Although pulmonary complications are a common and well-known problem in SCI, there is little information about their management. Current practice is mainly based on clinical experience and expert opinion. Management of care with appropriate interventions and prevention of pulmonary complications of SCI will be discussed with, support for a return to the maximal level of functioning.
After completing this course, the learner will be able to:
Respiratory complications are the main cause of morbidity and mortality in the acute phase of spinal cord injury (SCI), with an incidence of 36% to 83%. Approximately two-thirds of patients with acute SCI will experience complications such as atelectasis, pneumonia, and respiratory failure, which will require mechanical ventilation.1,2The degree of respiratory dysfunction is related to the extent and level of the neurological injury, in such a way that high cervical and thoracic injuries are at the highest risk.3 Various studies have suggested an increasing trend in cervical injuries, in particular, C1–C4 injuries, with an increased rate of SCI resulting in mechanical ventilation dependency.4,5
Respiratory dysfunction that leads to respiratory complications in SCI may be related to 3 factors6:
Although pulmonary complications are a common and well-known problem in SCI, there is little information about their management. Current practice is mainly based on clinical experience and expert opinion.7 Promptness of prevention and treatment, as well as, a multidisciplinary treatment approach by professionals experienced in the treatment of SCI, reduces respiratory complications.
Patients with high SCI can sometimes utilize oral, pharyngeal, and laryngeal muscles for short-term ventilation by projecting boluses of air past the glottis (glossopharyngeal breathing), although these muscles are not traditionally thought of as muscles of respiration.
Normally, expiration is passive and does not require use of these muscles. However, these muscles are crucial when forced exhalation is needed, such as during exercise or coughing. When the ability to generate forced exhalation for coughing is impaired, removal of airway secretions is ineffective. In addition, these muscles contribute to normal function of the diaphragm in three important ways9-13:
Movement of the Rib Cage during Inspiration (Figure 2)
Movement of the Rib Cage during Expiration (Figure 2)
Movement of the Rib Cage During Respiration
How to remember what happens to the intercostal muscles during respiration:
The process of inspiration involves contraction of the diaphragm and the external intercostal muscles that allow the chest cavity to expand. At high levels of ventilator activity, the accessory muscles are recruited to aid in this process. Expiration is largely passive but can be augmented by the forceful contraction of the muscles of the abdominal wall.6,14
The degree of respiratory failure associated with traumatic injuries to the spinal cord depends on the level of the spinal lesion. In general, functional impairment worsens as the level of injury is more rostral (i.e. superior in relationship to areas of the spinal cord). In addition, a complete SCI, defined as the absence of motor or sensory function below the injury (classified as American Spinal Injury Association (ASIA) score A), results in greater functional impairment than incomplete injuries (ASIA scores B–D). Other factors that are associated with pulmonary complications are age, preexisting medical illnesses, and associated major traumatic injuries.
Spirometry (meaning the measuring of breath) is the most common of the pulmonary function tests (PFTs). It measures lung function, specifically the amount (volume) and/or speed (flow) of air that can be inhaled and exhaled.
Spirometry generates pneumotachographs, which are charts that plot the volume and flow of air coming in and out of the lungs from one inhalation and one exhalation.
There are four lung volumes and four lung capacities. A lung capacity consists of two or more lung volumes.
The lung volumes are:
The four lung capacities are:
Individuals with SCI exhibit reduced lung volumes and flow rates as a result of respiratory muscle weakness. Changes in spirometric measurements in SCI are dependent on injury level and posture.14,15
The time factor is important because pulmonary function of quadriplegic/tetraplegic patients should improve as the muscle flaccidity associated with the initial phase of spinal shock converts to the spasticity of paralyzed muscles. This increase in muscle tone affects both intercostal and abdominal muscles and results in a decline in the end-expiratory volume and more effective diaphragmatic contraction.
Injury to the cervical or thoracic spinal cord affects the spinal nerves that innervate respiratory muscles. The diaphragm, the major muscle of inspiration, receives its innervation from the third, fourth, and fifth cervical spinal segments (Figure 3).
The respiration of patients with diaphragmatic paralysis commonly exhibits a paradoxical movement of the abdomen: the abdominal wall retracts during inspiration and protrudes during the expiration phase.
After the initial stage of spinal shock has passed, patients with quadriplegia/tetraplegia may develop abnormal spinal reflexes that involve the abdominal muscles. This spastic contraction reduces the elastic properties of the abdominal compartment of the respiratory system.
