Section XII

Medical Complications After Stroke

Richard D. Zorowitz, MD, and Gretchen E. Tietjen, MD

The general care of stroke survivors entails not only
treatment in the hyperacute and acute settings but also
prevention of secondary complications that hinder func-
tional recovery. Physicians, nurses, and allied health
professionals in both the acute care and rehabilitation
setting should be aware of the possible problems that a
stroke survivor may encounter and provide appropriate
preventative care and intervention where needed. The
secondary complications to be discussed in this section
include cardiovascular dysfunction, swallowing difficul-
ties, aspiration pneumonia, stress ulcers, seizures, deep
venous thrombosis and pulmonary embolus, bladder and
bowel dysfunction, contractures and pressure sores, and
depression.
Cardiovascular Dysfunction
Cerebrovascular and cardiovascular disease are both
manifestations of atherosclerotic disease, but each condi-
tion may also predispose to the other. With increased
sympathetic and decreased parasympathetic tone, electro-
cardiogram (ECG) abnormalities may occur in as many as
90% of stroke patients. 1 Cardiac dysfunction in the form
of life-threatening dysrhythmias or myocardial ischemia
make it prudent to consider monitoring the cardiac status
with telemetry during the first 24 to 48 hours after stroke. 2
With loss of autoregulation, elevated blood pressures (up
to a systolic blood pressure of 180 m m Hg) may be
necessary to maintain adequate cerebral blood flow and
cerebral perfusion. Sublingual nifedipine and other agents
that precipitously lower blood pressure should never be
given. After stroke, cardiac death is twice as common as
death related to recurrent stroke, equaling about 5% per
year. 3 Stroke survivors are likely to experience cardiovas-
From the Department of Physical Medicine and Rehabilitation,
Hospital of the University of Pennsylvania, Philadelphia, PA; and the
Division of Neurology,Medical College of Ohio, Toledo,OH.
Address reprint requests to Richard D. Zorowitz, MD, Department
of Physical Medicine and Rehabilitation, Hospital of the University of
Pennsylvania, 5 West Gates Building, 3400 Spruce Street, Philadel-
phia, PA 19104-4529.
Copyright 9 1999by National Stroke Association
1052-3057/ 99/ 0803-001253.00/ 0
cular dysfunction during recovery. Abnormalities in heart
rate, heart rhythm, blood pressure, or on ECG were found
in more than half of the stroke survivors undergoing a
rehabilitation program and may necessitate modification
of the program. 4 The presence of congestive heart failure
increased the risk of other cardiac abnormalities.
Swallowing Difficulties
Nearly one third of all stroke survivors will experience
difficulties with swallowing, which may be manifested by
a variety of symptoms, s Drooling reflects weakness of the
lips or inability to swallow saliva, or both. Dry mouth is
frequently a side effect of anticholinergic drugs. Difficulty
with chewing or prolonged feeding may result from weak
masticatory muscles or from cognitive deficits. Inappropri-
ate speaking or breathing while swallowing often reflects
organic brain disorders. Pocketing food or liquid in the
lateral recesses occurs with incoordination of the tongue
or inability of the cheeks to keep boluses in the midline.
Nasal leakage of food results from incompetence of the
nasopharyngeal port. Dyspraxia of the tongue may cause
difficulty with initiating and coordinating a swallow. The
sense of globus or food sticking in the throat originates
from either the pharynx or esophagus. A wet, gurgly
voice usually denotes a bolus that is resting above the true
vocal folds. Coughing or choking while eating or drinking
in stroke patients suggests penetration of a bolus through
the true vocal folds into the trachea. If the cough is
impaired, there may not be enough intraabdominal pres-
sure to force a bolus from the tracheobronchial tree, and
aspiration into the lungs occurs. Difficulty breathing may
be due to portions of a bolus obstructing the tracheobron-
chial tree.
The most serious complications of poststroke dyspha-
gia are malnutrition 6 and aspiration. Malnutrition may be
avoided by timely initiation of nasogastric tube feedings
in patients unable to safely swallow. In patients with
prolonged dysphagia, a gastrostomy tube is a practical
option for feeding. Aspiration in stroke patients may be
difficult to determine clinically, as nearly 60% of patients
who aspirate are not diagnosed during routine bedside
swallowing examination. Some researchers have associ-

192 Journal of Stroke and Cerebrovascular Diseases, Vol. 8, No. 3 (May-June), 1999: pp 192-196
MEDICAL COMPLICATIONS AFTER STROKE
ated the absence of a gag reflex with aspiration, although
this finding occurs in up to 10% of the normal population.
