Ch 7 - SCI: Medical Complications Flashcards
1
Q
What are SCI T6 and above patients at risk of?
A
Autonomic dysreflexia
Orthostatic hynpotension
2
Q
What are SCI T8 and above patients at risk of?
A
Cannot regulate and maintain normal body temperature
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°
4
Q
What are levels T1-L2 sympathetics responsible for?
A
Tachycardia
Vasoconstriction
Increased arterial pressure.
5
Q
What are levels T1-T7 sympathetics responsible for?
A
Heart and blood vessels supplied by T1–T7
6
Q
Which receptors sense decrease in BP?
A
Aortic and carotid baroreceptors
7
Q
What blood pressure management pathway is blocked following SCI?
A
Efferent pathway to increase sympathetic outflow
8
Q
What are non-pharmaceutical managements of hypotension?
A
– Trendelenburg/ recliner WC
– Elastic stocking/ abd binder/ace wrap LE
– Tilt table
– Fluid resuscitation
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
10
Q
What is Autonomic Dysreflexia?
A
Syndrome of massive imbalanced reflex sympathetic discharge in patients with SCI above the splanchnic outflow (T5–L2)
11
Q
What does a noxious stimulus cause in Autonomic Dysreflexia?
A
Increases sympathetic reflex spinal release
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
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
14
Q
What are signs of Autonomic Dysreflexia?
A
– Headache – Sweating/ flushing above level of SCI – Elevated BP – Piloerection – Pupillary constriction – Sinus congestion
15
Q
What is initial treatment for Autonomic Dysreflexia?
A
- Sit upright, loosen clothing and devices
- Identify and remove noxious stimulus
- Monitor BP ~2 to 5 min during the episode and monitor for symptoms for at least 2 hours after resolution
- Meds if BP is >150 mmHg, unable to find source quickly and prior to checking for fecal impaction
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
17
Q
What are pharmacologic treatments for Autonomic Dysreflexia in the ICU setting?
A
■ Diazoxide
■ Nitroprusside
■ Hydralazine
■ Labetalol
18
Q
What is recommended during delivery in patients with T6 or above SCI?
A
Spinal anesthesia
19
Q
What are complications of Autonomic Dysreflexia?
A
■ Retinal hemorrhage ■ CVA/SAH ■ Seizure ■ MI ■ Death
20
Q
What does the Corticopontine mesencephalic nuclei in the frontal lobe control?
A
– Inhibits PNS sacral micturition center
– Allows bladder storage
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
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
23
Q
What does the Motor cortex to pudendal nucleus control?
A
Voluntary control (contraction/inhibition) of external urethral sphincter
24
Q
Where is the origin of PNS efferents for voiding control?
A
Detrusor nucleus in intermediolateral gray matter at S2–S4 levels
25
Where is the course of PNS efferents for voiding control?
Travel through pelvic nerves to PNS receptors of detrusor muscle
26
What is the function of PNS efferents for voiding control?
Stimulation of cholinergic receptors causes bladder contraction and emptying
27
Where is the origin of SNS efferents for voiding control?
Intermediolateral gray matter from T11–L2
28
Where is the course of SNS efferents for voiding control?
Travel through hypogastric nerves to alpha (α-1) and beta (β-2) adrenergic receptors within the bladder and urethra
29
What is the function of SNS efferents for voiding control?
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
30
Where is the origin of somatic efferents for voiding control?
Pudendal nucleus of sacral segments (S2–S4)
31
Where is the course of somatic efferents for voiding control?
Travel through pudendal nerve to innervate striated muscle of external urethral sphincter
32
What is the function of somatic efferents for voiding control?
Voluntary contraction of external urethral sphincter prevents leakage or emptying
33
Where is the origin of afferent fibers for voiding control?
Detrusor muscle stretch receptors, external anal and urethral sphincters, perineum, genitalia
34
Where is the course of afferent fibers for voiding control?
Travel through the pelvic and pudendal nerves to the sacral cord
35
What is the function of afferent fibers for voiding control?
Myelinated A-delta (A-δ) fibers respond to bladder distention stim PNS emptying of bladder and unmyelinated C-fibers are silent
36
What innervates the internal urethral sphincter?
T11–L2 hypogastric nerve (sympathetic)
| Large number of α-adrenergic receptors
37
What is the function of the internal urethral sphincter?
– Contracts sphincter for storage
| – Smooth muscle, involuntary
38
What innervates the external urethral sphincter?
Innervated by pudendal nerve (S2–S4)
39
What is the function of the external urethral sphincter?
