Medical Complications in Traumatic Brain Injury

Introduction[edit | edit source]

Medical and neurological complications determine the final functional outcome, community reintegration as well as employment potential after a traumatic brain injury. Therefore, it is important to recognise the potential risks of those pathologies and to follow evidence based protocols to minimise the risk and extent of secondary complications. 

The long-term physical, cognitive, and behavioural complications are both related to the direct injury to the brain and also to the influence of central nervous system dysfunction and trauma on other organs and system. Several complications can occur immediately or soon after a traumatic brain injury, but others might not be recognised until the rehabilitation stage. Severe injuries increase the risk of a greater number and more-severe complications.

Presence of complications and injury related impairment impacts the quality of life of a person living with a traumatic brain injury. These problems can cause frustration, conflict and misunderstanding of people with a traumatic brain injury as well as family members or friends. [1] An individual’s risk of suicide as well as mood and anxiety disorders might be increased due to a combination of symptoms and neuropsychiatric factors which are often aggravated by the trauma.

Medical Complications[edit | edit source]

Medical complications include:

Infection[edit | edit source]

Traumatic brain injuries involving skull fractures or penetrating wounds can result in meninges damage. This can result in bacterial infection of the brain. An infection of the meninges (meningitis) could spread to the rest of the nervous system if not treated.

Sepsis, or multiple organ dysfunction syndrome are the leading causes of late morbidity and mortality in traumatic brain injury. The catecholamine surge that follows a systemic insult is directly involved in the regulation of cytokine expression in situations of acute stress producing a worsening clinical condition and, ultimately, a poor outcome. The trauma-induced catecholamine surge affects systemic organs and contributes to organ damage. [2]

Spasticity[edit | edit source]

Spacticity is one of the upper motor neuron features that develops rapidly, in some cases as early as one week post traumatic brain injury, and often results in orthopaedic sequelae. [3] Mild spasticity can have some benefits like maintaining muscle bulk or enhancing gait, but moderate to severe increased muscle tone and spasm can severely impact rehabilitation outcomes, functional recovery and ability to engage in activities of daily living. Moderate to severe spasticity requires structured management protocols.

Venous Thromboembolism[edit | edit source]

Venous thromboembolism (VTE) is a condition where a clot formed in the deep veins of a limb enters the circulation system and reaches the lungs causing pulmonary embolism which is a direct life-threatening condition. After traumatic brain injury the incidence of VTE is as high as 54% due to difficulties using anticoagulation in the acute post traumatic brain injury period. The VTE prophylaxis can be applied only after the risk of renewed intracranial haemorrhage decreases.

Paroxysmal Sympathetic Hyperactivity (PSH)[edit | edit source]

Sympathetic hyperactivity is “the storm after traumatic brain injury", observed for weeks or months and presenting with increased sympathetic activity: heart rate increase, blood pressure increase, respiratory rate increase, sweating, hyperthermia, motor posturing. [4] The PSH is related to poor outcome and results from disconnection syndrome which is the impairment of inhibitory control over excitatory autonomic centres.

Neuroendocrine Dysfunction / Post Traumatic Brain Injury Hypopituitarism[edit | edit source]

Clinically prevalent phenomenon related to damage of the pituitary gland, a small gland that sits at the base of the brain and regulates other endocrine glands, i.e. thyroid, adrenal glands, pineal gland. Damage to the pituitary gland is most prevalent in cases with skull fracture and affects its own function as well as affects other hormones production impacting homeostasis metabolism, mood, growth, sleep and other bodily functions. Hypopituitarism has been related to the presence of depression and fatigue. The resulting thyroid malfunction relates to neuropsychiatric issues, cardiac function decrease, anxiety, diabetes insipidus. 

Heterotopic Ossification[edit | edit source]

Incidence of 11-76%, with a 10-20% incidence of clinically significant heterotopic ossification (HO). It presents with abnormal formation of ectopic lamellar bone in soft tissue. The HO tends to form around the bigger joints such as the hip, knee and shoulder and causes a range of motion decrease with limited mobility, pain and decreased function. Timely use of prophylactic nonsteroidal anti-inflammatory drugs and diagnostic imaging modalities should be implemented early to prevent severe mobility impairment. Other approaches include use of bisphosphonates (limited evidence), radiation and physiotherapy allow mechanical improvement. Fully formed HO can be surgically excised when severe pain or lose of range of motion significantly impact mobility or personal care.

Bladder Bowel Dysfunction and Genitourinary Complications[edit | edit source]

Among the most common complications in patients with traumatic brain injury due to ineffective communication, cognitive deficits and behavioural difficulties. Urinary dysfunction relates to detrusor overactivity and often leads to longer stay at acute services and delayed rehabilitation. At discharge those patients demonstrate poorer functional recovery. Establishing the causes (e.g. urinary tract infection), use of appropriate medication and pelvic floor exercises improve the outcome. 

Neurogenic bowel conditions can be either incontinence or constipation. 68% of individuals admitted to rehabilitation might demonstrate faecal incontinence. Hydration, fibre intake, medication and toilet training can assist with these issues. Untreated bladder and bowel dysfunction impose a risk on tissue viability and should be addressed. 

