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Stroke-related pulmonary complications and abnormal respiratory patterns

Stroke-related pulmonary complications and abnormal respiratory patterns Find Print

TOPIC OUTLINE
Stroke-related pulmonary complications and abnormal
INTRODUCTION respiratory patterns
PNEUMONIA
Authors Section Editor Deputy Editor
Prevention
Julio A Chalela, MD Jose Biller, MD, FACP, John F Dashe, MD,
MECHANICAL VENTILATION Teresa L Jacobs, MD FAAN, FAHA PhD
OXYGEN DESATURATION
Disclosures
Sleep apnea
NEUROGENIC PULMONARY
EDEMA Last literature review version 19.3: Fri Sep 30 00:00:00 GMT
2011 | This topic last updated: Thu Jul 16 00:00:00 GMT
ABNORMAL RESPIRATORY
2009 (More)
PATTERNS
INTRODUCTION — Medical complications of acute ischemic
Cheyne-Stokes respiration
stroke are common and often lead to poor clinical outcomes. The
Periodic breathing
frequency of these complications must be recognized so that
Ataxic breathing
preventive strategies and appropriate treatment are employed.
Apneustic breathing
Gasping The major pulmonary complications of acute stroke will be
Central neurogenic reviewed here. Other medical complications of acute stroke are
hyperventilation discussed separately. (See "Medical complications of stroke" and
Apnea (aventilation) "Cardiac complications of stroke".)
REFERENCES PNEUMONIA — Pneumonia is one of the most common
GRAPHICSView All
respiratory complications of acute stroke, occurring in about 5
percent of patients [1]. The incidence of stroke-related
FIGURES pneumonia appears to be much higher in patients with acute
Stroke breathing patterns ischemic stroke admitted to a neurologic intensive care unit and
TABLES in those who require nasogastric tube feeding (21 and 44
Causes of NPE percent, respectively) [2,3].

RELATED TOPICS Pneumonia is the most common cause of fever within the first 48
Aspiration pneumonia in hours of acute stroke, and it is the most common medical
adults complication two to four weeks after a supratentorial ischemic
infarction [1,4,5]. In addition, retrospective data suggest that
Cardiac complications of
pneumonia and respiratory illness are the most frequent
stroke
diagnoses leading to hospital readmission in stroke survivors
Cheyne-Stokes breathing and throughout the first five years after ischemic stroke [6].
obstructive sleep apnea in
heart failure In a prospective study of 412 patients with acute stroke,
Control of ventilation independent risk factors for in-hospital pneumonia were age >65
years, dysarthria or no speech due to aphasia, severe poststroke
Diagnosis and treatment of
disability, cognitive impairment, and an abnormal water swallow
oropharyngeal dysphagia
test [7]. In an earlier prospective study of 124 patients with
Disorders of ventilatory
acute stroke treated in the intensive care unit, risk factors were
control
mechanical ventilation, abnormal chest radiograph on admission,
Hypoxic-ischemic brain injury and dysphagia [2]. In patients requiring nasogastric feeding,
Medical complications of independent risk factors for pneumonia were facial palsy and
stroke deceased level of consciousness [3].
Neurogenic pulmonary edema
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Aspiration is the cause of about 60 percent of post-stroke

pneumonia [1]. Aspiration pneumonia refers to the pulmonary
consequences resulting from the abnormal entry of fluid,
particulate exogenous substances, or endogenous secretions into
the lower airways. Most pneumonia arises following the
"aspiration" of microorganisms from the oral cavity or
nasopharynx.

Aspiration pneumonia following stroke is usually due to stroke-

related dysphagia (ie, impairment of motor and sensory
mechanisms involved in deglutition) or to a decreased level of
consciousness that results in compromise of the cough reflex and
glottic closure. (See "Medical complications of stroke", section on
'Dysphagia and aspiration'.)

The dependent pulmonary segments are usually affected in

aspiration pneumonia. The most common sites of involvement are
the posterior segments of the upper lobes or apical segments of
the lower lobes if aspiration occurs while recumbent, and the
lower lobes if the patient aspirates while upright or semi-upright.
Causative organisms and treatment of aspiration pneumonia are
discussed separately. (See "Aspiration pneumonia in adults".)

Patients with stroke-related pneumonia have a higher mortality

and a poorer long-term outcome when compared to patients
without pneumonia.

Prevention — Measures to prevent aspiration pneumonia in

patients with dysphagia include initial nulla per os (NPO) status
and subsequent dietary modifications for those who have
persistent dysphagia. (See "Diagnosis and treatment of
oropharyngeal dysphagia".)