– Prevents leakage or emptying
| – Skeletal muscle, voluntary
40
Where are Cholinergic muscarinic receptors located?
Located within the bladder wall, trigone, bladder neck, and urethra
41
Where are b-2 adrenergic receptors located?
Concentrated in the body of the bladder, also some in bladder neck
42
What happens when Norepinephrine (NE) binds to b-2 adrenergic receptors?
Cause relaxation to pormote bladder expansion and promote storage
43
Where are a-1 adrenergic receptors located?
Located within the base of the bladder and prostatic urethra
44
What happens when Norepinephrine (NE) binds to a-1 adrenergic receptors?
Cause contraction of internal sphincter to prommote storage
45
What does the bladder wall lack?
Baroreceptors
46
What happens when Ach binds to muscarinic receptors?
Stimulates cholinergic receptors in the bladder wall, trigone, neck, and urethra, causing bladder contraction and emptying
47
When should first sensation of bladder filling occur on cystometry?
100mL
48
What is a normal bladder capacity?
300-600 mL
49
What is functional bladder capacity?
Voided volume + residual urine volume
50
When should an intermittent catheterization (IC) program be established post-SCI?
Tolerate a fluid restriction of 2 L/day
| Early as 7 to 15 days post-injury
51
What volumes and frequency should an intermittent catheterization (IC) program be daily?
Volumes: <500 mL
Frequency: 4 to 5x/day
52
What is Vesicoureteral reflux?
Retrograde urine flow from the bladder toward kidneys caused by bladder wall hypertrophy and loss of the vesicoureteral angle
53
What is the failure with a LMN bladder?
Failure to empty from increased internal sphincter tension l/t overflow incontience
54
What is the failure with a UMN bladder?
Failure to store d/t overactive spasticy bladder from no sacral micturition center suppression
55
What are anticholinergic medications used for in SCI bladder treatment?
Relax detrusor and suppress uninhibited bladder contractions, thereby preventing long-term complication of vesicoureteral reflux
56
What are Alpha-blockers used for in SCI bladder treatment?
Open bladder neck
57
What is botox used for in SCI bladder treatment?
Detrusor wall
58
What is the normal function of the valve between the bladder and ureter?
Valve opens with bladder relaxation to bring urine from kidneys to bladder and closed during bladder contraction
59
What medications can be used to acidify urine for UTI prophylaxis?
Vitamin C supplementation
| Methenamine salts
60
When should Asymptomatic bacteriuria in SCI be treated?
```
Invasive procedures (cystoscopy, urodynamics)
Presence of vesicoureteral reflux
Growth of urease producing organisms (Proteus, Pseudomonas, Klebsiella, Providentia, Escherichia coli, Staphylococcus epidermidis)
```
61
What do Urea splitting organisms produce?
Struvite calculi made of ammonium and magnesium phosphate
62
When should UTI in SCI be treated?
```
– 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
What is the earliest sign of UTI complications?
Irregular, thickened bladder wall and small diverticuli
64
What are preventions to UTI?
Draining bladder at pressures <40 cm H2O, by IC, meds or surgical relief of outflow obstructions
65
Describe how pregnancy is affected after SCI.
Unchanged because fertility is unimpaired once menses return (~6-12 mo)
66
What may be the only manifestation of labor in SCI?
Autonomic dysreflexia
67
What innervates the internal anal sphincter?
SNS (T11–L2)
68
When does the internal anal sphincter normally relax?
Relaxes with filling of the rectum
69
What innervates the external anal sphincter?
Pudendal nerve (S2–S4)
70
When does the external anal sphincter normally relax?
Higher cortical centers and pontine defecation center send stimulus for EAS relaxation, allowing defecation
71
What causes colonic dysfunction in UMN SCI?
Loss of SNS/PNS input at the transverse and descending colon, EAS cannot voluntarily relax and pelvic floor muscles spastic
72
If bowel programs are done lying, on which side should a patient be?
Left side lying
73
What does docusate sodium cause?
Inc fat and fluid accumulation in the GI tract to soften stool
74
What does senna cause?
Stim peristalsis by acting on Auerbach’s plexus
75
What does glycerin suppository cause?
Draws water into stool and stretches rectal wall
76
What is Bisacodyl (Dulcolax®) suppository?
Oil base that stim peristalsis and sensory nerve endings
77
What is Magic Bullet® suppository?
Water base and acts faster than an oil base
78
What is Enemeez suppository?
