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PMR 03 - TBI > Day 3 - Neurological Complications > Flashcards

Day 3 - Neurological Complications Flashcards

1
Q

Posttraumatic Seizure (PTS) vs Posttraumatic Epilepsy (PTE)

A

Epilepsy: Recurrent (at least two)seizures unprovoked by any immediate identified cause that are 24 hours apart

PTS: Refers to a single recurrent seizure after TBI

PTE: Recurrent late seizure episodes not attributable to any other etiology than TBI

Majority of PTS are simple partial

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2
Q

Posttraumatic Seizures are also classified by onset 🔑🔑

A

Posttraumatic Epilepsy (PTE) = Posttraumatic Amnesia (PTA)

  1. Immediate PTS: Occurs within the first 24 hours postinjury
  2. Early PTS: Occurs within the first week (24 hours to 7 days)
  3. Late PTS: Occurs after the first week
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3
Q

Risk Factors Associated With Late Posttraumatic Seizures 🔑🔑

A
  1. Age
  2. Prolonged coma or PTA (>24 hours): 35%
  3. Depressed skull fracture: 3% to 70%
  4. Penetrating head injury: 33% to 50%
  5. Presence of foreign bodies
  6. Intracranial hematoma: 25% to 30%
  7. Early PTS (>24 hours to 7 days): 25%
  8. Focal signs such as aphasia and hemiplegia
  9. Alcohol abuse
  10. Use of TCAs
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4
Q

List 3 Major Components to make the diagnosis of Posttraumatic Epilepsy

A
  1. Clinical exam/findings
  2. EEG (standard, sleep-deprived, 24 hour)
  3. Prolactin level: ↑ prolactin level confirms true seizure activity, but normal level does not ruleout seizure activity
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5
Q

Posttraumatic Epilepsy (PTE) Prophylaxis 🔑🔑

A

Phenytoin, valproic acid or levetiracetam (Keppra) for 1 week

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6
Q

Posttraumatic Seizure (PTS) Treatment and when to stop 🔑🔑

A

Important to remember that all anticonvulsants may cause some degree of sedation and cognitivedeficits (usually psychomotor slowing).

Carbamazepine, valproic acid and levetiracetam (Keppra)

Consider withdrawal of antiepileptic drugs after a 2-year, seizure-free interval.

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7
Q

Complications of Posttraumatic Seizure (PTS)

A

Patient himself

  1. Status epilepticus
  2. Death
  3. Accidental injuries

Rehab and function

  1. Deterioration in overall functional status
  2. Negative impact on neurological recovery
  3. Loss of driving privileges

ERABI Model 7

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8
Q

List 4 cause for seizure in TBI patient. 🔑🔑

A

Structural

  • Hydrocephalus
  • Mass lesion (Hge, Abcess)

Metabolic

  • Electrolyte (Na, Ca, Mg)
  • Hypoglycemia
  • Uremia
  • Hepatic Encephalopathy

Infection

  • Sepsis
  • Encephalitis
  • Menengitis

Substance

  • Alcohol
  • Caffeine

Medications

  • TCA
  • Narcotics
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9
Q

Why TBI patient develop Ventriculomegaly?

A

Ventriculomegaly is usually due to cerebral atrophy and focal infarction of brain tissue (exvacuo changes).

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10
Q

List 3 classical manifestations of hydrocephalus in TBI patient and how to manage?

A

Classic triad of incontinence, ataxia/gait disturbance, and dementia.

Others: vomiting, mental status changes (confusion, drowsiness).

Managment: LP, shunt placement

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11
Q

List 5 most common affected cranial nerves in TBI and how do they present. 🔑

A

1. Olfactory nerve (CN I)

Anosmia, apparent loss of taste and CSF rhinorrhea

Result in decrease in appetite, weight loss

2. Facial nerve (CN VII)

Tactile sensation to the parts of the external ear

Taste sensation to the anterior two-thirds of the tongue

Muscles of facial expression

Salivary and lacrimal glands

3. Vestibulocochlear nerve (CN VIII)

Loss of hearing

Postural vertigo and nystagmus

4. Optic nerve (CN II)

Complete blindness

Blurring of vision

Homonymous hemianopsia.

5. Oculomotor nerves (CN IV > CN III > CN VI)

Diplopia

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12
Q

Time frame of hormonal profile for TBI patient? what do you order? 🔑🔑

A

Recommend that all patients undergo endocrine function evaluation at 3 months and at 1-year post injury regardless of injury severity.