The main physiologic consequence of expiratory muscle paralysis is an impaired cough. The cough reflex is preserved in cervical and upper thoracic SCI. However, the inability to cough adequately is caused by a weakness of the major muscles of expiration thus resulting in an accumulation of secretions.15
In acute quadriplegia/tetraplegia, some patients develop an unexplained production of excessive and tenacious bronchial mucus. Speculation presupposes that the bronchial mucus hypersecretion is caused by the unopposed vagal activity, perhaps related to the initial disappearance of peripheral sympathetic nervous system tone.21 This parasympathetic imbalance which predisposes the patient to atelectasis, pneumonia, and potentially respiratory failure include22-25:
Pulmonary physiologic changes due to SCI are related to the extent of neurological impairment. The American Spinal Injury Association Impairment Scale (AIS) is used to classify the degree of impairment that is based on strength in key muscles and on a sensory examination (Table 1).26
|American Spinal Injury Association (ASIA) Impairment Scale (AIS)* A Complete cord injury. No motor or sensory function is preserved in the sacral segments S4-5. B Sensory incomplete. Sensory but not motor function is preserved below the neurologic level and includes the sacral segments (light touch or pin prick at S4-5 or deep anal pressure) AND no motor function is preserved more than three levels below the motor level on either side of the body. C Motor incomplete. Motor function is preserved below the neurologic level and more than half of key muscle functions below the neurologic level of injury have a muscle grade <3 (Grades 0 to 2). D Motor incomplete. Motor function is preserved below the neurologic level and at least half or more of key muscle functions below the neurologic level of injury have a muscle grade ≥3. E Normal. Sensation and motor function are graded as normal in all segments and the patient had prior deficits.|
*Muscle function is graded using the International Standards for Neurologic Classification of Spinal Cord Injury.
*For an individual to receive a grade of C or D (i.e., motor incomplete status), he/she must have either:
*Patients without an initial spinal cord injury do not receive an AIS grade.
The patient’s strength in key muscle groups is assessed and graded. A muscle grade of 5/5 is normal, and a grade of 3/5 means the muscle can be moved against gravity.
Complete motor SCI includes: (see Table 1 above)
Incomplete motor SCI includes: (see Table 1 above)
With quadriplegia/tetraplegia, there is injury to at least one of the eight cervical segments of the spinal cord. With paraplegia, there is injury in the thoracic, lumbar, or sacral regions.
Pulmonary physiologic changes following SCI include:
In describing the occurrence of these changes, it is useful to consider SCI in three phases:
Immediately after SCI, flaccid paralysis occurs and affects all muscles caudal to the level of injury. This physiologic state is known as spinal shock. Subsequent improvements in pulmonary function are due primarily to27-31:
Starting from several days to up to four to six weeks, spinal reflexes return and eventually become exaggerated as the syndrome of spasticity develops.
The timing of respiratory failure was examined in 72 patients with traumatic cervical SCI.32 Among those who required mechanical ventilation, 90% of the episodes of respiratory failure occurred within the first three days after SCI. Improvement in respiratory muscle performance after SCI largely occurs in the first year following injury.31,33-35
The extent of ventilatory muscle impairment depends upon the degree and location of the injury, as well as, the duration of time since the injury. The higher the level and more complete the injury, the more likely that there will be respiratory muscle dysfunction (Table 2).
|Spinal Cord Level||Muscle Involvement||Effect on Respiration||Clinical Consequence|
|C1-3||Complete paralysis of all respiratory muscles||Vital capacity only 5-10% of normal. Absent cough.||Apnea and immediate death.|
|C3-6||Varied Impairment of diaphragmatic contraction||Vital capacity 20% of normal. Weak and ineffective cough.||Ventilation necessary in acute stages. Majority will be weaned from mechanical ventilation.|
|C6-8||Diaphragm and accessory cervical inspiratory muscles intact. Intercostals and abdominal muscles intact.||Expiration entirely passive. Secretion retention. No respiratory failure unless co-existing lung/chest injury/illness.|
|T2-4||Vital capacity 30-50% normal. Weak cough.|
Ventilatory muscles innervated below the level of a complete SCI are completely nonfunctional (AIS A or B), while the degree of ventilatory muscle compromise is variable in patients with incomplete injuries (AIS C or D) (see Table 1 above).