Thus, screening on admission for swallowing difficulty is probably

the most important measure to prevent pneumonia in patients
with acute stroke. Use of a formal screening protocol for
dysphagia for all patients admitted with stroke has been
associated with a significantly decreased risk of aspiration
pneumonia. (See "Medical complications of stroke", section on
'Dysphagia and aspiration'.)

A number of other interventions (eg, positioning, drugs, oral

hygiene, tube feeding, influenza vaccination, pneumococcal
vaccination) have been proposed to prevent aspiration in
hospitalized and nonhospitalized elderly patients. However, no
clinical trials have evaluated the utility of these measures
specifically in patients with stroke. (See "Aspiration pneumonia in
adults" and "Risk factors and prevention of hospital-acquired,
ventilator-associated, and healthcare-associated pneumonia in
adults" and "Pneumococcal vaccination in adults" and "Seasonal
influenza vaccination in adults".)

Angiotensin converting enzyme (ACE) inhibitors prevent the

breakdown of substance P, an important mediator of the cough
reflex, but there is conflicting evidence regarding the utility of
ACE inhibitors for preventing pneumonia in patients with stroke.
Data from several observational studies suggest that ACE

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inhibitors significantly lower the risk of aspiration pneumonia in

elderly Japanese patients with stroke [8,9]. However, post-hoc
analysis of a multinational randomized controlled trial found that
ACE inhibitor use was associated with a statistically nonsignificant
reduced risk of pneumonia in patients with a history of stroke or
TIA; a subgroup analysis found significant benefit for patients of
Asian ethnicity only [10]. In addition, a case-control trial from the
Netherlands reported that ACE inhibitor use was not associated
with a decreased incidence of pneumonia in a general (mostly
white) population [11].

MECHANICAL VENTILATION — Intubation and mechanical

ventilation of patients with ischemic stroke is usually performed
for inability to protect the airway, pulmonary edema, or seizures.
In a single-center retrospective series of 24 patients with
hemispheric ischemic stroke, mechanical ventilation was initiated
for bilateral pulmonary edema from heart failure (n = 10),
progression to stupor from brain swelling (n = 8), and
generalized seizures or status epilepticus (n = 6) [12].

The morbidity and mortality in patients intubated after acute

stroke is very high. In the study just cited, death occurred in 17
of the 24 patients (71 percent) [12]. Another retrospective study
found that among a group of 74 patients with ischemic stroke
receiving mechanical ventilation, 56 (76 percent) were either
dead or had severe disability requiring nursing home placement
at discharge [13].

Intubation is infrequently required in ischemic stroke, but the rate

may be more frequent in intracerebral hemorrhage. As an
example, intubation rates in one retrospective study for ischemic
stroke and intracerebral hemorrhage were 6 and 30 percent,
respectively [13].

Intubation and mechanical ventilation are indicated after acute

stroke for decreased level of consciousness from effects of the
stroke or seizure with inability to protect the airway. Additional
indications include partial airway obstruction, hypoventilation,
aspiration pneumonia, or pulmonary edema. (See "Overview of
mechanical ventilation" and "Physiologic and pathophysiologic
consequences of mechanical ventilation", section on 'Central
nervous system'.)

OXYGEN DESATURATION — In patients with acute hemiparetic

ischemic and hemorrhagic stroke, oxygen desaturation detected
by continuous pulse oximetry is associated with increased age,
higher National Institutes of Health Stroke Scale (NIHSS) score,
and the presence of dysphagia [14]. Even patients with stroke
deemed safe to eat have a greater likelihood of desaturation after
completion of a meal than do elderly controls [15]. Patients with
a history of cardiac and pulmonary diseases are also at higher
risk for desaturation [14]. In these studies, most patients were
asymptomatic during periods of desaturation, suggesting that
silent desaturation may be more common than previously
recognized. (See "Pulse oximetry".)

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Sleep apnea — The relationship of sleep disordered breathing

(including both obstructive sleep apnea and central sleep apnea
syndrome) as a possible risk factor for stroke and as a possible
complication of stroke is discussed separately. (See "Sleep related
breathing disorders and stroke".)

NEUROGENIC PULMONARY EDEMA — Neurogenic pulmonary

edema (NPE) is an increase in interstitial and alveolar fluid that
occurs in the setting of head trauma, seizures, or stroke,
particularly subarachnoid hemorrhage (table 1) [16]. The alveoli
are flooded with proteinaceous, hemorrhagic fluid.
Radiographically, it is indistinguishable from hydrostatic
pulmonary edema [17,18]. The pathophysiology is not clear, but
hemodynamic and permeability factors are cited. (See
"Neurogenic pulmonary edema".)