Sexual impairment related to frontal lobe damage and limbic system malfunction might present as hypersexuality, decreased sexual drive, lack of satisfaction or ejaculation dysfunction. Social and intimacy difficulties aggravate these sexual malfunctions. Resultant inappropriate sexual behaviour creates potential risks of difficulties forming relationships, aggression and criminalisation.

Nutritional Deficits [edit | edit source]

Endocrine and inflammatory processes after traumatic brain injury lead to excessive energy expenditure and consequent malnutrition, hyperglycaemia, hypercatabolism of proteins, lack of wound healing, muscle wasting and urinary nitrogen excretion. Enteral feeding with heavy protein supply can improve outcomes. Optimal nutrition facilitates better sleep behaviour, physical fitness, emotional status and fatigue management.

Sleep Disturbances[edit | edit source]

An extremely common complication amongst people living with traumatic brain injury. Includes insomnia, hypersomnia, excessive daytime sleeping and impaired circadian sleep-wake patterns.[5] The impact depends on the injured area and can be treated with sleep hygiene training, daytime exercises, caffeine intake limitation, CBT and medication.

Post-traumatic Headache[edit | edit source]

Commonly present after traumatic brain injury. Tension-type headaches are the most common form, but exacerbations of migraine-like headaches are also frequent. Headaches are often a long-term problem.

Neurological Complications[edit | edit source]

Neurological complications include:

Post-traumatic Seizures[edit | edit source]

Post-traumatic seizures frequently occur after moderate or severe traumatic brain injury. They may occur only in the early stages, or years after the injury (post-traumatic epilepsy). The post injury classification is:  

  • Immediate seizures (occurring within 24 h after injury) 
  • Early seizures (occur less than 1 week after injury) 
  • Late seizures (occur 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.  

Post-traumatic seizure relates to poor functional outcome. Phenytoin and levetiracetam are the most commonly used drugs in prevention and treatment of seizures. 

Hydrocephalus[edit | edit source]

Cerebrospinal fluid may build up in the cerebral ventricles causing increased pressure and swelling in the brain. As many as 70% of patients demonstrate ventricular enlargement 2 months post moderate to severe traumatic brain injury. Craniectomy, severe traumatic brain injury, older age, longer come, intracranial bleeding are possible risk factors. A plateau in rehabilitation progress or a functional decline might suggest the presence of post-traumatic hydrocephalus (PTH). Clinically a patient developing PTH might demonstrate headache, nausea, urinary incontinence, cognitive decline, papilledema, motor impairment. Diagnostic imaging in conjunction with a lumbar puncture are the usual diagnostic tools. The surgical implantation of a shunt to drain excess cerebrospinal fluid into the abdominal cavity is a treatment option. 

Cranial Nerve Disorders[edit | edit source]

Traumatic brain injury at the base of the skull can cause damage to the nerves that emerge directly from the brain or brainstem. Cranial nerve damage may result in: 

  • Paralysis of facial muscles or losing sensation in the face
  • 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[edit | edit source]

Visual dysfunction may present as blurred vision, sensitivity to light, reading difficulty, headaches with visual tasks, reduction or loss of visual field like hemianopsia, and difficulties with eye movements, gaze stabilisation deficits. These vision problems impact on other areas of functioning such as communication, mobility and balance. They can also impact on safety, e.g. visual field defects.

Neurosensory Deficit [edit | edit source]

May include somatosensory loss, persistent ringing in the ears, difficulty recognising objects, blind spots or double vision, bitter taste, a bad smell or difficulty smelling, paraesthesia like skin tingling, itching, numbness or pain. The array of problems experienced requires careful assessment to inform the most effective treatment as untreated the neurosensory deficits impact on other functions like motor control and the final level of functional recovery.

Spatial Neglect[edit | edit source]

Spatial neglect is a complex problem involving perception, movement and memory presenting as impaired attention to the side contralateral to the lesion. Presence of unilateral neglect severely impairs recovery. Therapeutic approaches should include teaching motor, sensory and compensatory strategies , however there is no clear evidence of clinical effectiveness or superiority of any particular approach.

Movement Disorders[edit | edit source]

Movement disorders can be demonstrated as hypokinetic or hyperkinetic phenomenon and might present as: tremor, chorea, dystonia, athetosis, ballism, myoclonus, parkinsonism, tics. [5] The movement disorder might be the only symptom or coexist with other movement or motor disorders. They can also be a side effect from medication, for example medications used to treat impaired cognition or arousal. Some pathologies like dystonia occur in acute phase post traumatic brain injury, but some like parkinsonism can occur decades after the trauma. The most common movement disorders after traumatic brain injury are tremors, dystonia, parkinsonism, myoclonus and these are more prevalent with severe injuries. The areas of the brain often involved in movement disorders are: basal ganglia, cerebellum, thalamus, subthalamus and white matter tracts. Treatments include addressing the cause, for example haematoma or hydrocephalus; through pharmacological and surgical interventions.