The phenomenon of silent aspiration increases as more
lesions are noted in different portions of the brain, with
the highest risk occurring in stroke survivors with bilat-
eral cerebral and brain-stem signs. 7 The risk of aspiration
also increases with prolongation in the pharyngeal transit
time. 8 Food consistencies (e.g., thin liquid, puree) that
result in aspiration of greater than 10% per bolus must be
avoided. 9
Aspiration Pneumonia
Pneumonia is responsible for 25% to 30% of deaths after
stroke and is the most common cause of nonneurological
death. 1~ Peak incidence of death related to poststroke
pneumonia occurs at 2 to 4 weeks. Pneumonia is fre-
quently due to aspiration of oropharyngeal contents. 11
The most common organisms include Pseudomonas aerugi-
nosa, Escherichia coli, Staphylococcus aureus, and Klebsiella
pneumoniae. A study of 441 stroke patients demonstrated a
20-fold increase in the incidence of aspiration pneumonia
in patients who were proven aspirators by a videofluoro-
graphic examination. The highest incidence of aspiration
pneumonia was found in stroke survivors with brain-
stern and right hemispheric lesions. 12
Stress Ulcers
Incidence of gastrointestinal bleeding after acute stroke
is 1% to 3%, but gastric changes as determined by
endoscopic studies may be as high as 50%. 13 Nasogastric
feeding, use of aspirin and nonsteroidal antiinflammatory
drugs, and corticosteroids may precipitate erosive changes.
Anticoagulant and fibrinolytic abnormalities are occasion-
ally related to life-threatening gastrointestinal bleeding.
Antacids, histamine (H2) receptor antagonists, and sucral-
fate are recommended as prophylactic agents. Sucralfate
may decrease nosocomial pneumonia in ventilator-
dependent patients. 14
Seizures
Seizures occur in up to 20% of patients after stroke at a
frequency of 2.5% to 5.7% in the first 2 weeks after
stroke. 15'16Seizures are more common with cortical infarc-
tion and may also be more likely to occur with embolic
than with thrombotic stroke. Seizures should be treated
promptly because of the associated increase in cerebral
oxygen demand; however, the prophylactic use of antiepi-
leptic drugs (AEDs) in stroke patients without clinical
evidence of seizures is not advised. When the patient has
acute stroke-related seizures, AED monotherapy is usu-
ally sufficient to control seizures. The clinical effects of the
AED on the infarcted or perinfarction tissue is not known.
193
Deep Venous Thrombosis and Pulmonary
Embolism
Without prophylactic treatment, deep venous thrombo-
sis (DVT) may occur in up to 75% of stroke survivors.
Approximately 10% of stroke survivors with DVT de-
velop pulmonary embolism (PE). 17 The time from stroke
onset to rehabilitation is a significant predictor of DVT
formation, is Prevention of DVT includes administration
of low-dose unfractionated heparin (e.g., 5000 U subcuta-
neously every 8 to 12 hours) or the more costly low-
molecular-weight heparin (30 m g enoxaparin subcutane-
ously every 12 hours or 2500 IU dalteparin subcutaneously
every 24 hours). Complementary use of external pneu-
matic compression or gradient elastic stockings to main-
tain venous flow is recommended. Stroke survivors who
ambulate 50 feet in the parallel bars with assistance or an
assistance device have a fivefold decrease in their risk of
DVT. Ambulating 50 feet outside of the parallel bars
reduces the risk of DVT 12-fold. 19
The treatment for DVT includes anticoagulation with
unfractionated heparin to prolong the adjusted partial
thromboplastin time (aPTT) to a range corresponding
with a heparin level of 0.2 to 0.4 U/mL. 2~ Bedrest is
maintained for a minimum of 24 hours as heparin be-
comes therapeutic. 21Heparin and warfarin may be started
concurrently but therapeutic heparin therapy should be
continued until warfarin prolongs the prothrombin time
to an international normalized ratio (INR) of 2.0 to 3.0.
