Chapter 22: Neurologic Impairment Flashcards

1
Q

(TRUE/FALSE) Nutrition support is understood to be a therapy to attenuate the metabolic response to stress, prevent metabolic oxidative stress, and modulate the immune response.

A

TRUE.

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2
Q

**What are the nutrition requirements for TBI?

A
  • ENERGY: IC, if unable use 140% x the Harris-Benedict equation.
  • PROTEIN: 1.3 to 1.5 g/kg/d
  • Early nutrition is key, start EN ASAP
  • Supplementation with zinc and IGF-1 has been shown to improve outcomes after TBI.
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3
Q

Define hyponatremia. What can it contribute to?

A
  • Serum sodium less than 135 mg/dL.
  • Contributes to worsening cerebral edema, intracranial pressure elevations and death from herniation
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4
Q

Define SIAD. How does it relate to TBI? What is the primary treatment?

A
  • SIAD = Syndrome of Inappropriate Anti-Diuresis
  • TBI is a common cause of SIAD, which results in euvolemic hyponatremia
  • FR is primary treatment
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5
Q

Define CSW (Cerebral Salt Wasting). How does it relate to TBI? What is the treatment/management?

A
  • A rare hypovolemic hyponatremia characterized by increased natriuresis (excretion of sodium in the urine).
  • Like SAID, CSW is usually transient after TBI
  • CSW is a diagnosis of exclusion
  • Managed with IV Sodium supplemention
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6
Q

Define diabetes insipidus.

A
  • A hypernatremic state characterized by a deficiency in vasopressin (neurogenic- most common type), lack of response to vasopressin (nephrogenic), OR accelerated degradation of vasopressin (gestational).
  • BASICALLY: DAMAGE TO THE HYPOTHALAMUS OR POSTERIOR PITUITARY, usually as a result of rotational forces sustained in MVC, reduces central vasopressin production leading to neurogenic diabetes insipidius after TBI.
  • Supplementation of salt-free water and replacement of vasopressin can reduce serum sodium to normal levels
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7
Q

(FILL IN THE BLANKS)

As with hyponatremia, hypernatremia should be corrected NO FASTER than X to X mEq/L/d to avoid worsening of cerebral edema.

A
  • 10 to 12 mEq/L/day
  • (relates to previous 3 conditions: SIAD, CSW, Diabetes insipidus).
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8
Q

What medications (4) used in TBI treatment have been shown to reduce measured energy expenditure?

A
  • Proproanolol
    • Reduced by 5 to 18%
  • Morphine
    • Reduced up to 8%
  • Pentobarbital (used to reduce intracranial pressure)
    • Reduced up to 32%
  • NMBAS (also used to reduce intracranial pressure)
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9
Q

At present, which pharmaconutrients lack the available information to recommend specific dosing strategies for patients with TBI?

A
  • L-arginine
    • Clinical research has not found that arginine supp in trauma and TBI improves outcomes
  • Glutamine
    • Low plasma glutamine concentration at ICU admission is an independent risk factor for post-ICU morality in critically ill patients; but early provision of glutamine did not improve outcomes in large-scale study
  • Omega-3 FA
    • No clinical data available
  • Antioxidants
    • Ascorbic acid and alpha-tocopheral levels; not enough information
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10
Q

**What are the nutrition recommendations for energy and protein for patients with SCI (spinal cord injury?)

A
  • ** ENERGY: IC first, or 15% less than Harris-Benedict equation (no validated predictive equation best determines the SCI energy expenditure)
  • PROTEIN: 1.5 to 2.0 g/kg/d (immediately following a SCI)
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11
Q

**What are the general energy recommendations for weight maintenance for quadriplegic patients?

A

** 20 to 22 kcal/kg/d OR 55 to 90% of the Harris-Benedict equation.

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12
Q

**What are the general energy recommendations for weight maintenance for paraplegic patients?

A

** Energy recommendations are increased slightly to 22 to 24 kcal/kg/d OR 80 to 90% of the Harris-Benedict equation)

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13
Q

**What is the protein intake for patients in long-term care after a SCI?

A

**Healthy patients; 0.8 to 1.0 g/kg/d

If pressure injuries: 1.25 to 1.5 g/kg/d with energy (30 to 35 kcal/kg/d), sufficient daily fluid, and vitamin/mineral supplementation if intake is poor or deficiencies are suspected.

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14
Q

**Healthy patients; 0.8 to 1.0 g/kg/d

If pressure injuries: 1.25 to 1.5 g/kg/d with energy (30 to 35 kcal/kg/d), sufficient daily fluid, and vitamin/mineral supplementation if intake is poor or deficiencies are suspected.

