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BR 3rd Ed > Ch 7 - SCI: Medical Complications > Flashcards

Ch 7 - SCI: Medical Complications Flashcards

1
Q

What are SCI T6 and above patients at risk of?

A

Autonomic dysreflexia

Orthostatic hynpotension

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2
Q

What are SCI T8 and above patients at risk of?

A

Cnnot regulate and maintain normal body temperature

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3
Q

What is orthostatic hypotension?

A

State of transient reflex depression caused by a lack of sympathetic outflow and triggered by tilting the patient upright >60°

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4
Q

What are levels T1-L2 responsible for?

A

Tachycardia
Vasoconstriction
Increased arterial pressure.

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5
Q

What are levels T1-T7 responsible for?

A

Heart and blood vessels supplied by T1–T7

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6
Q

Which receptors sense decrease in BP?

A

Aortic and carotid baroreceptors

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7
Q

What pathway is blocked following SCI?

A

Efferent pathway to increase sympathetic outflow

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8
Q

What are non-pharmaceutical managements of hypotension?

A

– Trendelenburg/ recliner WC
– Elastic stocking/ abd binder/ace wrap LE
– Tilt table
– Fluid resuscitation

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9
Q

What are pharmaceutical managements of hypotension?

A

■ Na tabs 1 gram QID
■ Midodrine (ProAmatine) (α-1 adrenergic agonist): 2.5 to 10 mg TID
■ Florinef® (mineralocorticoid): 0.05 to 0.1 mg daily

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10
Q

What is Autonomic Dysreflexia?

A

Syndrome of massive imbalanced reflex sympathetic discharge in patients with SCI above the splanchnic outflow (T5–L2)

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11
Q

What does a noxious stimulus cause in Autonomic Dysreflexia?

A

Increases sympathetic reflex spinal release

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12
Q

When does Autonomic Dysreflexia appear?

A

2 to 4 weeks post-injury
W/in 1st year in >90% of cases
Classically in complete SCI

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13
Q

What are the MCC of Autonomic Dysreflexia?

A 
– Bladder: Blocked catheter/distended bladder
– Bowel: Fecal impaction
– Abd emergency (appendicitis, cholecystis, pancreatitis)
– Labor
– PUs
– Fractures
– Ingrown toenails
– Orgasm
– Urinary tract infections
– Epididymitis
– Bladder stones
 – Gastric ulcers
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14
Q

What are signs of Autonomic Dysreflexia?

A 
– Headache
– Sweating/ flushing above level of SCI
– Elevated BP
– Piloerection
– Pupillary constriction
– Sinus congestion
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15
Q

What are treatments for Autonomic Dysreflexia?

A
  1. Sit upright, loosen clothing and devices
  2. Identify and remove noxious stimulus
  3. Monitor BP ~2 to 5 min during the episode and monitor for symptoms for at least 2 hours after resolution
  4. Meds if BP is >150 mmHg, unable to find source quickly and prior to checking for fecal impaction
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16
Q

What are pharmacologic treatments for Autonomic Dysreflexia?

A

■ Nitropaste: ½ to 2 inches, and removed once noxious stimulus is corrected
■ Clonidine: 0.3 to 0.4 mg
■ Procardia® 10 mg chew and swallow

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17
Q

What are pharmacologic treatments for Autonomic Dysreflexia in the ICU setting?

A

■ Diazoxide
■ Nitroprusside
■ Hydralazine
■ Labetalol

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18
Q

What is recommended during delivery in patients with T6 or above SCI?

A

Spinal anesthesia

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19
Q

What are complications of Autonomic Dysreflexia?

A 
■ Retinal hemorrhage
■ CVA/SAH
■ Seizure
■ MI
■ Death
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20
Q

What does the Corticopontine mesencephalic nuclei in the frontal lobe control?

A

– Inhibits PNS sacral micturition center

– Allows bladder storage

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21
Q

What does the Pontine mesencephalic nuclei in the Pons control?

A

– Coordinates bladder contraction and sphincter relaxation

– Loss of control from this center can result in detrusor sphincter dyssynergia

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22
Q

What does the Pelvic and pudendal nuclei: Sacral micturition control?

A

– Integrate stimuli from cephalic centers

– Mediate PNS sacral (S2–S4) micturition reflex

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23
Q

What does the Motor cortex to pudendal nucleus control?

A

Voluntary control (contraction/inhibition) of external urethral sphincter

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24
Q

Where is the origin of PNS efferents for voiding control?

