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PassPMR - 02 Acquired Brain Injury > 4- Medical Complications > Flashcards

4- Medical Complications Flashcards

1
Q

What type of neurogenic bladder do TBI patient develop? Urodynamic Result? Managment?🔑🔑

A

TYPE

  • Uninhibited detrusor contraction (UMN)

PRESENTATION

  1. Frequent urge incontinent
  2. Poor perception of bladder fullness
  3. Poor sphincter control
  4. Empties completely

URODYNAMIC STUDY

  1. Bladder volume is reduced
  2. Empties completely
  3. Small voids with normal residuals.
  4. Normal postvoiding intravesicular residual volumes

MANAGEMENT

  1. Time-void program (regular scheduled interval)
  2. Collecting device: Diaper for cognitive impairment
  3. Anticholinergic meds antimuscarinic effects on smooth muscle
    • Antimuscarinic effects on smooth muscle → decreases detrusor tone → increases bladder capacity
    • Oxybutynin (Ditropan): Extended-release: 5-10 mg/day PO; may be increased by 5 mg/day at weekly intervals; not to exceed 30 mg/day
    • Vesicare: 5 mg PO qDay, may increase to 10 mg/day if well tolerated
    • S/E: anticholenergic effects

Cuccurollo 4th Edition Chapter 2 TBI pg88

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2
Q

List 4 cognitive side effects of anticholinergic medications

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

Bowel dysfunction in TBI. 🔑🔑

A

Type

  1. Incontinence (Infection causing diarrhea, fecal impaction)
  2. Constipation (Impaired physical mobility, dehydration)

Management

  • Dietary: hydration and high fiber diet
  • Stool softeners
  • Stimulant suppositories
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4
Q

Two most common hormones affected in TBI. 🔑🔑 What life-threatening neuroendocrine abnormalities should be monitored post ABI? 🔑🔑

A

MOST COMMON

  1. Growth Hormone
  2. ADH

LIFE THREATENING

  1. ACTH deficiency
    • Low blood sugar (hypoglycemia)
    • Low sodium (hyponatremia)
    • Low blood pressure (hypotension)
  2. ADH abnormalities
    • DI can cause life-threatening hypernatremia
    • SIADH can cause life-threatening hyponatremia

ERABI Module 10

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5
Q

List the hormones released by the anterior (6) and posterior (2) pituitary glands 🔑🔑 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

ANTERIOR PITUITARY

  1. Prolactine
  2. FSH
  3. LH
  4. TSH & FT4
  5. ACTH → AM cortisol
  6. GH → Insulin growth factor (IGF)-I

POSTERIOR PITUITARY

  1. ADH
  2. Oxytocin

ERABI Module 10

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6
Q

With a TBI and shearing of the pituitary stalk, which part of the pituitary will be affected – anterior pituitary or posterior, and why?

A

Anterior pituitary will be affected, as blood supply travels through the stalk/infundibulum.

Posterior pituitary spared, because blood supply is through base of the skull.

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7
Q

List 5 risk factors for hypothalamic-pituitary axis dysfunction after an ABI?

A

Injury Severity

Location of injury (basal skull fractures, diffuse axonal injury)

Increased intracranial pressure

Glasgow Coma Scale score 3-12

Length of intensive care unit stay

Length of time post injury

ERABI Model 10

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8
Q

List 6 sign and symptoms of GH deficiency 🔑

A

COGNITIVE

  1. Sleep disturbance, insomnia
  2. Low self-esteem
  3. Depression
  4. Headaches
  5. Decreased cognitive function, concentration, and memory

PREFORMANCE

  1. Fatigue, low energy
  2. Reduced exercise tolerance
  3. Reduced lean body mass and muscle wasting
  4. Increased visceral adiposity
  5. Dyslipidemia