Alternatively, low-molecular-weight heparin (enoxaparin
1 mg per kg of body weight subcutaneously twice daily)
with warfarin starting on the second da)~ can be used
safely and effectively to treat DVT until warfarin is
therapeutic and eliminates the need for intravenous lines
and frequent laboratory monitoring. 22 Long-term antico-
agulation should be continued for at least 3 months after
DVT and at least 6 months after PE. Patients with
recurrent DVT or PE, or continuing risk factors such as
antithrombin III deficiency, protein C or S deficiency,
lupus anticoagulant, anticardiolipin or other antiphospho-
lipid antibodies, elevated homocysteine, folate deficiency,
and factor V Leiden deficiency, may be treated with
warfarin indefinitely. Low-molecular-weight heparin or
adjusted-dose standard (unfractionated) heparin therapy
to prolong the aPTT to a time corresponding to a plasma
heparin level greater than 2.0 U / m L should be considered
if warfarin therapy is contraindicated. An inferior vena
cava filter may be considered if anticoagulation therapy is
contraindicated.
Bladder Dysfunction
Bladder dysfunction is a common complication after
stroke, occurring in over half of stroke survivors within 1
week of stroke onset. Over the first year, the incidence of
bladder dysfunction gradually decreases until it is similar
194
to that of the normal geriatric population. Associated
factors include significant impairments in motor function
and mobility and problems with cognition or communica-
tion. The most common symptoms of poststroke bladder
dysfunction include urinary frequency, urgency, and incon-
tinence. Bladder dysfunction, often characterized by al-
tered tone, is not associated with any specific lesion site.
The most common bladder dysfunction is detrusor hyper-
reflexia. Some persons develop uninhibited bladder con-
tractions with small amounts of urine (<200 mL) and may
not empty the bladder completely. Muscarinic receptor
agonists, such as tolterodine tartrate, may be effective for
treatment of urinary frequency, urgency, and urge inconti-
nence. Areflexic or hyporeflexic bladders may require
catheterization. Enlarged or cancerous prostates can ob-
struct the bladder outlet.
Postvoid residuals with the use of a bladder scanner or
catheter will help to characterize bladder dysfunction.
When pharmacological management of bladder dysfunc-
tion is required, more complete assessment can be per-
formed by using urodynamics (i.e., filling the bladder
with water while measuring water pressures and electri-
cal activity of the sphincter). 23Indwelling catheters should
be avoided because of the increased risk of bacteruria and
infection. On removing a catheter, obtain a urinalysis and
urine culture to determine whether treatment of residual
colonization is needed.
Bowel Dysfunction
Many stroke survivors have bowel incontinence or
constipation. The use of toileting programs and bowel
programs increase the chance that a stroke survivor is
continent of both bowel and bladder. Several simple
principles may be applied in the treatment of bowel
dysfunction. First, the patient should be allowed to use a
toilet or commode to facilitate the use of gravity and
intraabdominal pressure during defecation. Second, the
patient should be well hydrated and eating a diet ad-
equate in fiber. Stool softeners and bowel stimulants will
help the patient maintain regularity. Finally, periodic
review of the bowel program will allow simplification
over time and ensure compliance.
Contractures and Pressure Sores
Contractures and pressure sores caused by immobility
after stroke are usually preventable. The stroke survivor
should lie on the unaffected side to divert edema from the
affected side and to prevent contractures. Hip and knee
contractures are prevented by periodically having the
patient assume the prone position. Weakened limbs must
be properly supported during transfers and repositioning
to prevent traction injuries of brachial and lumbosacral
plexi. Pressure-relief ankle foot orthoses should be placed
R. D. Z O R O W I T Z A N D G. E. TIETJEN
on immobile feet to maintain the ankle in a neutral
position and prevent heel pressure. Footboards will pre-
vent bed linens from causing friction injuries to the lower
extremities but may not prevent the ankle from assuming
an equinovarus position. For the hands, resting splints or
rolls will prevent increased tone and contractures. Intrave-
nous lines should be placed in the unaffected upper limb
to prevent phlebitis or noxious stimuli from causing the
affected upper limb to assume a flexor synergy pattern
that might facilitate contracture.
Pressure sores may be caused by both extrinsic and
intrinsic factors. Pressure, shear forces, friction, and mois-
ture facilitate skin breakdown. Anemia, contractures,
spasticity, diabetes mellitus, deficiencies of vitamins and
minerals, edema, and obesity may prevent timely healing
of pressure sores when they occur. The location of pres-
sure sores is position dependent. If the stroke patient is
confined to bed, the sacrum, heels, occiput, elbows, dorsal
thorax, and ear rim are predisposed to pressure sores. If
the patient is positioned on his side, pressure sores
usually develop on the lateral malleolus, greater trochan-
ter, ribs, shoulder, ear, and lateral knee. In a sitting
position, pressure sores are apt to occur on the ischial
tuberosity, sacrum, posterior knee, foot, and shoulder. The
basic premise in the treatment of these sores is removal of
pressure by periodically turning the patient and vigorous,
regular incontinence care. Thorough cleaning and applica-
tion of commercially available dressings, such as Granu-
lex (Dow Hickam, Sugarland, TX), Duoderm (ConvaTec
Ltd., Princeton, NJ), and Opsite (Smith and Nephew,
Largo, FL), may be helpful in treating more superficial
decubiti. Damp-to-dry dressings that are frequently
changed will help debride necrotic tissue. Surgical graft-
ing may be considered as a last resort when more
conservative means of treatment fail to close the wound.