A

Detrusor nucleus in intermediolateral gray matter at S2–S4 levels

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25
Q

Where is the course of PNS efferents for voiding control?

A

Travel through pelvic nerves to PNS receptors of detrusor muscle

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26
Q

What is the function of PNS efferents for voiding control?

A

Stimulation of cholinergic receptors causes bladder contraction and emptying

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27
Q

Where is the origin of SNS efferents for voiding control?

A

Intermediolateral gray matter from T11–L2

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28
Q

Where is the course of SNS efferents for voiding control?

A

Travel through hypogastric nerves to alpha (α-1) and beta (β-2) adrenergic receptors within the bladder and urethra

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29
Q

What is the function of SNS efferents for voiding control?

A

Stim of β-2 adrenergic rec w/in bladder body causes smooth muscle relaxation (compliance) + stim of α-1 adrenergic rec w/in bladder base; prostatic urethra causes smooth muscle contraction (increase outlet resistance) = urine storage

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30
Q

Where is the origin of somatic efferents for voiding control?

A

Pudendal nucleus of sacral segments (S2–S4)

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31
Q

Where is the course of somatic efferents for voiding control?

A

Travel through pudendal nerve to innervate striated muscle of external urethral sphincter

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32
Q

What is the function of somatic efferents for voiding control?

A

Voluntary contraction of external urethral sphincter prevents leakage or emptying

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33
Q

Where is the origin of afferent fibers for voiding control?

A

Detrusor muscle stretch receptors, external anal and urethral sphincters, perineum, genitalia

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34
Q

Where is the course of afferent fibers for voiding control?

A

Travel through the pelvic and pudendal nerves to the sacral cord

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35
Q

What is the function of afferent fibers for voiding control?

A

Myelinated A-delta (A-δ) fibers respond to bladder distention stim PNS emptying of bladder and unmyelinated C-fibers are silent

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36
Q

What innervates the internal sphincter?

A

T11–L2 hypogastric nerve (sympathetic)

Large number of α-adrenergic receptors

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37
Q

What is the function of the internal sphincter?

A

– Contracts sphincter for storage

– Smooth muscle, involuntary

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38
Q

What innervates the external sphincter?

A

Innervated by pudendal nerve (S2–S4)

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39
Q

What is the function of the external sphincter?

A

– Prevents leakage or emptying

– Skeletal muscle, voluntary

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40
Q

Where are Cholinergic muscarinic receptors located?

A

Located within the bladder wall, trigone, bladder neck, and urethra

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41
Q

Where are b-2 adrenergic receptors located?

A

Concentrated in the body of the bladder, also some in bladder neck

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42
Q

What happens when Norepinephrine (NE) binds to b-2 adrenergic receptors?

A

Cause relaxation to pormote bladder expansion and promote storage

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43
Q

Where are a-1 adrenergic receptors located?

A

Located within the base of the bladder and prostatic urethra

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44
Q

What happens when Norepinephrine (NE) binds to a-1 adrenergic receptors?

A

Cause contraction of internal sphincter to prommote storage

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45
Q

What does the bladder wall lack?

A

Baroreceptors

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46
Q

What happens when Ach binds to muscarinic receptors?

A

Stimulates cholinergic receptors in the bladder wall, trigone, neck, and urethra, causing bladder contraction and emptying

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47
Q

When should first sensation of bladder filling occur on csystometry?

A

100mL

48
Q

What is a normal bladder capacity?

A

300-600 mL

49
Q

What is functional bladder capacity?

A

Voided volume + residual urine volume

50
Q

When should an intermittent catheterization (IC) program should be established post-SCI?

A

Tolerate a fluid restriction of 2 L/day

Early as 7 to 15 days post-injury

51
Q

What volumes and frequency should an intermittent catheterization (IC) program be daily?

A

Volumes: <500 mL
Frequency: 4 to 5x/day

52
Q

What is Vesicoureteral reflux?

A

Retrograde urine flow from the bladder toward kidneys caused by bladder wall hypertrophy and loss of the vesicoureteral angle

53
Q

What is the failure with a LMN bladder?

A

Failure to empty from increased internal sphincter tension l/t overflow incontience

54
Q

What is the failure with a UMN bladder?

A

Failure to store d/t overactive spasticy bladder from no sacral micturition center suppression

55
Q

What are Anticholinergic medications used for in SCI bladder treatment?