Lung and chest wall compliance, when measured 1 to 12 months after SCI, is reduced in patients with quadriplegia/tetraplegia, compared with normal subjects.39 The decrease in compliance has been attributed to the accompanying reduction in lung volumes and possibly changes in surfactant that can occur with ventilation at reduced lung volumes.35 Although the abdomen is highly compliant in quadriplegia/tetraplegia, the rib cage compartment of the chest wall is stiff because of intercostal muscle spasticity and ankylosis of the rib articulations with the spine and sternum. It is believed that ankylosis of rib articulations results from an inability to inspire to total lung capacity due to inspiratory muscle weakness.35,39-42
Subjects with quadriplegia/tetraplegia demonstrate reversible expiratory airflow limitation, which is usually only apparent when a bronchodilator is administered, as the predominant abnormality is a restrictive ventilatory defect. Loss of postganglionic sympathetic innervation to the airways is a potential mechanism contributing to airflow limitation, although the functional significance of direct sympathetic airway innervation is thought to be minor or absent. The reversibility of this airflow limitation was demonstrated by the administration of inhaled ipratropiu bromide, an anticholinergic agent, which caused an increase in expiratory airflow.43,44 This reversibility suggests that unopposed vagal cholinergic (bronchoconstrictor) activity also contributes to airflow limitation. An alternate explanation is reduced airway smooth muscle relaxation secondary to lack of inhalation to a normal total lung capacity.43-47 Abnormalities of sympathetic or parasympathetic nervous system activity may also be responsible for airway hyperresponsiveness noted after SCI causing quadriplegia/tetraplegia.48
Abnormalities of sympathetic or parasympathetic nervous system activity may also be responsible for airway hyperresponsiveness noted after SCI causing quadriplegia/tetraplegia.48
Individuals with quadriplegia/tetraplegia have an abnormally small increase in ventilatory drive in response to hypercapnia.49,50 As an example, a study of nine quadriplegic/tetraplegic subjects and eight able-bodied controls found that the ventilatory response to hypercapnia among quadriplegics/tetraplegics was approximately one-fourth that of the controls.50 The mechanism for a blunted response to hypercapnia is not fully explained by respiratory muscle weakness, as patients with comparable respiratory muscle weakness due to other causes do not exhibit the same blunted response.
One hypothesis is that the blunted response is related to a decrease in blood pressure in the sitting position. This was examined in a study of 12 subjects with quadriplegia/tetraplegia that found a normal ventilatory response to hypercapnia in the supine position and a reduced response in the sitting position.51 The ventilatory response was normal in the supine position, but decreased in the sitting position. The ventilatory response correlated better with blood pressure changes than with improved chest cage mechanics associated with the supine position.
Sleep-disordered breathing has been reported in individuals with SCI and is predominantly obstructive or a combination of obstructive and central.
Some of the techniques for performing PFTs need to be modified in the patient with a SCI. In addition, changes in respiratory muscle performance following SCI result in abnormal PFT results that can be predicted based on the level and completeness of SCI and other factors.
Standardized techniques for performing PFTs and calculating predicted values need to be adjusted due to the practical challenges posed by SCI patients. For example:
The objective of monitoring diaphragmatic function in patients with acute SCI is to help in the decisions on managing the airway.
The two most important markers that predict the need for intubation are the level of the injury and the ASIA classification.
The goals for patients who are intubated are to:
The studies on phrenic nerve conduction, although essential for assessing the possibility of using diaphragmatic pacemakers, do not properly differentiate between patients who can be weaned and those who become ventilator dependent. Pathological studies do not distinguish between neuropraxia, atrophy, and axonotmesis. Similarly, normal results do not guarantee a sufficient diaphragmatic force.66 For similar reasons, diaphragmatic fluoroscopy does not predict the possibility of weaning from the respirator and should not be used as a prognostic marker.66
In recent years, interest has grown in the use of ultrasound as a noninvasive, bedside approach to evaluating diaphragm function.67,68 Vivier et al.69 found that the relation between diaphragm thickness measured by inspiration and expiration using ultrasound correlated adequately with the work of breathing during noninvasive ventilation. Kim et al.70 recently demonstrated that diaphragm dysfunction diagnosed by M-mode ultrasound predicted weaning failure. However, the use of diaphragm ultrasound in patients with acute spinal cord injury has not been prospectively studied.
As with monitoring the need for intubation, spirometry with measurement of the VC and the maximum negative inspiratory pressure are the best bedside markers for initiating weaning.6,66,71
More direct measures of diaphragmatic function such as transdiaphragmatic pressure and negative inspiration force diaphragm needle electromyography are invasive and of little use in clinical practice.6,66 Noninvasive studies such as the estimation of diaphragm dysfunction using airway occlusion pressure during magnetic stimulation of the phrenic nerves are correlated with the duration of ventilatory support but their use in clinical practice is unknown.72
To ventilate a patient with acute SCI, the peculiarities that exclusively affect these patients must be considered.
Although patients with acute traumatic SCI can usually be said to have “healthy” lungs,71 up to 60% of the patients may have sustained associated chest trauma.