Depression
Depression is the most underdiagnosed and under-
treated complication after stroke. Loss or alteration of
catecholamine-containing neurons may result in major
depression. Correlation with lesion site is controversial. 24
Reactive depression involving grief over loss of function
can interfere with active participation in the recovery
process. 25,26Depression during the early stages of recov-
ery may be due to adjustment to the new disability. 27
Depression in the chronic stages of stroke recovery is
more prevalent. Eighty percent of stroke survivors who
are depressed in the early phase of recovery remain
depressed 6 months after the stroke. Of these, 33% to 40%
will remain depressed for up to 2 years or more post-
stroke, largely because of the social isolation that disabil-
ity brings to the stroke survivor. 28Fewer than 5% of stroke
survivors with depression are actually treated with medi-
cation. Many types of antidepressants (Table 1) may be
effective treatments for poststroke depression. 29,3~Fluox-
MEDICAL COMPLICATIONS AFTER STROKE 195
Table 1. Antidepressants used in post-stroke depression

Dosage Serum level

Antidepressant type (rag/day) (ng/mL) Side effects

Tricyclic
Nortriptyline (Pamelor; Sandoz Pharmaceuticals, East 25-150 50-150 Hypotension, tachycardia, confusion,
Hanover, NJ) dry mouth, Agranulocytosis, anxiety,
urinary retention, weight gain, con-
stipation, seizure, insomnia
Imipramine 25-150
(Tofranil; Ciba Geneva, Summit, NJ)
Amitriptyline (Elavil; Zeneca, Wilmington, DE) 25-150 50-150
Triazolopyridine
Trazadone (Desyrel; Apathecon, Princeton, N J) 25-400
Serotonin-specific reuptake inhibitors
Flnoxetine (Prozac; Dista, Indianapolis, IN) 20-40
Sertraline (Zoloft; Pfizer Inc., New York, NY) 25-200
Peroxetine (Paxil; Smith Kline Beecham Pharmaceuti- 10-50
cals, Philadelphia, PA)
Bupropion (Wellbutrin; Glaxo Wellcome Inc., Research 150-300
Triangle Park, NC)
Venlafaxine (Effexor; Wyeth-Ayerst, Philadelphia, PA) 75-375

etine treats depression as well as producing significant
functional recovery. 31 Other serotonin-specific release in-
hibitors (SSRI) may also be useful agents in treating
poststroke depression. Citalopram (Forest Pharmaceuti-
cals, St. Louis, MO), the only SSRI tested for poststroke
depression, is not available in the United States. 32 Psycho-
therapy may also be helpful in nonaphasic stroke survi-
vors. A psychiatric consultation may be necessary for
stroke survivors in which monotherapy is ineffective or
who have psychiatric histories.
References
1. Goldstein D. The electrocardiogram in stroke with rela-
tionship to pathophysiological type and comparison to
prior tracings. Stroke 1979;10:253,
2. Sen S, Tstober T, Thonnes W, et al. Electrocardiographic
changes following acute ischemic or hemorrhagic stroke.
In: DiPasquale G, Pinelli G, eds. Heart-brain interactions.
Berlin: Springer-Verlag, 1992:13-18.
3. Canadian Cooperative Study Group. Randomized trial of
aspirin and sulfinpyrazone in threatened stroke. N Engl J
Med 1978;299:53-59.
4. Roth EJ, Mueller K, Green D. Cardiovascular response to
physical therapy in stroke rehabilitation. NeuroRehabil
1992;2:7-15.
5. Veis SL, Logemann JA. Swallowing disorders in persons
with cerebrovascular accident. Arch Phys Med Rehabil
1985;66:372-375.
6. Logemann JA. Evaluation and treatment of swallowing
disorders. Boston: College-Hill Press, 1983.
7. Horner J, Massey EW. Silent aspiration following stroke.
Neurology 1988;38:317-319.
