires an adequate supply of oxygen to function, while the respiratory system It needs instructions from the brain to function.
Respiratory dysfunction is the most common medical complication in the setting of traumatic brain injury, respiratory complications are directly related to mortality, and both are related to the severity of the injury. Up to a third of patients with severe traumatic brain injury will develop acute Respiratory Distress Syndrome (ARDS). In this syndrome, inflammation occurs at the alveolar-capillary interface, causing fluid and protein to enter the interstitial space and alveoli. Between 20% and 30% of patients with ARDS die from pulmonary infiltrates leading to Respiratory failure.
Read more about Respiratory Management for Traumatic Brain Injury
deep vein thrombosis and pulmonary embolism
Deep vein thrombosis (DVT) is the formation of one or more blood clots in a large vein in the body, followed by a pulmonary embolism (PE), in which an artery in the lung is blocked by material that has moved from the rest of the body through the blood (embolism) remains an important cause of morbidity and mortality in patients with traumatic brain injury and is particularly vulnerable during the first 2-3 weeks after injury. After traumatic brain injury, DVT occurs in up to 54% due to difficulty in administering anticoagulants in the acute phase Prophylaxis after traumatic brain injury is usually only available after the risk of recurrent intracranial hemorrhage has been reduced.
Read more about deep vein thrombosis and pulmonary embolism
Paroxysmal sympathetic hyperactivity (PSH)
Hypersympathetic hypersympathetic is “a storm observed weeks or months after traumatic brain injury and manifested by increased sympathetic activity: increased heart rate blood pressure increased respiratory rate increased sweating hyperthermia exercise posture.  PSH is associated with poor Consequences and consequences of disconnection syndrome, which is impaired inhibitory control of excitatory autonomic centers.
Neuroendocrine dysfunction/post-traumatic hypopituitarism
The clinically common phenomenon associated with damage to the pituitary gland is a small gland located at the base of the brain that regulates other endocrine glands, the thyroid adrenal pineal gland. Pituitary gland damage is most prevalent in skull fracture cases and affects itself Function as well as affect the production of other hormones affect homeostasis metabolism mood growth sleep and other bodily functions. Hypopituitarism is associated with the presence of depression and fatigue. Resulting thyroid dysfunction linked to neuropsychiatric problems heart function Reduce anxiety and diabetes insipidus.
Heterotopic ossification, also known as heterotopic ossification and myositis ossificans, is the formation of pathological bone in muscle or soft tissue that can lead to stiffness and impaired function in severe cases. It usually appears around the joints, mainly in the hip, and the first signs are These include periarticular swelling, reduced range of motion, with or without fever, cramps, and pain, which are clinically similar to fractures and deep vein thrombosis. Ultrasound CT scan or bone scan can be used to provide a definitive diagnosis of heterotopic ossification, although A blood test can also give some indication.
Clinically significant heterotopic ossification has been reported to occur in 11-76% of traumatic brain injuries and in 10-20% of cases. It manifests as abnormal formation of heterotopic lamellar bone in soft tissue. Heterotopic ossification tends to form around larger joints, such as As in the hip, knee and shoulder joints, it results in reduced range of motion, pain and decreased function with limited mobility. Timely use of prophylactic NSAIDs and diagnostic imaging should be implemented early to prevent severe mobility impairment. Other methods Including the use of bisphosphonates (limited evidence) Radiotherapy and physical therapy can improve mechanical properties. Completely formed heterotopic ossifications may be surgically removed when severe pain or loss of range of motion significantly interferes with mobility or personal care.
Read more about the prevention and management of heterotopic ossification here
Bladder bowel dysfunction and genitourinary complications
Cognitive deficits and behavioral difficulties due to ineffective communication, one of the most common complications in patients with traumatic brain injury. Urinary dysfunction is associated with detrusor overactivity, often resulting in longer acute care and delayed recovery. when discharged These patients showed poor functional recovery. Determining the cause (such as a urinary tract infection), using appropriate medications, and pelvic floor exercises can improve outcomes.