GROWTH

  1. Osteoporosis

ERABI Module 10 pg11

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9
Q

List 3 clinical features of Acromegaly. 🔑

A
  1. Frontal bossing
  2. Skeletal overgrowth deformities (large hands/feet, thick heel pad, frontal bossing, prognathism, macroglossia)
  3. Obstructive sleep apnea
  4. Hypertension
  5. Glucose intolerance / DM
  6. Peripheral nerve entrapment syndromes (CTS)
  7. Cardiomegaly
  8. Arthritis/joint pain
  9. Hyperhidrosis
  10. Soft tissue swelling and enlargement of extremities

https://emedicine.medscape.com/article/925446-clinical

Greenberg textbook pg 441

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10
Q

List 6 sign and symptoms of ACTH deficiency 🔑

A
  1. Low blood pressure
  2. Low serum sodium (hyponatremia)
  3. Hypoglycemia
  4. Fatigue
  5. Weakness
  6. Hair loss
  7. Nausea and/or vomiting
  8. Loss of appetite (anorexia)
  9. Low quality of life
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11
Q

What are risk factors for hypopituitarism in TBI?

A
  1. Moderate-severe TBI (with GCS 10 or less)
  2. Diffuse brain swelling
  3. Hypotensive/hypoxic episode

Ref: Brain Injury Medicine p680

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12
Q

List 2 types of Hyponatremia in TBI

A

1- Normal extracellular volume (isovolemia)

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

2- Reduced extracellular volume (hypovolemia) ← Common Exam Q

Cerebral salt wasting (CSW)

Cuccurollo 4th Edition Chapter 2 TBI pg90

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13
Q

Patient with TBI and hyponatremia 🔑🔑 EXAM
List 2 Differential diagnoses & mechanism of each.
List 1 Investigation to distinguish between your DDx (Mention the results)
List 1 Specific treatment for each differential diagnosis.?

A

CSW (HypoNa+, Hypovolemia)

  1. Salt wasting (inability to resorb Na).
  2. Secondary volume depletion (hypovolemia).
  3. Resultant release of ADH (appropriate).

SIADH (HypoNa, Isovolemia)

  1. Inappropriate secretion ADH (plasma iso or hypo-osmolality).
  2. Inability to excrete water (water resorbed through aquaporins)
  3. Resultant hyponatremia and concentrated urine

DI (HyperNa+, Isovolemia)

  1. Disruption of ADH secretion from posterior pituitary (Fracture near sella turcica, tearing pituitary stalk, etc).
  2. Inability to resorb water from kidneys

Cuccurollo 4th Edition Chapter 2 TBI pg90

ERABI Module 10 pg16

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14
Q

How to differentiate between DI and CSW (3 marks) 🔑🔑

A

DI

  1. High Serum Na+
  2. High Serum Osmolality
  3. Low Urine Osmolality

CSW

  1. Hypovolemia (Decreased blood volume)
  2. Signs of dehydration

Cuccurollo 4th Edition Chapter 2 TBI pg91

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15
Q

For patients with disorders of sodium, such as hyponatremia (low serum sodium) or hypernatremia (high serum sodium), patients should be assessed for (4 marks) 🔑

A
  1. Serum sodium
  2. Serum osmolality
  3. Urine sodium
  4. Urine osmolality
  5. Total body volume (hydration status)
  6. Urine output
  7. Serum ADH
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16
Q

List 6 causes of SAIDH and why its “Inappropriate” 🔑 List 4 drugs causes SAIDH 🔑🔑

A

ADH inappropriate

  • Because of excess of ADH leading to water retention resulting and plasma hypo-osmolality (i.e., euvolemic hyponatremia).