8. Splaingard ML, Hutchins B, Sulton LD, et al. Aspiration
in rehabilitation patients: Videofluoroscopy vs. bedside
clinical assessment. Arch Phys Med Rehabil 1988;69:637-
640.
9. Chen MYM, Ott DJ, Peele VN, et al. Oropharynx in
patients with cerebrovascular disease: Evaluation with
videofluoroscopy. Radiology 1990;176:641-643.
10. Smithard DG, O'Neill PA, Park C, et al. Complications
and outcome after acute stroke. Stroke 1996;27:1200-1204.
11. Johnson ER, McKenzie SW, Sievers A. Aspiration pneumo-
nia in stroke. Arch Phys Med Rehabil 1993;74:973-976.
12. Teasell RW, McRae M, Marchuk Y, et al. Pneumonia
associated with aspiration following stroke. Arch Phys
Med Rehabil 1996;77:707-709.
13. Kitamura T, Ito K. Acute gastric changes in patients with
acute stroke. With reference to gastroendoscopic find-
ings. Stroke 1976;7:460-463.
14. Driks MR, Craven DE, Celli BR, et al. Nosocomial
pneumonia in intubated patients given sucralfate as
compared with antacids and histamine type 2 blockers. N
Engl J Med 1987;317:1376-1382.
15. Kilpatrick CJ, Davis SM, Tress BM, et al. Epileptic
seizures at the onset of acute stroke. Arch Neuro11990;47:
1517-1560.
16. Shinton RA, Gill JS, Melnick SC. The frequenc36 and
prognosis of epileptic seizures at the onset of stroke. J
Neurol Neurosurg Psychiatry 1988;51:273-276.
17. Ginsberg JS. Management of venous thromboembolism.
N Engl J Med 1996;335:1816-1828.
18. Pambianco G, Orchard T, Landau P. Deep venous throm-
bosis: Prevention in stroke patients during rehabilitation.
Arch Phys Med Rehabil 1995;76:324-330.
19. Bromfield EB, Reding MB. Relative risk of deep venous
thrombosis or pulmonary embolism post-stroke based
upon ambulatory status. J Neurol Rehab 1988;2:51-56.
20. Turpie AG. Prophylaxis of venous thromboembolism in
stroke patients. Semin Thromb Hemost 1997;23:155-157.
21. Hyers TM, Hull RD, Weg JG. Antithrombotic therapy for
venous thromboembolic disease. Chest 1995;108:335S-
351S (suppl).
196
22. Levine M, Gent M, Hirsh J, et al. A comparison of
low-molecular-weight heparin administered primarily at
home with unfractionated heparin administered in the
hospital for proximal deep-vein thrombosis. N Engl J
Med 1996;334:677-681.
23. Nitti VW, Adler H, Combs AJ. The role of urodynamics in
the evaluation of voiding dysfunction in men after
cerebrovascular accident. J Uro11996;155:263-266.
24. House A, Dennis M, Warlow C, et al. Mood disorders
after stroke and their relation to lesion location. Brain
1990;113:1113-1129.
25. Stern RA, Bachman DL. Depressive symptoms following
stroke. Am J Psychiatry 1991;148:351-356.
26. Starkstein SE, Fedoroff JP, Price TR, et al. Catastrophic
reaction after cerebrovascular lesions, frequency,, corre-
lates, and validation of a scale. J Neuropsychiatry Clin
Neurosci 1993;5:189-193.
R. D. Z O R O W I T Z A N D G. E. TIETJEN
27. Coll P, Erickson RV. Mood disorders associated with sh:oke.
Phys Med Rehab: State of the Art Reviews 1989;3:619-628.
28. Astrom M, Adolfsson R, Asptund K. Major depression in
stroke patients. A 3-year longitudinal study. Stroke 1993;
24:976-982.
29. Reding MJ, Orto LA, et al. Antidepressant therapy after
stroke: A double-blind trial. Arch Neuro11986;43:763-765.
30. Lipsey JR, Robinson RG. Nortriptyline treatment of
post-stroke depression: A double-blind study. Lancet
1984;1:297-300.
31. Dam M, Tonin P, De Boni A, et al. Effects of fluoxetine and
maprotiline on functional recovery in poststroke hemiple-
gic patients undergoing rehabilitation therapy. Stroke
1996;27:1211-1214.
32. Andersen G, Bestergaard K, Lauritzen L. Effective treat-
ment of poststroke depression with the selective seroto-
nin reuptake inhibitor citalopram. Stroke 1994;25:1099-1104.