In this continuing education course we will focus on the management of patients with acute SCI and “healthy” lungs. In contrast to the abundance of the literature on mechanical ventilation in acute pulmonary lesions, the literature on the management of specific complications of acute SCI is very limited and of low quality.
The preservation of diaphragmatic function should be a primary objective in all patients undergoing mechanical ventilation. Diaphragmatic dysfunction is a common cause of weaning failure.73 The consequences of this dysfunction in patients who depend almost exclusively on the diaphragm to maintain effective inspiration are clear.
Although the negative effect of mechanical ventilation on the respiratory musculature has been known for many years, the specific diaphragmatic impairment was recently reported by Vassilakopoulos and given the name “ventilator-induced diaphragmatic dysfunction” (VIDD).73,74
Diaphragmatic atrophy occurs early after only 18 hours of inactivity and appears to be related to an increase in muscle proteolysis.75,76 Diaphragmatic atrophy increases with ventilation time and causes a progressive reduction in diaphragmatic function.
VIDD has been linked to diaphragmatic inactivity caused by controlled ventilation. It has been shown in animal models that assist modes attenuate VIDD.77 These findings have not been confirmed in humans, and no difference has been found in the onset of VIDD between patients ventilated with pressure control and those ventilated with pressure support.78
Patients ventilated with pressure control is often used. Pressure support ventilation (PSV) is often avoided due to the lack of evidence for a better prognosis and the risk of inadequate ventilation and exhaustion in patients with reduced respiratory reserve. The objective is to maintain some level of diaphragmatic contraction, ensuring total respiratory support. Achieving this objective requires adequate interaction between the patient and the respirator and the avoidance of asynchrony.
Asynchrony can occur at any time in the respiratory cycle. With a perfect patient-ventilator interaction, the respirator should trigger in synchrony with the electrical impulses originating in the central nervous system.79 Up to 25% of patients present some type of asynchrony while on mechanical ventilation.80 Most of the ventilators in use today trigger inspiration by a signal measured within the ventilator circuit. The signal may be a fall in the pressure of the airway (pressure trigger) or a variation in the flow signal (flow trigger). Although it was initially believed that the flow trigger produced a better patient-respirator interaction, with current respirators, no differences have been found.81-83
In recent years, a new modality of ventilation has been reported: neutrally adjusted ventilator assist (NAVA).84 In this modality, the signal used by the respirator to deliver assistance is not the flow or the airway pressure, but rather the diaphragmatic electromyogram signal collected from electrodes placed on an esophageal catheter. Despite its promising theoretical advantages, to date there is little evidence of the superiority of NAVA compared with other ventilatory modalities.85
Common practice in some clinical settings is to use the flow trigger. The lowest level possible is used that avoids the auto trigger. In case an ineffective trigger is detected, the presence of auto-PEEP (positive end-expiratory pressure) must be ruled out. Overcoming intrinsic PEEP in a patient with muscular weakness is imperative because intrinsic PEEP is one of the most frequent causes of an ineffective trigger. Lengthening the expiratory time, using bronchodilators, adding external PEEP, and reducing the sensitivity of the trigger are alternatives that can improve synchrony.
Traditionally, the use of tidal volumes between 15 and 20 mL/kg has been recommended, with the goal of avoiding or treating atelectasis. This recommendation is based on the theory that high volumes improve the production of surfactant, prevent the collapse of the airway, promote recruitment, and are better tolerated by the patient.7,24,65,71 The clinical evidence for this recommendation is based on retrospective studies and case series.
One of the most referenced studies to justify this method for ventilating patients with SCI was published in the journal Spinal Cord in 1999.86 Peterson retrospectively reviewed 42 patients with SCI and found that those who were ventilated with >20 mL/kg were weaned 21 days earlier than those ventilated with <20 mL/kg (37.6 days versus 58.7 days). Several limitations in this study include:
Only one clinical trial has compared these two approaches.87 The study, reported exclusively as a poster, included only 16 patients ventilated 2 weeks after the injury. There were no differences between ventilating with 10 mL/kg and 20 mL/kg.
To facilitate the removal of secretions, the postural drainage and manually assisted coughing techniques are considered essential. The use of mechanical devices such as intrapulmonary percussive ventilation71 and mechanical insufflation-exsufflation (MIE)24 have not been prospectively assessed in acute patients undergoing mechanical ventilation. Retrospective studies suggest their efficacy for reducing the number of hospitalizations in chronic patients88 and for reducing the weaning time.24 In a survey on the use of MIE, only 49% of the centers that responded acknowledged using the technique routinely.89
Regarding PEEP, the standard recommendation is to use 0 cm H2O (ZEEP). The theory behind this recommendation is that it can increase air trapping in patients with expiratory muscle impairment. Considering that expiration is a passive phenomenon, it is difficult to justify this reasoning. The use of PEEP increases the residual functional capacity and may prevent the collapse and cyclic closure of alveoli, one of the causes directly related to the onset of ventilator-associated lung injury (VALI).90 Lacking evidence to support it, recommending the use of ZEEP no longer seems reasonable for the ventilation of patients with spinal injuries, at least in the acute phase.