NPE occurs in a minority of patients with acute stroke, usually

following subarachnoid hemorrhage or uncontrolled seizures [19].

Animal studies suggest that a sudden increase in intracranial

pressure or hypothalamic lesions may result in a massive
sympathetic discharge with redistribution of blood to the
pulmonary circulation resulting in high pulmonary pressures and
increased permeability [16-18,20]. Increased sympathetic tone
may lead to increased afterload, left ventricular failure, elevated
pulmonary wedge pressure, and transudation of fluid into the
alveoli. Reduced left ventricle relaxation, excessive venous return,
and direct neurogenic cardiac inhibition have also been postulated
as possible mechanisms [16,20].

Some authors have hypothesized a "blast injury" to the

endothelium, in which the sudden increase in pulmonary capillary
pressure leads to mechanical disruption of the endothelium and
increased capillary permeability. Extravascular pulmonary water
may be increased even in patients with normal wedge pressures
[16]. NPE has also been attributed to acute constriction of
lymphatic vessels, which leads to decreased lymphatic flow and
filling of the interstitial space and eventually the alveoli [16].

NPE develops abruptly and progresses quickly after the onset of

the neurologic insult. In contrast, aspiration pneumonia usually
takes longer to become manifest. The typical patient with NPE is
dyspneic, tachycardic, and hypertensive, with bilateral rales. The
chest radiograph reveals bilateral infiltrates that tend to be more
interstitial than alveolar, and the cardiac silhouette may appear
normal or enlarged [16,17]. At the time of diagnosis, the cardiac
filling pressures are usually normal. Central to the diagnosis of
NPE is a strong index of suspicion when pulmonary congestion
develops in patients with head trauma (especially with elevated

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intracranial pressure), seizures or status epilepticus, or

subarachnoid hemorrhage [16,18,20].

Most cases of NPE resolve spontaneously and are well tolerated,

but the condition can be fatal in severe cases.

Treatment of NPE is largely supportive and directed mainly

towards treatment of the underlying neurologic condition
[16,18,20]. Mechanical ventilation often has already been
instituted as part of the treatment for the primary neurologic
disorder. Many authors recommend positive end expiratory
pressure, but theoretical concerns exist about decreasing cerebral
perfusion in patients with elevated intracranial pressure.

Dobutamine has been used successfully and is believed to act by

reducing afterload and by increasing cardiac contractility [17].
Osmotic diuretics may be useful in relieving both the cerebral and
pulmonary edema [16]. Other therapeutic measures include loop
diuretics, alpha-adrenergic blockers such as phentolamine, and
antihistamines to attempt to reverse increased pulmonary
vascular permeability.

In some patients, florid pulmonary edema does not occur, but

transient respiratory difficulty and hypoxemia with a normal chest
radiograph are evident soon after a stroke. The term "neurogenic
pulmonary dysfunction" has been used to describe this condition.
Some authors consider neurogenic pulmonary dysfunction a more
benign variant of NPE, and it may reflect neural disruption of
normal ventilation-perfusion relationships, microatelectasis,
and/or retained secretions [16].

ABNORMAL RESPIRATORY PATTERNS — Abnormal respiratory

patterns are a common consequence of stroke. Abnormal
breathing patterns are recognized in approximately 60 percent of
patients with acute neurologic disorders, including acute stroke.
In a subset of these patients, underlying cardiac and respiratory
abnormalities account for the abnormal breathing pattern
[21,22].

Among the recognized abnormal respiratory patterns are Cheyne-

Stokes breathing, periodic breathing, central neurogenic
hyperventilation, apneustic breathing, central sleep apnea, ataxic
breathing, and failure of automatic breathing (Ondine's curse)
[21] (figure 1).

Abnormal breathing patterns are more common among patients

with impaired consciousness, with severe deficits, during sleep,
and in patients with medullary infarcts [19,22]. Most respiratory
patterns do not have prognostic significance or imply involvement
of specific areas of the central nervous system [19,21,22]. Only
sustained tachypnea with low PaCO2 is associated with poor
outcome [19]. (See "Control of ventilation" and "Disorders of
ventilatory control".)