A

**

EN start within 24 to 48 hours of admission.

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15
Q

**What are the energy requirements for patients with acute stroke?

A
  • **IC is the gold standard; no equation has been validated to precisely determine the energy expenditure for the stroke population.
  • Based on available data, the energy requirements following an ischemic stroke are likely close to estimated BMR via Harris-Benedict equation or Penn-State equation.
  • Patients with hemorrhagic stroke, especially SAH, have elevated energy needs as compared with estimates of BMR.
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16
Q

**What are the protein requirements for patients following an acute stroke?

A

** Recommended protein goals range from 1.0 to 1.5 g/kg/d

17
Q

If hypernatremia protocols aim for serum sodium ranges of 140 to 150 mg/dL to minimize cerebral edema, what should you recommend?

A

A concentrated enteral formula with 1.5 to 2.0 kcal/mL may be appropriate to provide less water. Then advancing to a standard formula as the patient progresses.

18
Q

Explain the level 1 dysphagia diet.

A

PUREED (homogenous, very cohesive, and pudding-like in texture, requiring very little chewing ability.

19
Q

Explain the level II dysphagia diet.

A

MECHANICALLY ALTERED

  • Cohesive, moist, semisolid foods, requiring some chewing
20
Q

Explain the level III dysphagia diet.

A

SOFT FOODS that requiring more chewing; most advanced dysphagia diet.

21
Q

(TRUE/FALSE)

Although overeating creates risks for SCI patients, poor intake may increase the risk of pressure ulcers. When pressure ulcer incidence was examined in SCI patients, a higher percentage of underweight patients developed pressure ulcers compared to healthy weight, overweight or obese patients with SCI.

A

TRUE.

Monitoring weekly weight changes throughout the rehab program is useful in guiding adjustments in energy requirements.

22
Q

Explain implication of nutrition status in patients with ALS.

A
  • ALS = Lou Gehrig’s disease; a rapidly progressing, degenerative motor neuron disease that results in significant muscle weakness and atrophy
  • 75% of ALS patients will experience bulbar involvement (includes muscles that control speech, swallowing, and chewing, that can lead to substantial weight loss)
  • Malnutrition is an independent prognostic factor of ALS survival; 8-fold increase in poor nutrition status
  • Early nutrition interventions has been shown to maintain good nutrition status for a longer period of time.
  • PEG placement earlier in the disease process is more effective at preserving nutrition status for a longer period of time.
    • ***It is recommended that PEG is placed whle forced vital capacity is more than 50% of predicted value or when patients has dysphagia or a BMI less than 20 or loses 5 to 10% of UBW.
23
Q

**What are the energy requirements for patients with ALS?

A
  • **Mifflin St. Jeor and Harris-Benedict equations have been shown to be the most accurate methods, with HB being the most practical
  • Some research supports increasing the calculated resting energy expenditure by 10%
    • Others: recommend energy needs to be 120% greater than BMR by IC and 130% x HB equation.
  • As the ratio of organ mass to muscle mass increases, patients may require 34 to 35 kcal/kg/d
24
Q

**What are the protein requirements for patients with ALS?

A

** Ranges from 0.8 to 1.2 g/kg/day

25
Q

Explain the ketogenic diet.

A
  • Well documented use for therapy in controlling seizures in the pediatric population
  • To decrease seizures, a 4:1 ratio of fat to CHO and protein is recommended; which can be titrated down as the disease state stabilizes.
  • Note many medications contain CHOs and must be taken into account when calculating diet.
26
Q

Explain the modified Atkins diet.

A
  • A 1:1 ratio fat to protein and CHO can be used once a patient’s seizure frequency is more stable.
  • Shown to reduce seizures in adults and adolescents with drug-resistant epilepsy.
27
Q

Limited information is known about nutrition and Parkinson’s disease. What is the overall pattern with body weight patterns in Parkinsons?

A
  • In the beginning stages of the disease, body weight increases, likely due to a decrease in motor function.
  • As the disease progresses, weight loss occurs. It is theorized that the metabolic rate increases because of worsening rigidity and dyskinesia.
28
Q

Explain the relationship between carbidopa/levodopa drug therapy and protein intake.

A
  • The medication and protein compete for transport in the SI and blood-brain barrier.
  • Fluctuations in absorption in leveodopa can affect motor function, and this drug therapy. has been associated with decreased intake of protein.
  • Higher levodopa requirements have been associated with increased constipation, and diet mgmt is recommended.