Drugs

  1. Carbamazepine (Tegretol)
  2. Amitriptyline
  3. Nicotine
  4. Morphine

Others

  1. CNS diseases
    • Thrombotic or hemorrhagic events
    • Meningitis, Encephalitis
    • Brain abscess
    • CNS neoplasm
    • Traumatic Brain Injury
  2. Head trauma
  3. Lung disease
    • Pneumonia, CF, TB
  4. Malignancy
    • Lung CA

Cuccurollo 4th edition Chapter 2 TBI pg90 & Flash Cards

17
Q

List 6 sign and symptoms SIADH 🔑🔑

A

💡 Edema (peripheral/soft tissue) almost always absent

  1. Low serum sodium (hyponatremia)
  2. Increased body weight
  3. Low appetite (anorexia)
  4. Nausea and vomiting
  5. Altered mental status, ranging from restlessness or irritability to confusion to coma
  6. Seizures

Cuccurollo 4th edition Chapter 2 TBI pg90

ERABI Module 10 pg17

18
Q

List 3 Treatments of SAIDH 🔑

A
  1. Fluid restriction to approximately 1.0 L/d
  2. 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).
  3. Demeclocycline, which normalizes serum Na+ by inhibiting ADH action in the kidney

Cuccurollo 4th Edition Chapter 2 TBI pg91

Sodium may be corrected no more than 10 mEq/L over 24 hours

19
Q

List 4 sign and symptoms of DI. It has diabetes in it. 🔑🔑

A
  1. Large amounts of dilute urine (polyuria)
  2. Incredible thirst (polydipsia)
  3. Elevated serum sodium (hypernatremia).
  4. Dehydration
  5. Weakness
  6. Fever
  7. Psychic disturbances
20
Q

State 3 differential diagnoses for hyponatremia in a patient with TBI 🔑🔑

A
  1. Cerebral salt wasting (CSW): often seen in SAH.
  2. Syndrome of inappropriate anti-diuretic hormone secretion (SIADH).
  3. psychogenic polydipsia.

Ref: Cuccurullo pg 87-88; Brain injury medicine pg 662.

21
Q

Explain Autonomic Instability in TBI and management

A

AD in TBI

2 weeks of TBI, there is surge of circulating catecholamines: epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine are released from direct trauma.

Presentation & Management

  1. Hypertension & Tachycardia → Beta blockers (propranolol)
  2. Hyperthermia & Perspiration → NSAIDs, Acetaminophen, Cooling blankets
  3. Spasticity → Dantrolene Sodium
  4. Dopamine agonists: Amantadine, bromocriptine

Anterior hypothalamus—temperature sensitive

Posterior hypothalamus—heat dissipation center

Cuccurollo 4th Editio Chapter 2 TBI pg79

22
Q

Drug of choice for post TBI hypertension. 🔑

A

Propranolol

  1. Plasma catecholamine levels
  2. Heart rate
  3. Myocardial oxygen demand
  4. Improves pulmonary ventilation-perfusion inequality

Cuccurollo 4th Edition Chapter 2 TBI pg87

23
Q

What is Heterotopic ossification? commonest location? 🔑🔑

A

Formation of mature lamellar bone in extra skeletal soft tissue

Most frequently deposited around a joint.

  1. Hip (anteromedial aspects, most common)
  2. Knee
  3. Shoulder
  4. Elbow.

SCI: 1 to 3 months status post-injury is most common; peak at 2 months

TBI: Period of greater risk to develop HO is 3 to 4 months postinjury

Cuccurullo 4th Edition Chapter 2 TBI pg86 & Chapter 7 SCI pg594

24
Q

List 6 Risk factors for Heterotopic ossification 🔑🔑

A

HO in SCI patient

  1. Complete injury
  2. Young age
  3. Spasticity
  4. Trauma
  5. Pressure ulcers

Cuccurollo 4th Editoin Chapter 2 TBI pg86

Cuccurollo 4th Edition Chapter 7 SCI pg594

DeLisa 5th Edition Chapter 43 Burn pg1137

SCIRE

25
Q

Staging Heterotopic Ossification (HO) 🔑🔑 EXAM 2021

26
Q

Differentials of HO. 4 marks 🔑🔑

A
  1. Deep vein thrombosis (DVT)
  2. Tumor
  3. Septic joint
  4. Hematoma
  5. Cellulitis
  6. Fracture
  7. Compartment Syndrome
  8. Rheumatological (RA, gout).
  9. Impending pressure ulcer.