  1. AM cortisol → Addison Disease or Diabetes insipidus
  2. Urinary free cortisol
  3. Insulin growth factor (IGF)-I → Growth hormone deficiency
  4. Follicle-stimulatinghormone (FSH)
  5. luteinizing hormone (LH)
  6. Testosterone → Hypogonadism
  7. Estradiol
  8. Prolactin
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13
Q

List 6 causes of hypothalamic-pituitary axis disruption

A

Direct

  1. Acceleration-deceleration
  2. Basal Skull Fracture

Indirect

  1. Brain edema
  2. Hypoxia
  3. Raised ICP and hydrocephalus
  4. Reduced cerebral perfusion from shock
  5. Inflammation

ERABI

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14
Q

List 6 sign and symptoms of Hypopituitarism

A
  • Fatigue
  • Decreased cognitive function, concentration, and memory
  • Mood disturbance, depression, and irritability
  • Weight gain
  • Decreased muscle mass and increased fat mass
  • Sleep disturbance
  • Amenorrhea, decreased libido, and/or erectile dysfunction
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15
Q

List 6 sign and symptoms of ACTH deficiency

A

Salt (BP & Na)

  1. Low blood pressure
  2. Low serum sodium (hyponatremia)

Sugar (Glu)

  1. Hypoglycemia
  2. Fatigue

Sex (Hair & Strength)

  1. Weakness
  2. Hair loss
  3. Nausea and/or vomiting

Stress (QOL)

  1. Loss of appetite (anorexia)
  2. Low quality of life
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16
Q

Life threatening complications. What to monitor? 🔑🔑

A
  1. ACTH deficiency can cause life-threateningly low levels of cortisol and can result in low blood sugar (hypoglycemia), low sodium (hyponatremia), and low blood pressure (hypotension).
  2. ADH abnormalities can cause DI and SIADH which result in life-threatening increases in serum sodium, while SIADH can cause life-threatening reductions in serum sodium.
17
Q

List 6 causes of SAIDH and why its “Inappropriate” 🔑

A

ADH excess is considered to be inappropriate because of excess of ADH in normal or increased plasma volume. Leading to Water retention resulting and plasma hypo-osmolality (i.e., euvolemic hyponatremia).

  1. CNS diseases
    • Thrombotic or hemorrhagic events
    • Meningitis, Encephalitis
    • Brain abscess
    • CNS neoplasm
  2. Head trauma
  3. Lung disease
    • Pneumonia
  4. Malignancy
    • Lung CA
  5. Drugs
    • Carbamazepine
    • Amitriptyline
18
Q

List 6 sign and symptoms SIADH 🔑

A
  1. Low serum sodium (hyponatremia)
  2. Peripheral edema
  3. Increased body weight
  4. Low appetite (anorexia)
  5. Cerebral edema
  6. Nausea and vomiting
  7. Altered mental status
  8. Seizures
19
Q

Treatment of SAIDH 🔑

A
  1. Fluid restriction to approximately 1.0 L/d
  2. Loop diuretic Furosemide (Lasix)
  3. Hypertonic saline (e.g., 3% NaCl solution)—200 to 300 mL should be infused IV over 3 to 4hr (Fast correction >Pontine myelinolysis, or CHF). Sodium may be corrected no more than 10 mEq/L over 24 hours
20
Q

How to differentiate between CSW and SIADH 🔑

A
  1. CSW, hyponatremia is not dilutional (as in SIADH)
  2. CSW patients are volume depleted.
  3. Signs of dehydration are present
21
Q

Treatment of CSW

A
  1. Hydration/fluid replacement
  2. Electrolyte (Na+) correction
22
Q

One Key difference between DI compared to CSW and SIADH

A

Hypernatremia

23
Q

List 4 sign and symptoms of DI

A
  1. Large amounts of dilute urine (polyuria)
  2. Diluted urine
  3. Incredible thirst (polydipsia)
  4. Elevated serum sodium (hypernatremia).
  5. Dehydration
  6. Weakness
  7. Fever
  8. Psychic disturbances
24
Q

Treatment of DI

A

DDAVP (desmopressin acetate)—analog of ADH

25
Q
A
26
Q

What type of neurogenic bladder do TBI patient develop? Managment?

A

Neurogenic bladder with uninhibited detrusor reflex (contraction):

  • Frequently incontinent
  • Bladder volume is reduced
  • Empties completely with normal post voiding intravesicular residual volumes

Managment

  • Time-void program (regular scheduled interval)
  • Anticholinergic meds (decreases detrusor tone → increases bladder capacity)
27
Q

Cognitive side effects of Anticholinergic medications

A
  1. Sedation - Drowsiness
  2. Dizzyness
  3. Confusion
  4. Hallucination
  5. Impaired concentration
  6. Impaired memory
28
Q

Explain Autonomic Instability in TBI and management

A

First 2 weeks of injury = surge of circulating catecholamines Epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine are released from direct trauma.

  1. Hypertension & Tachycardia → Beta blockers
  2. Hyperthermia & Perspiration → NSAIDs, Acetaminophen, Cooling blankets
  3. Spasticity → Dantrolene Sodium

PMR 03 - TBI (8 decks)

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