Traumatic Brain Injury: Complications

The following are the most important diseases or complications that may be contributed to by traumatic brain injury:

Respiratory system (J00-J99)

Blood, hematopoietic organs – immune system (D50-D90).

  • Blood coagulation disorders, unspecified

Endocrine, nutritional, and metabolic disorders (E00-E90).

  • Pituitary insufficiency – hypofunction of the pituitary gland (pituitary gland).
  • Inadequate ADH secretion (antidiuretic syndrome).

Factors influencing health status and leading to health care utilization (Z00-Z99).

  • Suicide (suicide) (1.9-fold risk).

Cardiovascular system (I00-I99)

  • Cardiovascular failure
  • Ischemic insult (stroke) (approximately 25-33% of patients).

Infectious and parasitic diseases (A00-B99).

  • Brain abscess – encapsulated collection of pus in the brain.
  • Infections, unspecified
  • Meningitis (meningitis)

Mouth, esophagus (esophagus), stomach, and intestines (K00-K67; K90-K93).

  • Gastric ulceration (stomach ulcers).

Psyche – nervous system (F00-F99; G00-G99)

  • Apallic syndrome (decerebration syndrome) – functional failure of the cerebrum.
  • Chronic traumatic encephalopathy (“brain dysfunction”) – due to repetitive mild TBI.
  • Epilepsy
  • Fatigue syndrome (possibly due to depression, anxiety, and sleep disturbances following an STH) – studies suggest that a shortened REM (rapid eye movement) portion of sleep and decreased melatonin production may also play a role
  • Memory disorders
  • Cranial nerve injuries
  • Cerebral edema – swelling of the brain resulting from an increase in cerebral volume and pressure.
  • Hydrocephalus (hydrocephalus; pathological enlargement of the liquid-filled fluid spaces (cerebral ventricles) of the brain).
  • Insomnia (sleep disorders; prevalence / incidence of disease: 29%).
  • Intracranial hemorrhage (brain hemorrhage)* Note:Intracranial hemorrhage may be delayed with anticoagulants; patients on DOAK therapy with blunt traumatic brain injury should have another cranial CT 12 hours after the accident.
    • Epidural hemorrhage
      • Arterial epidural hematoma – rupture of arterial vessels (A. meningea media) inside on the skull bone; typical is a symptomless or asymptomatic interval (which may be absent! ), latency: minutes to hours. Progressive hemorrhage with increasing pressure on the dura mater (hard meninges) and brain inward. Symptoms: Nausea (nausea)/vomiting, in 20-25% of cases initial unconsciousness followed by an awake interval of several hours and renewed unconsciousness; pupil dilation on the affected side; trepanation (“opening of the skull”) required!
      • Venous fracture hematoma – venous blood seeps from the fracture gap (fracture gap) into the epidural space; bleeding, if progressive, is slow and small.
    • Subdural hemorrhage (subdural hematoma; subdural hematoma, SDH) – hematoma (bruise) under (lat. sub) the hard meninges between the dura mater and arachnoid.
      • Acute subdural hematoma Symptoms: Disturbances of consciousness up to unconsciousness
      • Chronic subdural hematoma symptoms: uncharacteristic complaints, such as a feeling of pressure in the head, cephalgia (headache), vertigo (dizziness), restriction or loss of orientation and ability to concentrate
    • Subarachnoid hemorrhage – bleeding under the arachnoid (spider skin) Guiding symptom: thunderclap headache/destructive headache (sudden headache event) with nausea (nausea)/vomiting.
  • Concentration disorders
  • Locked-in syndrome – complete paralysis with the exception of the eye muscles with complete preservation of consciousness.
  • Alzheimer’s disease
  • Parkinson’s disease – patients with trauma aged ≥ 55 years have a 44% increased risk of developing Parkinson’s disease within the next 5 to 7 years
  • Paresis (paralysis), unspecified.
  • Postcommotion syndrome (PCS; synonym: chronic posttraumatic syndrome (CPS)) or postcontusion symptoms with headache, dizziness, difficulty concentrating, etc; may last weeks to years [also possible in patients with mild TBI).
  • Psychosis
  • “Second impact syndrome” (SIS) – Suffering a second trauma before the effects of the first have fully subsided; in this context, minor trauma can quickly lead to malignant cerebral edema (“brain swelling”); therefore, strict adherence to the guideline: no more same-day competition (“no return to play the same day”); for more information, see “Further therapy/rehabilitation”
  • Sleep-wake rhythm disorders (prevalence/disease frequency 50%).
  • Behavioral changes

* Under clopidogrel, clustered intracranial hemorrhage/bleeding within the skull – even in mild TBI.

Symptoms and abnormal clinical and laboratory findings not classified elsewhere (R00-R99).

  • Cephalgia (headache)-post-traumatic headache (PTH, “post-traumatic-headache”) (10-95%)
    • Risk factors that favor the development of PTH include.
      • Severity of the TBI
      • Younger age
      • Female sex
      • Abnormalities in the CT
      • Headache already in the emergency room
  • Olfactory disorders (dysosmia)

Injuries, poisonings, and other consequences of external causes (S00-T98).

  • Pneumencephalon – penetration of air into the skull.
  • Posttraumatic coma – triggered by brainstem dysfunction.

Prognostic factors

  • Advocate for a poor outcome (death or disability) with a GCS score of 3:
    • Increased intracranial pressure
    • Bilateral absence of pupillary recurrence

    One in seven patients has a good chance of surviving without major limitations.

Risk factors for the occurrence of intracranial injury sequelae.

According to a meta-analysis, the occurrence of intracranial injury sequelae depends significantly on various risk factors. For adults, the following positive likelihood ratios (+LR; indicates how many times more often a positive test result occurs in individuals with disease/risk factors compared with individuals without disease/risk factors.) were found regarding intracranial injury sequelae:

Likelihood Ratio (LR). Risk factors
+LR > 10 Impression fracture of the skull (injury in which the skull bone has been depressed), basilar skull fracture, radiologically proven skull fracture, or posttraumatic seizure
+LR 5-10 Focal neurologic deficit, persistent vomiting, declining Glasgow Come Scale (GCS), or previous neurosurgical intervention
+LR 2-5 Fall, coagulopathy, chronic alcohol use, age > 60 years, collision as pedestrian with motor vehicle, any seizure, unspecified vomiting, amnesia, GCS < 15 points

Note: Unconsciousness and headache as isolated criteria are not relevant risk factors. Further notes