Medical Complications in Traumatic Brain Injury

Introduction

Medical and neurological complications determine ultimate functional outcome in community reintegration and employment after traumatic brain injury. It is therefore important to recognize the potential risks of those diseases and to follow evidence-based policy to. risk and extent of secondary complications.

Long-term physical psychosocial complications are both related to direct injury to the brain and also to the effects of central nervous system dysfunction and trauma on other organs and systems. Many complications can occur immediately or shortly after a traumatic brain injury but others may not be known until rehabilitation. A serious injury increases the risk of more numerous and serious complications.

The complications and injury-related problem affect the quality of life of a person living with traumatic brain injury. These problems can lead to frustrating conflicts and misunderstandings with people with traumatic brain injury as well as with family or friends. [1] An an individual’s risk for suicide and mood and anxiety disorders may be increased by a combination of symptoms and neuropsychological factors that tend to exacerbate the trauma.

Medical Complications

Medical complications include:

Infection

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 multiple organ dysfunction syndrome is a major cause of late morbidity and mortality in traumatic brain injury. Catecholamine surge after systemic injury is directly involved in the regulation of cytokine expression in acute stress situations leading to disease exacerbation Clinical status, final outcome is poor. The surge of catecholamines caused by trauma can affect organs throughout the body and lead to organ damage. [2]

Spasticity

Spasticity, one of the upper motor neuron hallmarks, can develop rapidly in some cases as early as a week after traumatic brain injury and often results in orthopedic sequelae. [3] Mild spasticity may have some benefits, such as maintaining muscle mass or enhancing gait, but moderate to severe Increased muscle tone and spasticity can seriously affect rehabilitation outcomes, functional recovery and the ability to participate in activities of daily living. Moderate to severe spasticity requires a structured management protocol.

Respiratory Dysfunction

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 needs 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 Excessive Activity (PSH) .

sympathetic overactivity is “a storm following a traumatic brain injury that is seen for weeks or months and results in increased sympathetic activity: increased heart rate increased blood pressure increased respiratory rate sweating burn great motor posturing. [4] PSH is associated with poverty the result is a disconnection syndrome in which inhibitory control over excitatory autonomic centers is impaired.

Neuroendocrine Dysfunction / Posttraumatic Brain Injury Hypopituitarism

A common clinical phenomenon associated with damage to the pituitary gland a small gland that lives beneath the brain and regulates other endocrine glands ie. thyroid adrenal gland pineal gland. The pituitary gland is severely damaged in cases of skull fracture and affects its own function as well as affect the production of other hormones that affect homeostasis metabolism mind growth sleep and other bodily functions. Hypopituitarism has been associated with the presence of depression and fatigue. Consequent thyroid dysfunction involves neuropsychological issues related to cardiac function reduce anxiety diabetes unpleasantness.

Heterotopic Ossification

Heterotopic ossification, also known as ectopic ossification and myositis ossificans, is a pathological bone formation in tendons or soft tissues that, when severe, can lead to ankylosis and impaired function. It is most common around the joints especially in the hips with the first symptoms including decreased swelling around the joint with decreased range of motion with cranial tenderness and pain which are clinical symptoms similar to those associated with rheumatoid arthritis and deep lymph nodes. Ultrasound CT Scan or Bone Scan is used to detect definite heterotopic ossification though blood tests can also be indicative.

In traumatic brain injury the incidence has been reported to be between 11-76% with 10-20% of cases of clinically significant heterotopic ossification. It is characterized by abnormal formation of ectopic lamellar bone in soft tissues. Heterotopic ossification is usually formed around the major joints such as as the hip knee and shoulder are responsible for some reduction of movements when immobilizing pain is minimal and inactive. Timely administration of prophylactic nonsteroidal anti-inflammatory drugs and diagnostic imaging modalities should be implemented early to prevent severe immobility. Other methods of working including the use of bisphosphonates (limited evidence) radiation and physical therapy for technical improvement for. Complete heterotopic ossification can be surgically resected when severe pain or loss of mobility significantly affects mobility or self-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.

Nutritional Deficits 

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.

Pressure Ulcers

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. [5] 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. [6] 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. [7]

Read more about pressure ulcer prevention and management here

Sleep Disturbances

Sleep disturbances are a very common problem in people living with traumatic brain injury. They include insomnia hypersomnia excessive daytime sleepiness and impaired circadian sleep-wake patterns.[8] The impact depends on the injured area and can be treated with sexual hygiene training afternoon exercise caffeine intake restriction CBT and medication.

Post-traumatic Headache

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

Neurological complications include:

Post-traumatic Seizures

Post-traumatic seizures often occur after moderate or severe traumatic brain injury. They may occur only early in the injury or years after (post-traumatic epilepsy). Post-injury classifications are:

• Immediate seizures (within 24 hours of injury)
• Early seizures (less than 1 week after injury)
• Late concussion (appears more than a week after injury).