Cuccurollo 4th Edition Chapter 2 TBI pg86

Braddom, 1335.

27
Q

List 4 Complications of HO 🔑🔑

A
  1. SKIN: Pressure ulcer
  2. VESSELS: DVT, Lymphedema
  3. NERVES: Peripheral nerve injury (entrapment), Increased spasticity
  4. MUSCLE: Compartment syndrome
  5. JOINT: Ankyloses
  6. BONE: Fracture through nascent bone
  7. TENDON: Contracture, Impair function and mobility

Cuccurollo 4th Edition Chapter 2 TBI pg86

Cuccurollo 4th Edition Chapter 7 SCI pg595

ERABI Model 9 pg10-11

Varghese et al. Nonarticular complication of heterotopic ossification: a clinical review. Arch Phys Med Rehabil 1991 Nov;72(12)1009-13

28
Q

List 4 Investigations of HO 🔑🔑

A

Blood

  1. CBC with differential (r/o infection)
  2. ESR/CRP (Inflammation)
  3. CRP, and erythrocyte sedimentation rate (ESR)
  4. Alkaline phosphatase (Heterotopic Ossification).
  5. Creatine phosphokinase (CPK)

Imaging

  1. Plain film: 2-3 weeks to 3 months
  2. Ultrasound dopplers (DVT).
  3. Ultrasound MSK (Bursitis)
  4. Triple phase bone scan (Heterotopic Ossification).
  5. CT scan or MRI scan in indicated for other pathologies

Cuccurollo 4th Edition Chapter 7 SCI pg595

29
Q

Treatment for HO. 5 marks 🔑🔑 EXAM

A

CONSERVATIVE THERAPY

Passive & Active ROM

Modalities: Shockwave and Radiotherapy

NSAID with high CPK or CRP

  • Naproxen 375 mg TID for 4-6 weeks
  • Indomethacin 25 mg TID for 4-6 weeks

Etidronate

  • Prophylaxis: 20mg/kg per day for 2 weeks → 10mg/kg per day for 10 weeks
  • Normal CPK: 20 mg/kg/day 3 months → 10 mg/kg/day for 3 months
  • Elevated CPK: 20 mg/kg/day 6 months

SURGICAL THERAPY

  1. Surgery can be considered when HO severely limits ROM, impairing function

Cuccurollo 4th Edition Chpater 7 SCI pg595

Delisa 5th Edition Chapter 27 SCI Edition p695

30
Q

Write bisphosphonate prescription for treatment of HO. 🔑🔑 EXAM

A

PROPHYLAXIS

20mg/kg per day for 2 weeks → 10mg/kg per day for 10 weeks

TREATMENT

Etidronate for 6 months

  • Normal CPK: 20 mg/kg/day 3 months → 10 mg/kg/day for 3 months
  • Elevated CPK: 20 mg/kg/day 6 months + addition to NSAIDs (e.g., naproxen 375 mg TID or indomethacin 75 mg/day).

Monitor phosphate levels if using etidronate as it is a bisphosphonate.

Cuccurollo 4th Edition Chpater 7 SCI pg595

Delisa 5th Edition Chapter 27 SCI Edition p695

31
Q

When do you consider surgery for HO (heterotopic ossification)?🔑 Prophylactic dose of Bisphosphonates post op 🔑🔑 EXAM

A

INDICATION → HO Complications

  1. After bone is mature (12–18 months postinjury with normal bone scan)
  2. When joint mobility severely restricted
  3. When interferes with self-care
  4. When interferes with sitting in wheelchair
  5. Pressure ulcers.
  6. Nerve compression.
  7. Compression of vasculature.

POST OPERATIVE TREATMENT

  1. Bisphosphonates for 3 to 12 months
  2. NSAIDS for 6 weeks or more
  3. Radiation (optional)

Cuccurollo 4th Edition Chapter 2 TBI pg86

Cuccurollo 4th Edition Chapter 7 SCI pg595

Braddom p1335

PassPMR - 02 Acquired Brain Injury (6 decks)

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