A

Relax detrusor and suppress uninhibited bladder contractions, thereby preventing long-term complication of vesicoureteral reflux

56
Q

What are Alpha-blockers used for in SCI bladder treatment?

A

Open bladder neck

57
Q

What is botox used for in SCI bladder treatment?

A

Detrusor wall

58
Q

What is the normal function of the valve between the bladder and ureter?

A

Valve opens with bladder relaxation to bring urine from kidneys to bladder and closed during bladder contraction

59
Q

What medications can be used to acidify urine for UTI prophylaxis?

A

Vitamin C supplementation

Methenamine salts

60
Q

When should Asymptomatic bacteriuria in SCI be treated?

A 
Invasive procedures (cystoscopy, urodynamics)
Presence of vesicoureteral reflux
Growth of urease producing organisms (Proteus, Pseudomonas, Klebsiella, Providentia, Escherichia coli, Staphylococcus epidermidis)
61
Q

What do Urea splitting organisms produce?

A

Struvite calculi made of ammonium and magnesium phosphate

62
Q

When should UTI in SCI be treated?

A 
– Significant bacteriuria
A. Clean catch: >100,000 org/ mL
B. Cath: >100 org/mL
– Pyuria: >10 leuk/mm2
– Fever, malaise, inc spasticity or neurogenic pain
63
Q

What is the earliest sign of UTI complications?

A

Irregular, thickened bladder wall and small diverticuli

64
Q

What are preventions to UTI?

A

Draining bladder at

pressures <40 cm H2O, by IC, meds or surgical relief of outflow obstructions

65
Q

Describe how pregnancy is affected after SCI.

A

Unchanged because fertility is unimpaired once menses return (~6-12 mo)

66
Q

What may be the only manifestation of labor in SCI?

A

Autonomic dysreflexia

67
Q

What innervates the internal anal sphincter?

A

SNS (T11–L2)

68
Q

When does the internal anal sphincter normally relax?

A

Relaxes with filling of the rectum

69
Q

What innervates the external anal sphincter?

A

Pudendal nerve (S2–S4)

70
Q

When does the external anal sphincter normally relax?

A

Higher cortical centers and pontine defecation center send stimulus for EAS relaxation, allowing defecation

71
Q

What causes colonic dysfunction in UMN SCI?

A

Loss of SNS/PNS input at the transverse and descending colon, EAS cannot voluntarily relax and pelvic floor muscles spastic

72
Q

If bowel programs are done lying which side should a patient be?

A

Left side lying

73
Q

What does docusate sodium cause?

A

Inc fat and fluid accumulation in the GI tract to soften stool

74
Q

What does senna cause?

A

Stim peristalsis by acting on Auerbach’s plexus

75
Q

What does glycerin suppository cause?

A

Draws water into stool and stretches rectal wall

76
Q

What is Bisacodyl (Dulcolax®) suppository?

A

Oil base that stim peristalsis and sensory nerve endings

77
Q

What is Magic Bullet® suppository?

A

Water base and acts faster than an oil base

78
Q

What is Enemeez suppository?

A

5 mL mini-enemas of docusate sodium

Bowel Program

79
Q

What is the gastrocolic reflex?

A

Contraction of the colon occurring with gastric distention

80
Q

What is the retocolic reflex?

A

Occurs when rectal contents stretch the bowel wall reflexively, relaxing the internal anal sphincter

81
Q

What are causes of GIB in SCI?

A
  • Perforating and bleeding ulcers
  • Most common early after injury
  • Steroids may increase risk
82
Q

What is the MCC of emergency abdominal surgery in chronic SCI?

A

Cholecysitis

Increased risk: 3x greater in SCI

83
Q

When is the timing of pancreatitis in SCI?

A

1st month post injury

84
Q

What is superior mesenteric artery (SMA) syndrome?

A

3rd portion of the duodenum is intermittently compressed by overlying SMA resulting in GI obstruction

85
Q

What are causes of superior mesenteric artery (SMA) syndrome?

A

– Rapid weight loss
– Prolonged supine position
– Spinal orthosis
– Flaccid abdominal wall causes hyperextension of the back

86
Q

What are symptoms of superior mesenteric artery (SMA) syndrome?

A

– Post-prandial nausea and vomiting
– Bloating
– Abdominal pain

87
Q

How is superior mesenteric artery (SMA) syndrome diagnosed?

A

UGI series shows abrupt duodenal obstruction to barium flow

88
Q

What are treatments of superior mesenteric artery (SMA) syndrome?