Dizziness / Balance Disorders[edit | edit source]

Dizziness and balance disorders are a common traumatic brain injury complication with dizziness being reported by 80% of people. The aetiology might be complex including vestibular impairment, sensory integration problems, visual or proprioceptive. Main pathologies include BPPV, central vestibular or peripheral problems, like vestibular nerve damage or injury to the semicircular canals of the ear. Physiotherapeutic treatment depends on the pathology aetiology. 

Sleep / Wake Disorders[edit | edit source]

Post traumatic brain injury the restorative function of sleep is diminished, and sleep pathology is very common. Contributing factors include biochemical and structural changes to the brain especially reticular system, thalamus and hypothalamus, medicinal such as unmanaged pain, behavioural with napping during the day and caffeine intake, and can be environmental. For example where there is no clear day/night distinction in the hospital ward. Treatment approaches include sleep hygiene training, pharmacological agents such as melatonin, benzodiazepines or zolpidem, exercises and light therapy. 

Fatigue[edit | edit source]

Fatigue in people with traumatic brain injury have impacts that are central, for example causing difficulty with cognitive tasks (linked to caudate activation in the Basal Ganglia[6]) and peripheral resulting in musculoskeletal tiredness. The presence of fatigue can have negative impacts on the participation in rehabilitation. Treatment includes environmental adjustments and sometimes medication such as modafinil.

Behavioural & Emotional[edit | edit source]

Behavioural and emotional changes including agitation, difficulty with self-control, lack of awareness of abilities, risky behaviour, verbal or physical outbursts, alcohol misuse, binge drinking, anxiety and depression, mood swings, irritability, anger, lack of empathy for others. All these issues can significantly impact a rehabilitation outcome and community reintegration.  These behavioural changes can have negative impacts on relationships, employment and criminal activity. The neuropsychologist and neuropsychiatrist are an integral part of the MDT working with people after brain injury and an integrated behaviour management programme needs to be followed by all the professionals and relatives involved. Post-traumatic depression is further associated with cognitive decline, anxiety disorders, substance abuse, dysregulation of emotional expression, and aggressive outbursts.

Cognitive Decline[edit | edit source]

Following areas can be affected and impact on information processing, communication, movement 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

Degenerative Brain Diseases and Dementia[edit | edit source]

Often resulting from repeated or severe traumatic brain injuries; People living with traumatic brain injury are at approximately 4 times greater risk of developing dementia and earlier in life compared to the general population. Repetitive injuries have been related to Chronic Traumatic Encephalopathy (CTE) or Dementia Pugilistica (Boxer’s Dementia) whilst a single brain injury has been related to Alzheimer’s type symptoms. The exacerbation of degenerative brain diseases following traumatic brain injury is also related to genetic background. 

Altered Consciousness[edit | edit source]

Moderate to severe traumatic brain injury, can result in changes to a person’s state of consciousness, awareness or responsiveness. Different states of consciousness include:

  1. Coma: A person in a coma is unconscious, unaware of self and environment and unable to respond to any stimulus. This results from widespread damage to all parts of the brain. The person with traumatic brain injury may emerge from a coma or enter a vegetative state at various times after the trauma.
  2. Vegetative State (VS): Related to widespread damage to the brain. The person is unaware of surroundings, but might open eyes, make sounds, respond to reflexes or move. The person can remain in VS permanently, but some patients can make a transition to a minimally conscious state.
  3. Minimally Conscious State: A condition of severely altered consciousness but with some signs of self-awareness or awareness of an environment. It is sometimes an intermittent state between coma or VS and some degree of consciousness recovery.
  4. Brain Death: Is declared when there is no measurable activity in the brain and the brainstem. In a person who has been declared brain dead, removal of breathing devices will result in cessation of breathing and eventual heart failure. Brain death is considered irreversible.

Communication Deficits[edit | edit source]

Potential issues with communication can include:

  • Difficulty understanding speech or writing
  • Difficulty speaking or writing
  • Inability to organize thoughts and ideas
  • Trouble following and participating in conversations
  • Trouble with turn taking or topic selection in conversations
  • Problems with changes in tone, pitch or emphasis to express emotions, attitudes or subtle differences in meaning
  • Difficulty understanding nonverbal signals
  • Trouble reading cues from listeners
  • Trouble starting or stopping conversations
  • Inability to use the muscles needed to form words (dysarthria)

References[edit | edit source]

  1. 26.05.2019
  2. Kinoshita K. Traumatic brain injury: pathophysiology for neurocritical care. Journal of Intensive Care. 2016. 4:29-39. DOI 10.1186/s40560-016-0138-3
  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.
  4. Meyfroidt G, Baguley DJ, Menon DK. Paroxysmal sympathetic hyperactivity: the storm after acute brain injury. The Lancet Neurology. 2017. 16(9):721-729.
  5. 5.0 5.1 Eapen BC, Cifu DX. Editor. Rehabilitation After Traumatic Brain Injury. Elsevier2018
  6. 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