Neurogenic bowel disease can be incontinence or constipation. 68% of people undergoing rehabilitation may exhibit fecal incontinence. Hydration, fiber intake, medication and toilet training can help with these problems. Untreated bladder and bowel dysfunction can have Organizational vitality should be addressed.
Sexual dysfunction associated with frontal lobe damage and limbic system dysfunction may manifest as hyposexuality, decreased libido, lack of satisfaction, or ejaculatory dysfunction. Social and intimacy difficulties exacerbate these sexual dysfunctions. sexual misconduct Creates a potential risk of aggression and criminalization of difficult-to-form relationships.
Endocrine and inflammatory processes after traumatic brain injury lead to excessive energy expenditure and consequent malnutrition hyperglycemia protein catabolism deficient wound healing muscle atrophy and urinary nitrogen excretion. Enteral feeding with a large protein supply can improve result. Optimal nutrition can help improve sleep behavior, physical health, emotional state and fatigue management.
People with traumatic brain injuries are at high risk of developing pressure sores. The National Pressure Ulcer Advisory Panel (NPUAP) defines a pressure ulcer as an area of unrelieved pressure on a specific area, usually located on a bony prominence, resulting in ischemic cell death and tissue necrosis.  A pressure ulcer is a localized injury to the skin and/or underlying tissue, usually over a bony protrusion, due to pressure or a combination of pressure and shear.  Pressure sores can develop within hours, but their effects can last for months and even lead to death. A sort of Many contributing or confounding factors have been associated with pressure ulcers; however, the significance of these factors has yet to be elucidated. Tissue damage is related to extrinsic and intrinsic factors. Extrinsic factors include pressure shear friction immobility and moisture while Intrinsic factors associated with the patient’s condition, such as sepsis, local infection, decreased autonomic control, altered level of consciousness, increasing age, vaso-occlusive disease, anemia, malnutrition, sensory loss, spasticity, and contractures. 
Read more about pressure ulcer prevention and management here
Sleep disturbance is an extremely common complication in patients with traumatic brain injury. These include insomnia, narcolepsy, excessive daytime sleepiness, and impaired circadian sleep-wake patterns.  Effects depend on the site of injury and can be treated with sleep hygiene training Daytime exercise caffeine restriction CBT and medication.
Post-traumatic headaches usually occur after a traumatic brain injury. Tension-type headaches are the most common form, but exacerbations of migraine-like headaches are also common. Headaches are usually a long-term problem.
Neurological complications include:
Post-traumatic seizures often occur after moderate or severe traumatic brain injury. They may occur only early in the injury or years after the injury (post-traumatic epilepsy). Post-injury classifications are:
- Immediate seizures (within 24 hours of injury)
- Early seizures (less than 1 week after injury)
- Late seizures (occurring more than a week after the injury).
Risk Factors include:
- Bilateral contusion
- Dural penetration
- Subdural haematoma
- Multiple intracranial surgeries
- Midline shift > 5mm
- Presence of serious injury as measured by GCS.
Posttraumatic seizures are associated with poor functional outcomes. Phenytoin and levetiracetam are the most commonly used drugs for the prevention and treatment of seizures.
Hydrocephalus occurs when cerebrospinal fluid builds up in the ventricles of the brain, causing increased pressure and swelling in the brain. Up to 70% of patients show ventricular enlargement 2 months after moderate-to-severe traumatic brain injury. Craniotomy for severe traumatic brain injury Older age and longer duration of intracranial hemorrhage are possible risk factors. Smooth progress in recovery or decreased function may indicate posttraumatic hydrocephalus. Clinically, patients with posttraumatic hydrocephalus may present with headache, nausea, and urine Urinary incontinence Cognitive decline Papilledema Movement disorders. Diagnostic imaging combined with lumbar puncture is a commonly used diagnostic tool. Surgical implantation of a shunt to drain excess cerebrospinal fluid into the abdominal cavity is a treatment option.