A

– Eat small, frequent meals upright
– Lie in the left lateral decubitus position after eating
– Metoclopramide
– Rarely duodenojejunostomy

89
Q

What leads to hypercalciuria in SCI?

A
  • Immobilizationpromotes b one resorption
  • Hypercalciuric for 18 months
  • Vitamin D and parathyroid hormone are not involved
90
Q

Whend does hypercalcemia in SCI occur?

A
  • Adolescent and young adult males more often than older female
  • Tetraplegia> paraplegia
  • ~4 to 8 wks after SCI
91
Q

What increases urinary excretion of Ca?

A

IV fluid hydration with normal saline

92
Q

When does osteoporosis occur in SCI?

A

3 months to first year post-injury

93
Q

What are the most frequent pulmonary complications in SCI?

A

Pneumonia
Atelectasis
Ventilatory failure

94
Q

What are risk factors for pulmonary complications in SCI?

A
  • Older age
  • Obesity—restrictive respiratory deficits
  • H/o COPD, asthma, and smoking
95
Q

What is the leading cause of death in SCI?

A

Pneumonia

96
Q

What are contraindications to phrenic nerve pacing?

A

– Denervated diaphragm (EMG)

– Significant lung impairment

97
Q

What are benefits of phrenic nerve pacing?

A

– Inc arterial oxygenation despite dec alveolar ventilation
– Longer survival
– Inc daily function 2/2 conditioning of the diaphragm

98
Q

What are signs of phrenic nerve pacemaker failure?

A 
■Sharp chest pain
■ SOB
■ Absence of breath
■ Erratic pacing 
■ Must maintain adequate ventilation via manual resuscitation bag
99
Q

What are causes of phrenic nerve pacemaker failure?

A

■Diaphragmatic failure—due to overly aggressive pacing schedule
■ Infection of lung and/or phrenic nerve
■ Meds: sedatives, tranquilizers, and narcotics
■ Upper airway obstruction—tracheal aspiration
■ Phrenic nerve damage from overstimulation or surgery

100
Q

Describe a phrenic motor study set up.

A

– Recording site: Diaphragm muscle
– G1: Two finger breaths above xiphoid process
– G2: Anterior costal margin 16 cm from G1
– Stim: Lateral neck, posterior to SCM muscle ~3 cm above clavicle

101
Q

What lung pattern do tetraplegics develop?

A

Restrictive lung pattern

102
Q

What are contraindications of mechanical cough assist?

A

Bullous emphysema

103
Q

What can tracheal suctioning cause?

A

Inc vagal tone leading to bradycardia (only suction as you withdraw catheter)

104
Q

What is the order of occurrence of joints with HO in SCI?

A

Hhip/knee/shoulder/elbow

105
Q

What is the onset of HO in SCI?

A

1 to 4 months status post-injury is most common

106
Q

What are risk factors of HO in SCI?

A 
– Spasticity
– Completeness of injuries
– Trauma or prior surgery to joint
– Age (younger)
– Pressure ulcer in proximity of joint
– Presence of DVT
107
Q

What is the incidence of DVT in SCI?

A

47% to 100% w/o ppx

14% w/ appropriate chemoprophylaxis

108
Q

What patients MC get DVT in SCI?

A

Neurologically complete

Tetraplegia

109
Q

What is the onset of DVT in SCI?

A

– MC 2 weeks after SCI

– Dec ~8-12 weeks post-SCI

110
Q

What is the gold standard of diagnosis of DVT in SCI?

A

Venogram

111
Q

What is the leading cause of death in acute SCI?

A

Pulmonary embolism

112
Q

What is the gold standard of diagnosis of PE in SCI?

A

Pulmonary arteriogram

113
Q

What is the most effective DVT ppx in SCI?

A

LMWH

114
Q

What is the duration of DVT ppx in incomplete SCI and ambulating?

A

Continue until discharge

115
Q

What is the duration of DVT ppx in complete SCI?

A

■ At least 8 weeks post-injury in uncomplicated complete motor injury
■ Continue 12 weeks post-injury, or can consider until discharge from rehabilitation
■ >12 weeks in persons with complete motor injury and other risk factors (lower limb fracture, h/o thrombosis, cancer, heart failure, obesity, or age >70)

116
Q

What are uses of FES in SCI?

A
  • Avoid complications of muscle inactivity
  • Producing extremity motion for functional activities
  • Provide a CV conditioning program

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