Risk Factors include:  

• Bilateral contusion 
• Dural penetration 
• Subdural haematoma 
• Multiple intracranial surgeries 
• Midline shift > 5mm 
• Presence of severe injury measured by GCS.

Posttraumatic constipation is about the consequences of poor functioning. Phenytoin and levetiracetam are the drugs most commonly used to prevent and treat epilepsy.

Hydrocephalus

Hydrocephalus occurs when cerebrospinal fluid builds up in the brain cavity, which increases pressure and causes swelling of the brain. As many as 70% of patients exhibit ventricular enlargement 2 months after moderate to severe traumatic brain injury. Craniectomy severe traumatic brain injury advanced age occurs intracranial bleeding are potential risk factors. A plateau of cosmetic improvement or decreased function may indicate the presence of posttraumatic hydrocephalus. Clinically, a patient who develops post-traumatic hydrocephalus may present with urinary headaches incontinence moderate mental retardation papilledema motor weakness. Diagnostic imaging in conjunction with spinal closure is the most common diagnostic tool. Surgery to insert a shunt to drain excess cerebrospinal fluid into the abdomen 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
• Dizziness
• Ringing in the ear
• Hearing Loss

Visual Dysfunction

Visual dysfunction may manifest as blurred vision Sensitivity to light Difficulty reading Headaches with reduction in visual tasks or loss of visual field such as hemianopia and eye movement difficulties Deficit 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.

Neuro-sensory Deficit 

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 The most effective treatment is untreated neurosensory deficits that affect other functions such as motor control and a final level of functional recovery.

Spatial Neglect

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.

Movement Disorders

Movement disorders can be expressed as a hypokinetic or hyperkinetic phenomenon and can manifest as: tremor chorea dystonia athetosis ballism myoclonus parkinsonism tics. [8] Movement disorders may be the only symptom or coexist with other movement or motor neuropathies. They can also be partial effects of drugs for example drugs to treat cognitive impairment or stimulation. Some diseases like dystonia occur in the acute phase post traumatic brain injury but others like parkinsonism can develop decades after the trauma. Common movement disorders after traumatic brain injury are tremors dystonia parkinsonism myoclonus and these are more common in severe injuries. Brain areas commonly involved in movement disorders are: basal ganglia cerebellum thalamus subthalamus and white matter tracts. Treatments include dealing with the underlying cause for example hematoma or fluid in the head; through pharmaceutical and surgical interventions.

Dizziness / Balance Disorders

Confusion and balance disturbance is a common traumatic brain injury with 80% of people reporting dementia. The etiology may be complex including vestibular impairment sensory integration problems with vision or proprioceptive. Major pathologies include BPPV central vestibular or extrinsic problems such as damage to the vestibular nerve or injury to the semicircular nerve of the ear. Physical therapy depends on the cause of the disorder.

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

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 [9]) 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.

Cognitive Decline

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
• Reasoning
• Judgment
• Attention or concentration
• Executive functioning problems
• Problem-solving
• Multitasking
• Organisation
• Planning
• Decisionmaking
• Beginning or completing tasks

Brain Degeneration and Mental Illness

Usually from repeated or severe traumatic brain injury; People living with traumatic brain injury are at approximately 4 times the risk of developing dementia and early in life compared to the general population. Repetitive injuries have been associated with Chronic Traumatic Encephalopathy (CTE) or Dementia Pugilistica (Boxer’s Dementia) when a single brain injury has been shown to be associated with Alzheimer’s type symptoms. The severity of traumatic brain diseases after traumatic brain injury is also associated with genetics.

Altered Consciousness

Moderate to severe traumatic brain injury can cause changes in a person’s mental state in terms of perception or behavior. Conscious states include:

1. 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.
2. Vegetative state (VS): Associated with extensive damage to the brain. The person is unaware of their surroundings, but may open their eyes in response to sounds, reflections or movement. The person can remain in VS permanently, but some patients can transition to a minimally conscious state.
3. Minimal state of consciousness: A condition in which consciousness is severely altered but there are some signs of self-awareness or awareness of the environment. It is sometimes an intermittent state between coma or VS and some degree of regaining consciousness.
4. Brain Death: Announced when there is no measurable activity in the brain and brainstem. For someone who has been declared brain dead, removal of the breathing device will cause breathing to stop and eventually heart failure. Brain death is considered irreversible.

Communication Deficits

Potential communication problems 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
• Problems with turn taking or topic choice in conversation
• Problems with changes in pitch or emphasis to convey emotional behavior or subtle differences in meaning
• Nonverbal cues are difficult to understand
• Trouble reading cues from listeners
• Difficulty starting or stopping a conversation
• Muscles needed for dysarthria .