11. Complications include the following: 1. Posttraumatic
seizures: Frequently occur after moderate or severe TBI 2.
Hydrocephalus 3. Deep vein thrombosis 4. Heterotopic ossification:
Incidence of 11-76%, with a 10-20% incidence of clinically
significant heterotopic ossification 5. Spasticity 6.
Gastrointestinal and genitourinary complications: Among the most
common sequelae in patients with TBI 7. Gait abnormalities 8.
Agitation: Common after TBI
12. Long-term physical, cognitive, and behavioral impairments
1. Insomnia 2. Cognitive decline 3. Posttraumatic headache:
Tension-type headaches are the most common form, but exacerbations
of migraine-like headaches are also frequent 4. Posttraumatic
depression: Depression after TBI is further associated with
cognitive decline,anxiety disorders, substance abuse, dysregulation
of emotional expression, and aggressive outbursts
13. seizure (97-2- 59) 2 Carbamazepine
14. Incidence Varies greatly according to the severity of the
injury, the time since the injury, and the presence of risk factors
(see below). 5% of hospitalized TBI patients (closed-head injury)
have late PTS. 45% of hospitalized TBI patients have 1 or more
seizures in the first week after the injury (early PTS) (Rosenthal
et al, 1990). 5066% of PTS occur within 1 year; 7580% occur within
2 years - Most PTS occur 13 months after injury. 50% patients with
PTS will have only 1 seizure, and 25% have no more than 3
episodes.
15. Therapeutic anticonvulsant medications are usually started
once late seizures occur. In the TBI population, carbamazepine
(partial seizures) and valproic acid (generalized seizures) are
often preferred to medications that are more sedating or associated
with cognitive impairment (such as phenobarbital and phenytoin).
Their superiority over phenytoin has been debated, but the
differences among these 3 agents are probably minimal;
carbamazepine may be as sedating as phenytoin (Brain Injury Special
Interest Group of the AAPM&R, 1998).
16. Important to remember that all anticonvulsants may cause
some degree of sedation and cognitive deficits (usually psychomotor
slowing). Phenobarbital is clearly associated with greater
cognitive impairment and should not be used as first choice of
anticonvulsant therapy in the TBI patient. Long-term use of
phenytoin has been associated with adverse cognitive effects.
Animal and clinical (extrapolated from strokes) studies suggest
that phenytoin may impede recovery from brain injury (Dikmen,
1991).
17. Second-generation anticonvulsants, such as gabapentin and
lamotrigine, may also be used for treatment of PTS as adjuvant
agents (not approved yet for monotherapy). These agents appear to
have fewer cognitive side effects but are still under investigation
in the TBI population.
18. Risk Factors Associated With Late Posttraumatic
Seizures
21. HETEROTOPIC OSSIFICATION (HO) HO is the formation of mature
lamellar bone in extra skeletal soft tissue. Common in TBI:
incidence of 1176%. Incidence of clinically significant cases is 10
20%.
22. Risk Factors Prolonged coma (> 2 weeks) Immobility Limb
spasticity increased muscle tone (in the involved extremity)
Associated long-bone fracture Pressure ulcers Edema Period of
greater risk to develop HO: 3 to 4 months postinjury
23. Signs/Symptoms Most common: pain and decreased ROM. Also:
local swelling, erythema, warmth in joint, muscle guarding,
low-grade fever. In addition to pain and decreased ROM,
complications of HO include bony ankylosis, peripheral nerve
compression, vascular compression, and lymphedema. Joints most
commonly involved: 1. Hips (most common) 2. Elbows/shoulders 3.
Knees
24. Diagnostic Tests Serum Alkaline Phosphatase (SAP) SAP
elevation may be the earliest and least expensive method of
detection of HO. It has poor specificity (may be elevated for
multiple reasons, such as fractures, hepatic dysfunction,
etc.)
25. Bone Scan Sensitive method for early detection of HO. HO
can be seen within the first 24 weeks after injury in Phase I
(blood-flow phase) and Phase II (blood-pool phase) of a triple
phase bone scan, and in Phase III (static phase/delayed images) in
48 weeks with normalization by 7 to 12 months. Plain X-Rays Require
3 weeks to 2 months postinjury to reveal HO. Useful to confirm
maturity of HO.
26. Fever (100.5F) and left knee pain developed in 22-y-old man
after closed cranial trauma, raising concern about osteomyelitis or
other local infection. Initial radiography findings were normal.
(A) 67Ga image shows intense increased uptake in anteromedial
aspect of distal left thigh. (B) From left to right, selected flow
study images, blood pool images, and delayed bone scan images
obtained shortly thereafter show increased flow, hyperemia, and
increased uptake, respectively, also in anteromedial aspect of
distal left knee. (C) Subsequently obtained radiograph shows HO at
this site. (D) Three-phase bone scan 18 mo after injury shows
significantly less abnormal activity on (from left to right) flow
study images, blood pool images, and delayed bone scan images.
(Reprinted with permission of (58).)
27. HO Prophylaxis ROM exercises Control of spasticity
Nonsteroidal anti-inflammatory drugs (NSAIDs) Radiation used
perioperatively to inhibit HO in total hip replacement patients;
concerns about decreased risk of neoplasia limit its use in younger
patient populations. Radiation in TBI patients for HO prophylaxis
would require essentially irradiation of the whole body (as HO can
develop practically at any joint), which is not practical.
28. Treatment Bisphosphonates and NSAIDs (particularly
indomethacin) have been used on patients to arrest early HO and to
prevent postop recurrence, but their efficacy has not been clearly
proven (TBI population). ROM exercises: used for prophylaxis and
treatment for developing HO to prevent ankylosis. Surgical
resection of HO indicated only if function is the goal (eg,
hygiene, ADLs, transfers). Surgical resection usually postponed 12
to 18 months to allow maturation of HO.