Cranial Nerve Disorders
Traumatic brain injury at the base of the skull causes damage to the nerves that go directly out of the brain or brainstem. Damage to the cranial nerves can cause:
- Facial muscle paralysis or loss of facial sensation
- Loss of or altered sense of smell
- Loss of or altered sense of taste
- Loss of vision or double vision
- Swallowing problems
- Ringing in the ear
- Hearing Loss
Visual dysfunction may manifest as blurred vision Sensitivity to light Difficulty reading Headaches with reduced visual tasks or loss of visual field such as hemianopia and eye movement difficulties Deficits in gaze stability. These vision problems can affect other areas of function, such as Communication mobility and balance. They can also affect safety, such as vision defects.
May include loss of somatosensory perception Persistent tinnitus Difficulty recognizing objects Blind spot or double vision A range of issues encountered that require careful assessment to inform Most Effective Treatment Untreated neurosensory deficits can affect other functions such as motor control and the ultimate level of functional recovery.
Spatial neglect is a complex problem involving sensorimotor and memory, manifested by impaired attention to the side opposite the lesion. The presence of unilateral neglect seriously undermines recovery. Treatment approaches should include teaching motor sensation and compensation strategies However, there is no clear evidence of the clinical effectiveness or superiority of any particular approach.
Dyskinesias can manifest as hypokinesia or hyperkinesia and may manifest as: tremor chorea dystonia athetosis elastic myoclonus parkinsonism convulsions.  Dyskinesia may be the only symptom or coexist with other movements or movement disorders. they can also be a party The effects of medications, such as those used to treat cognitive impairment or arousal disorders. Some conditions, such as dystonia, occur in the acute phase after traumatic brain injury, but some conditions, such as Parkinson’s disease, may develop decades after trauma. Most Common Movement Disorder After Traumatic Brain Injury It’s tremors, dystonia, Parkinsonism, myoclonus, which are more prevalent in serious injuries. Brain regions frequently involved in movement disorders are: basal ganglia, cerebellum, thalamus, subthalamus, and white matter tracts. Treatment consists of addressing the cause, such as a hematoma or Hydrocephalus; by medical and surgical intervention.
Dizziness / Balance Disorders
Dizziness and balance disturbances are a common complication of traumatic brain injury, reported by 80% of people. The etiology may be complex and include vestibular impairment, sensory integration problems, vision or proprioception. Primary pathology includes BPPV central vestibular or Peripheral problems, such as damage to the vestibular nerve or to the semicircular canals of the ear. Physical therapy depends on the etiology of the pathology.
Sleep / Wake Disorders
The restorative function of sleep is impaired after traumatic brain injury, and sleep pathology is very common. Contributing factors include biochemical and structural changes in the brain, particularly the reticular system, thalamus, and hypothalamus Medicinal use, such as uncontrollable pain behavior during naps Daytime and caffeine intake and environment. For example, hospital wards do not have a clear division of day and night. Treatment includes sleep hygiene training pharmaceutical preparations such as melatonin, benzodiazepines or zolpidem, exercise and light therapy.
Fatigue in patients with traumatic brain injury can have major effects, for example leading to difficulties with cognitive tasks (associated with activation of the caudate nucleus in the basal ganglia ) and peripherally leading to musculoskeletal fatigue. The presence of fatigue can negatively affect the body Get involved in recovery. Treatment includes environmental modifications and sometimes medications such as modafinil.
Behavioural & Emotional
Changes in behavior and mood, including agitation Difficulty with self-control Lack of awareness of competence Risky behavior Verbal or physical outbursts Alcohol abuse Overeating Anxiety and depression Mood swings Irritability Anger Lack of empathy for others. These questions can Significantly affects rehabilitation outcomes and community reintegration. These behavioral changes can negatively impact interpersonal employment and criminal activity. Neuropsychologists and neuropsychiatrists are an integral part of MDT and work with people after brain injury, All relevant professionals and relatives need to follow a comprehensive behavior management plan. Post-traumatic depression is further associated with cognitive decline, anxiety disorders, substance abuse, dysregulated emotional expression, and aggressive outbursts.