Cheyne-Stokes respiration — Cheyne-Stokes respiration is

characterized by recurrent central apnea alternating with a
crescendo-decrescendo pattern of tidal volume. It is the most
commonly recognized abnormal respiratory pattern after stroke,
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but in approximately 90 percent of patients it reflects underlying

cardiopulmonary disease [22]. (See "Cheyne-Stokes breathing
and obstructive sleep apnea in heart failure".)

Initially believed to be due to bilateral forebrain disease or diffuse

bihemispheric disease, Cheyne-Stokes respiration is now known
to occur with unilateral hemispheric and brainstem infarcts
[19,22]. Cheyne-Stokes respiration has little prognostic value
[19,22]. However, hypocapnia is almost always present and may
require treatment to prevent cerebral vasoconstriction and
exacerbation of the underlying neurologic condition. Hypoxemia is
frequently present due to concomitant heart and lung disease.

Periodic breathing — Periodic breathing, a variant of Cheyne-

Stokes respiration, is characterized by regular, recurrent cycles of
changing tidal volumes in which the lowest tidal volume is less
than half the maximal tidal volume in that cycle [19]. It is the
most frequent abnormal respiratory pattern directly related to
stroke rather than underlying systemic disease, occurring in
approximately 25 percent of patients [19,22]. Periodic breathing
may be more common among patients with subarachnoid
hemorrhage [19].

Ataxic breathing — Ataxic breathing is a rare respiratory

pattern characterized by an erratic rate and depth of breathing,
alternating with interspersed episodes of apnea [23]. It is the
only respiratory pattern with true localizing value and is indicative
of a medullary lesion. It may occur in patients with
neurodegenerative disorders (such as Shy-Drager syndrome) but
when developing acutely should always raise suspicion for a
medullary stroke.

Ataxic breathing is caused by dysfunction of the dorsal respiratory

neurons in the medulla that control the rhythmicity of breathing.
In one case series of 227 patients, ataxic breathing was found in
all 12 patients with medullary strokes [19]. Ataxic breathing is
not necessarily associated with poor outcome.

Apneustic breathing — Apneustic breathing is characterized by

sustained deep inspiration lasting several seconds followed by a
rapid exhalation and a brief post-expiratory phase. Its presence
reflects dysfunction of the inspiratory cut-off mechanism localized
in the inferomedial posterior region of the pons [23]. The pattern
is rarely observed because patients usually have severe bulbar
dysfunction and require mechanical ventilation [22,23]. Weaning
from mechanical ventilation is often difficult, and long-term
ventilation via tracheostomy is often necessary.

Gasping — Gasping is an abnormal breathing pattern

characterized by an attenuated inspiratory period followed by a
disproportionately long period of expiration. Associated abnormal
involuntary movements such as platysma contraction and neck
hyperextension are common [19,23]. Gasping is more commonly
seen in medullary strokes but overall has poor localizing value.
Respiratory failure almost invariably ensues.

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Central neurogenic hyperventilation — Central neurogenic

hyperventilation is a rare ventilatory disorder characterized by
rapid deep breaths leading to hypocapnia [24]. The diagnosis
cannot be made in the presence of radiographic evidence of
pulmonary congestion or sepsis nor in the presence of respiratory
stimulants. It may occur following stroke, head trauma, and brain
tumors. When the pH is higher than 7.46 and the PaCO2 lower
than 35 mmHg, the prognosis is generally poor, particularly if the
patient is obtunded [25]. The mechanism of hyperventilation is
not clear, but the frequent association between cerebral
neoplasms and central hyperventilation as well as the presence of
acidic CSF suggests that hydrogen ions in the cerebrospinal fluid
may stimulate chemosensitive areas in the brainstem and
produce rapid respiration [26]. (See "Control of ventilation".)

Apnea (aventilation) — Complete apnea following stroke is

extremely rare in the absence of brain death, but it may be seen
with the development of medullary or high spinal cord lesions
[23,27]. It has been described rarely after unilateral brainstem
infarction [27]. It is diagnosed by determining absent respirations
in fully alert patients after stimulation with CO2, in a similar
manner to that performed when brain death is suspected [27].
(See "Hypoxic-ischemic brain injury".)

The prognosis for recovery is generally poor. Complete apnea

during sleep with normal ventilation during wakefulness has been
termed Ondine's curse. It occurs due to an interruption of the
brainstem respiratory generators or their spinal projections but
with preserved integrity of corticospinal pathways which control
the more voluntary aspects of respiratory control. Ondine's curse
is generally treated with mechanical ventilation during sleep. In
some patients spontaneous improvement may occur [21,23].
(See "Disorders of ventilatory control".)

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