TBI: Medical and Neurologic complications after TBI

Question 1

What is heterotopic ossification (HO)?

Answer 1

Formation of mature lamellar bone in extra skeletal soft tissue

Heterotopic ossification can occur in various conditions and is characterized by abnormal bone growth outside of the skeleton.

Question 2

What are the risk factors (6) for developing heterotopic ossification?

Answer 2

• Coma >2 Weeks
• Immobility
• Spasticity
• Long bone fracture
• Ulcers
• Edema

HO typically develops 3-4 months post-injury.

Question 3

2 most common signs of HO?

Answer 3

Pain and decreased range of motion (ROM)

Question 4

What is the primary location for heterotopic ossification after TBI?

Answer 4

HIPS

Question 5

What laboratory findings may be elevated early in cases of heterotopic ossification?

Answer 5

Serum alkaline phosphatase

Elevated levels can indicate bone turnover and should be monitored in patients at risk for HO.

Question 6

When can heterotopic ossification be detected by bone scan?

Answer 6

Weeks 2-4 in phase 1 and phase 2, and weeks 4-8 in phase 3

Bone scans are useful for early detection of HO before it becomes visible on X-rays.

Question 7

How long does it take for X-rays to reveal heterotopic ossification after an injury?

Answer 7

3 weeks to 2 months post-injury

X-rays will show maturity of HO after this period.

Question 8

What are 3 prophylactic measures to prevent heterotopic ossification?

Answer 8

• Range of motion (ROM) exercises
• Control of spasticity
• NSAIDs

Question 9

What treatment options are available for heterotopic ossification?

Answer 9

• Bisphosphonates
• NSAIDs (e.g., indomethacin)
• ROM exercises to prevent ankylosis
• Surgical resection to restore function (usually wait 12-18 months)

Treatment aims to manage symptoms and restore mobility while allowing HO to mature.

Question 10

True or False: Radiation can be used to inhibit heterotopic ossification in traumatic brain injury (TBI) patients.

Answer 10

False

Radiation is effective in total hip replacement patients but is contraindicated in TBI patients.

Question 11

What medicaiton is used for post TBI HTN?

Answer 11

propranolol

due to sympathetic overdrive, transitory and will resovle

–– Plasma catecholamine levels
–– Cardiac index
–– Myocardial oxygen demand
–– Heart rate
–– Improves pulmonary ventilation-perfusion inequality

Question 12

What is the the gold standard for diagnosis of clinically suspected DVT

Answer 12

contrast venography

Question 13

which ranchos los amgios level is associated with poor ability to wearn patient off alt feeding?

Answer 13

5

Question 14

How does spasticity in acute TBI affect total body energy use?

Answer 14

Increased muscle tone causes hypermetabolism, raising energy use from 100% to 140%.

Question 15

What is the recommended duration for G and J tubes to decrease complications?

Answer 15

At least 30 days.

Question 16

What should be done if a patient with enteral feeding has GERD and recurrent aspiration?

Answer 16

Consider distal tube placement.

Question 17

How can esophagitis be reduced in patients with enteral feeding?

Answer 17

Head elevation and antacids can help reduce esophagitis.

Question 18

What is the most common cause of feeding intolerance in enteral feeding? how to treat?

Answer 18

High gastric residue. Tx with NG delivered erythromycin

Question 19

What GI medication should not be used in TBI due to sedation and extrapyramidal side effects?

Answer 19

Metoclopramide.

Question 20

What are the risks associated with parental feeding?

Answer 20

Line complications (infection, clots, edema), electrolyte, and metabolic abnormalities.

Question 21

What is thge most common hormone in hypothalamic pituitary dysfunction associated with TBI and its prevalence in TBI?

Answer 21

Growth factor
50%

Question 22

What is the evaluation timeline for endocrine function tests after TBI?

Answer 22

3 months and 1 year.

Question 23

What causes SIADH?

Answer 23

inc ADH secretion > water retention -> NA excretion in urine maintained by hypervolemia, suppression of RAAS and inc plasma concentration of ANP(atrial natriuretic peptide)

Question 24

What symptoms are associated with mild hyponatremia?

Answer 24

Anorexia and nausea/vomiting.

Question 25

What are severe symptoms of hyponatremia?

Answer 25

Increased body weight and symptoms of cerebral edema (restlessness, irritability, confusion, convulsions, coma).

Question 26

What is the treatment for severe hyponatremia?

Answer 26

• Fluid restriction to 1L daily,
• monitor weight and serum sodium,
• if severe, 300ml 3% NaCl IV over 3-4 hours.

Question 27

What is the maximum rate of sodium correction to avoid pontine myelinolysis?

Answer 27

Limit to 10 mEq/L over 24 hours.

Question 28

What is the treatment for chronic SIADH?

Answer 28

Demeclocycline, which inhibits ADH action in the kidney.

Question 29

What is diabetes insipidus (DI)?

Answer 29

Deficiency of ADH (vasopressin).

Question 30

What are the symptoms of diabetes insipidus?

Answer 30

Polyuria, thirst, polydipsia, weakness, fever, psychic symptoms, and hypernatremia due to volume depletion.

Question 31

What is the usual prognosis for diabetes insipidus after TBI?

Answer 31

Usually spontaneous resolution in 6 months.

neural pathways heal over time

Question 32

What medication is an analog of ADH used in diabetes insipidus treatment?

Answer 32

DDAVP (desmopressin).

Question 33

What medication potentiates the effects of ADH on renal tubules and can be used in DI?

Answer 33

Chlorpropamide.