The following areas may be affected and affect information processing, communication, motor execution, and balance skills:
- Memory: sensory memory working memory short-term long-term semantic memory procedural memory episodic memory
- Learning new skills and information
- Attention or concentration
- Executive functioning problems
- Beginning or completing tasks
Degenerative Brain Disease and Dementia
Usually caused by repeated or severe traumatic brain injuries; compared with the general population, people with traumatic brain injuries are approximately 4 times more likely to develop dementia and live earlier. Repetitive Injury Linked to Chronic Trauma Encephalopathy (CTE) or dementia pugilistica (Dementia pugilistica), while a single brain injury is associated with Alzheimer’s symptoms. Exacerbation of degenerative encephalopathy after traumatic brain injury has also been associated with genetic background.
Moderate to severe traumatic brain injury can cause changes in a person’s state of consciousness or ability to respond. Different states of consciousness include:
- Coma: A person in a coma is unconscious, unaware of himself or his environment, and unable to respond to any stimuli. This is due to widespread damage to all parts of the brain. Patients with traumatic brain injury may emerge from a coma or enter a vegetative state at various times after trauma.
- Vegetative State (VS): Involves extensive brain damage. The person is unaware of the surroundings but may be open to sounds responding to reflexes or moving. The person may remain in VS forever but some patients may transition to an unconscious state.
- Minimally Conscious State: A state of severe consciousness alteration but with some signs of self-awareness or awareness of the environment. Sometimes it is an intermittent state between coma or VS and a degree of recovery of consciousness.
- Brain Death: Declared when there is no measurable activity in the brain and brainstem. In a person who has been declared brain dead, the removal of ventilators will stop breathing and eventually cardiac arrest. Brain death is considered irreversible.
Possible connection issues could include:
- It is difficult to understand speech or writing
- Difficulty speaking or writing
- Inability to organize thoughts and ideas
- The problem behind discussion is participation
- Having trouble taking turns or choosing topics in a conversation
- Problems with inflection or emphasis expressing emotional attitudes or nuances of meaning
- Difficulty understanding nonverbal signals
- Trouble reading cues from listeners
- Can’t start or stop a conversation
- Inability to use the muscles needed to form words (dysarthria)
- ↑ https://www.mayoclinic.org/diseases-conditions/traumatic-brain-injury/symptoms-causes/syc-20378557accessed 26.05.2019
- ↑ Kinoshita K. Traumatic brain injury: pathophysiology for neurocritical care. Journal of Intensive Care. 2016. 4:29-39. DOI 10.1186/s40560-016-0138-3
- ↑ Bose P, Hou J, Thompson FJ. Traumatic Brain Injury (TBI)- Induced Spasticity: Neurobiology, Treatment, and Rehabilitation. In: Kobeissy FH, editor. Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects. Boca Raton: CRC Press/Taylor & Francis; 2015. Chapter 14.
- ↑ Meyfroidt G, Baguley DJ, Menon DK. Paroxysmal sympathetic hyperactivity: the storm after acute brain injury. The Lancet Neurology. 2017. 16(9):721-729.
- ↑ http://emedicine.medscape.com/article/190115-overview
- ↑ National Pressure Ulcer Advisory Panel. NPUAP pressure ulcer Stages/Categories.
- ↑ Kruger EA, Pires M, Ngann Y, Sterling M, Rubayi S. Comprehensive Management of Pressure Ulcers in Spinal Cord Injury: Current Concepts and Future Trends. The Journal of Spinal Cord Medicine. 2013 Nov 1;36(6):572-85.
- ↑ Jump up to:8.0 8.1 Eapen BC, Cifu DX. Editor. Rehabilitation After Traumatic Brain Injury. Elsevier2018
- ↑ Wylie GR, Dobryakova E, DeLuca J, Chiaravalloti N, Essad K, Genova H. Cognitive fatigue in individuals with traumatic brain injury is associated with caudate activation. Sci Rep. 2017;7(1):8973. Published 2017 Aug 21. doi:10.1038/s41598-017-08846-6