Comorbidities and Complications of TBI. Rocco A Chiappini, MD

Transcription

1 Comorbidities and Complications of TBI Rocco A Chiappini, MD

2 TBI: A Disease Process, Not an Event WHO definition of a chronic disease Permanent Caused by non-reversible pathological alterations Requires special training of patient May require a long period of observation, supervision or care

3 Masel and DeWitt, J Neurotrauma 2010 TBI increases long term mortality and decreases life expectancy. It is associated with increased incidence of seizures, sleep disorders, neurodegenerative disease, neuroendocrine dysregulation and psychiatric diseases as well as nonneurologic disorders such as sexual dysfunction, bladder and bowel

4 Masel and Dewitt J Neurotrauma 2010 incontinence and systemic metabolic dysregulation that may arise and/or persist for months or years after injury.

5 TBI Complications and Comorbidities Seizures Sleep disturbance Fatigue Infections Craniectomy Hydrocephalus Shunt issues

6 TBI Complications and Comorbidities Subdural/Epidural Hematoma Neuro-endocrine dysfunction Spasticity Post-traumatic headache

7 Seizures TBI is the leading cause of epilepsy in young adults Early seizures- within the first week Late seizures- after the first week Incidence of late seizures Nonpenetrating severe TBI 17% Penetrating TBI 35-65%

8 Seizures- risk factors Depressed skull fracture Bone/metal fragments Focal contusions Intracranial hemorrhage

9 Gunshot wound

10 Types of Seizures Partial 25% Generalized 25% Partial with secondary generalization 50%

11 Frontal Lobe Epilepsy Complex, semipurposeful motor automatisms

12 Temporal Lobe Epilepsy May have emotional symptoms like panic followed by post-ictal confusion or amnesia

13 Seizures Current Recommendations Prophylaxis for the first week Discontinue prophylaxis and monitor Treat late seizures with carbamazepine, valproate, lamotrigine or levetiracetam Avoid phenytoin

14 Sleep Disorders Guilleminault studied 184 TBI survivors Restless sleep 49% Regular loud snoring 36% Leg and body jerking during sleep 18%

15 Sleep Disorders Ouellet studied 452 TBI survivors (avg time since injury 8 years) 50% had symptoms of insomnia 30% met criteria for insomnia (general public 10%)

16 Sleep disorders TBI population Decreased REM Decreased total sleep time More frequent awakenings Decreased deep sleep stages

17 Sleep Disorders Causes Damage to brain centers involved in sleep (hypothalamus, midbrain, ascending reticular activating system) Disruption of circadian pacemaker in the hypothalamus with decrease in level of melatonin production

18 Pain Depression Anxiety Medications Environment Sleep Disorders Causes

19 Sleep Disorders Treatment Treat depression, anxiety, pain Treat sleep apnea if present Improve sleep hygiene Melatonin Hypnotics, TCAs, antiepileptics may be helpful although no studies have shown best pharmacotherapy for insomnia in TBI

20 Fatigue The awareness of a decreased capacity for physical and/or mental activity due to an imbalance in the availability, utilization and/or restoration of resources needed to perform activity.

21 Fatigue Physiologic- arises from depletion of energy, hormones, neurotransmitters, or neural connections Psychologic- weariness related to reduced motivation, prolonged mental activity or boredom

22 Fatigue Kreutzer found 46% of 722 outpatients with TBI self reported fatigue

23 Fatigue May result from diffuse neuronal injury, particularly from damage to brain centers that control arousal, attention and response speed including the ARAS, limbic system, anterior cingulate, basal ganglia Alteration in chemistry. Histamine and growth factor.

24 Fatigue

25 Exercise Sleep assessment Hormonal screening Light therapy Fatigue Treatments Assessment of meds. D/C meds that increase fatigue Try antidepressants with activating effect Modafinil

26 Infections Meningitis Headache, fever, stiff neck, confusion

27 Infections Subdural empyema Usually due to septic skull fracture Acute presentation with fever, headache, obtundation

28 Infections Brain abscess 3 times more likely with gunshot wound Usually 2-3 weeks post injury Headache, vomiting, change in mental status 50%, seizure 33%

29 Craniectomy Syndrome of the trephined Deficits that may improve with cranioplasty Headaches, apathy, hemiparesis, tremor, gait, cognitive dysfunction

30 Trephination

31 Hydrocephalus Occurs in about 40% of patients with severe TBI Usually begins to appear within the first 2 weeks post injury