5 mL mini-enemas of docusate sodium
| Bowel Program
79
What is the gastrocolic reflex?
Contraction of the colon occurring with gastric distention
80
What is the rectocolic reflex?
Occurs when rectal contents stretch the bowel wall reflexively, relaxing the internal anal sphincter
81
What are causes of GIB in SCI?
* Perforating and bleeding ulcers
* Most common early after injury
* Steroids may increase risk
82
What is the MCC of emergency abdominal surgery in chronic SCI?
Cholecysitis
| Increased risk: 3x greater in SCI
83
When is the timing of pancreatitis in SCI?
1st month post injury
84
What is superior mesenteric artery (SMA) syndrome?
3rd portion of the duodenum is intermittently compressed by overlying SMA resulting in GI obstruction
85
What are causes of superior mesenteric artery (SMA) syndrome?
– Rapid weight loss
– Prolonged supine position
– Spinal orthosis
– Flaccid abdominal wall causes hyperextension of the back
86
What are symptoms of superior mesenteric artery (SMA) syndrome?
– Post-prandial nausea and vomiting
– Bloating
– Abdominal pain
87
How is superior mesenteric artery (SMA) syndrome diagnosed?
UGI series shows abrupt duodenal obstruction to barium flow
88
What are treatments of superior mesenteric artery (SMA) syndrome?
– Eat small, frequent meals upright
– Lie in the left lateral decubitus position after eating
– Metoclopramide
– Rarely duodenojejunostomy
89
What leads to hypercalciuria in SCI?
* Immobilization promotes bone resorption
* Hypercalciuric for 18 months
* Vitamin D and parathyroid hormone are not involved
90
When does hypercalcemia in SCI occur?
* Adolescent and young adult males more often than older female
* Tetraplegia> paraplegia
* ~4 to 8 wks after SCI
91
What increases urinary excretion of Ca?
IV fluid hydration with normal saline
92
When does osteoporosis occur in SCI?
3 months to first year post-injury
93
What are the most frequent pulmonary complications in SCI?
Pneumonia
Atelectasis
Ventilatory failure
94
What are risk factors for pulmonary complications in SCI?
* Older age
* Obesity—restrictive respiratory deficits
* H/o COPD, asthma, and smoking
95
What is the leading cause of death in SCI?
Pneumonia
96
What are contraindications to phrenic nerve pacing?
– Denervated diaphragm (EMG)
| – Significant lung impairment
97
What are benefits of phrenic nerve pacing?
– Inc arterial oxygenation despite dec alveolar ventilation
– Longer survival
– Inc daily function 2/2 conditioning of the diaphragm
98
What are signs of phrenic nerve pacemaker failure?
```
■ Sharp chest pain
■ SOB
■ Absence of breath
■ Erratic pacing
■ Must maintain adequate ventilation via manual resuscitation bag
```
99
What are causes of phrenic nerve pacemaker failure?
■ 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
Describe a phrenic motor study set up.
– 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
What lung pattern do tetraplegics develop?
Restrictive lung pattern
102
What are contraindications of mechanical cough assist?
Bullous emphysema
103
What can tracheal suctioning cause?
Inc vagal tone leading to bradycardia (only suction as you withdraw catheter)
104
What is the order of occurrence of joints with HO in SCI?
Hip/knee/shoulder/elbow
105
What is the onset of HO in SCI?
1 to 4 months status post-injury is most common
106
What are risk factors of HO in SCI?
```
– Spasticity
– Completeness of injuries
– Trauma or prior surgery to joint
– Age (younger)
– Pressure ulcer in proximity of joint
– Presence of DVT
```
107
What is the incidence of DVT in SCI?
47% to 100% w/o ppx
| 14% w/ appropriate chemoprophylaxis
108
What patients MC get DVT in SCI?
Neurologically complete
| Tetraplegia
109
What is the onset of DVT in SCI?
– MC 2 weeks after SCI
| – Dec ~8-12 weeks post-SCI
110
What is the gold standard of diagnosis of DVT in SCI?
Venogram
111
What is the leading cause of death in acute SCI?
Pulmonary embolism
112
What is the gold standard of diagnosis of PE in SCI?
Pulmonary arteriogram
113
What is the most effective DVT ppx in SCI?
LMWH
114
What is the duration of DVT ppx in incomplete SCI and ambulating?
Continue until discharge
115
What is the duration of DVT ppx in complete SCI?
■ 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
What are uses of FES in SCI?
* Avoid complications of muscle inactivity
* Producing extremity motion for functional activities
* Provide a CV conditioning program