32 Hydrocephalus Communicating Different portions of the ventricular system are interconnected and fluid may exit the ventricular system freely to the cisterns and subarachnoid space

33 Hydrocephalus Non-communicating (obstructive) CSF flow is obstructed either between the ventricles or in exiting the ventricular system Due to cerebral edema, blood or infection which interferes with CSF flow May present with nausea, vomiting and lethargy

34 Shunting Study of 356 adults with VP shunts over 18 years. Incidence of revision 30%. Shunt failure Shunt infection Overdrainage

35 VP Shunt

36 Shunt failure Proximal occlusion of the ventricular catheter is the most common source of blockage (30%) Disconnection of shunt components account for 15% Distal shunt obstruction due to encystment and loculation of peritoneal contents around distal tip

37 Shunt infection 70% present within the first 2 months after shunt placement Low grade fever, malaise, irritability, nausea, erythema over shunt site

38 Overdrainage Not seen as much with modern shunt components (programmable valves) Orthostatic headache, dizziness, nausea, lethargy, diplopia Can lead to chronic subdural hematoma

39 Overdrainage

40 Subdural hematoma Change in mental status, signs of increased intracranial pressure Especially consider in older patients Treatment is neurosurgical; burr hole or craniotomy

41 Epidural hematoma Due to injury of the middle meningeal artery

42 Spasticity Components of UMNS Spasticity Mass synergy patterns Weakness Loss of finger dexterity

43 Spasticity Rule out exacerbating factors Non-pharmacological treatments Oral medications Intrathecal baclofen Focal treatments Surgery

44 Neuroendocrine Dysfunction More common than once thought Autopsy study of 100 patients with TBI found 62% had injury to pituitary Studies of hormone levels in patients with severe TBI found 36-69% had abnormal levels of at least 1 hormone

45 Pituitary Gland

46 Neuroendocrine Dysfunction All of the following have been reported abnormal in TBI survivors Antidiuretic hormone Cortisol Growth hormone Thyroxine FSH/LH Prolactin Glucagon Somatostatin

47 Normal Pressure Hydrocephalus Classic triad- incontinence, gait disorder and dementia Classic gait is short, wide based, magnetic steps Some believe this is the most common cause of post trauma HA IGF1 Urine assessment if polyuria Patients with moderate to severe TBI should undergo hormone evaluation at 3 months and 12 months post ICU discharge

48 Neuroendocrine Dysfunction Recommendations of Global Experts Consensus Panel 2005 Patients with moderate to severe TBI should undergo hormonal evaluation at 3 months and 12 months post ICU discharge

49 Neuroendocrine Dysfunction Hormone evaluation should include 9 AM cortisol level ft3, ft4 TSH FSH LH Testosterone in males E2 in females Prolactin IGF1

50 SIADH Inappropriate ADH release will produce hyponatremia by interfering with urinary dilution and decreasing excretion of ingested water Na < 135 Nausea, fatigue, muscle cramps, change in mental status, seizure, coma

51 Post Traumatic Headache Most common complaint after mtbi Consider causes such as hematomas, hydrocephalus, VP shunt malfunction Types Musculoskeletal Cervicogenic Neuralgic Post traumatic migraine Post traumatic sinus headache

52 Musculoskeletal Headache Referred pain from muscles such as trapezius and SCM Pattern often refers pain to retro or peri orbital area Treatment with trigger point management, acupuncture, postural correction, meds

53 Musculoskeletal HA

54 Cervicogenic Headache Pain referred from zygapophyseal joints of c-spine especially C2 and C3

55 Neuralgic Headache Most common is greater occipital nerve Splenius muscle spasm or overactivity exacerbates Ipsilateral frontotemporal scalp Treatment with trigger point management, gabapentin, TCAs, NSAIDs, blocks, surgical decompression

56 Occipital Neuralgia

57 Post Traumatic Migraine Described as throbbing, unilateral, worse with cough or bending over. May have visual issues, nausea, vomiting Treatment like migraine in general population. Prophylactic meds (NSAIDs, beta blockers, calcium channel blockers, TCAs, depakote) and abortive meds (triptans, ergot, dihydroergotamine). Possible role for botox

58 Post Traumatic Sinus HA Patient with history of facial bone fractures HA pattern may be based on drainage angles Frontal and ethmoid worse with supine Maxillary and sphenoid better supine

59 Sinuses