Standard practice in some settings with acute SCI patients undergoing mechanical ventilation and who have “healthy” lungs is to use an assisted, pressure-controlled, ventilation mode, adjusted to achieve tidal volumes of 10 to 12 mL/kg with 5 to 7 cm H2O of PEEP, with the pressure plateau always below 30 cm H2O. The goal is to maintain total ventilator support, allowing the patient to initiate most of the cycles and attempting to adjust the inspiratory time to adapt it to the neural inspiratory time. This same ventilation modality is continued once weaning has begun in the resting periods between trials of spontaneous respiration. In all cases of acute pulmonary lesion, the lung protective ventilation strategy is followed.
In the event of recurrent atelectasis that does not resolve despite assisted coughing, bronchodilators, postural drainage, and hydration, the VT can be increased by 100 mL/day up to 15 to 20 mL/kg, as long as the plateau pressure is maintained below 30 cm H2O.
Patients with cervical SCI have compromised respiratory functions and require mechanical ventilation based on the location and degree of the injury, both of which also affect their success in weaning from the respirator, which approaches 40% in patients with cervical injuries above C4, with increasing success in injuries below C5.91 The respiratory modality most commonly used in weaning is Progressive ventilator-free breathing (PVFB or T-tube),92 with noninvasive mechanical ventilation and tracheotomy also playing a role. Other adjuvant treatments include the use of phrenic/diaphragmatic pacemakers in patients who do not have spontaneous breathing and drug treatments whose actual benefit is still untested.
The start of weaning and the strategy to employ are determined by the following three factors:
Therefore, the patient’s respiratory function needs to be assessed before and during weaning.93 The best parameters to use for assessing the patients respiratory function are66:
Before the start of weaning, it is advisable to optimize the patients breathing by94:
Once the patient’s breathing has been optimized, the various weaning modalities should be assessed. The three general approaches to weaning are95:
Regardless of the weaning modality, all studies have observed that the time for the withdrawal of the respirator in patients with SCI ranges from weeks to months.99,100
Extubation is considered when, after 48 hours without ventilator support, the patient meets several requirements101:
Checks before extubation include:
The Role of Noninvasive Mechanical Ventilation (NIMV)
The use of NIMV has been proposed for patients with SCI as respiratory support both in acute conditions and in respirator weaning and as a long-term night support for patients in whom hypoventilation is detected.
Indications for the use of NIMV include:
Bach and Saporito101,102 and Tromans et al.103 describe the use of NIMV in acute conditions:
NIMV can be used with two ventilator modalities:
Both modalities may be used with or without supplemental oxygen and with an interface that can be nasal, oral or naso-oral.
Limitations to the use of NIMV include:
Phrenic or diaphragmatic pacemakers, whose use started in the 70s by Glenn et al. 106, are one of the forms of respiratory support that may be used in the withdrawal of the volumetric respirator as an alternative to long-term respiration in patients with SCI, thereby improving their quality of life.
Electrostimulation of the phrenic nerve consists of triggering diaphragmatic contractions through direct electrical stimulation of the phrenic nerve in the neck and chest. Candidates for electrostimulation include patients with:
It is therefore necessary, prior to implantation, to perform phrenic nerve conduction with bilateral, simultaneous diaphragmatic fluoroscopy. After its placement using thoracotomy, a period of conditioning is needed in order to improve the muscle tone of the diaphragm, which may have atrophied due to lack of use.
The daily duration of the electrophrenic respiration may be 16 hours to 24 hours, with nighttime ventilator support to support physiological recovery of the diaphragmatic muscle, in anticipation of the next day.
External diaphragmatic pacemakers are a modality that is more applicable to the ICU.109 This modality uses electrodes that are implanted directly using endoscopy within the diaphragmatic muscle and which are connected to an external stimulator implanted in the skin. This system can be used early on for the management of weaning in the ICU thus lessening the likelihood of complications by avoiding the need for major surgery.
In regard to quadriplegic/tetraplegic patients who have inadequate function of the phrenic nerves and in whom the implantation of phrenic/diaphragmatic pacemakers is not possible, there are experimental studies in animals that attempt to restore ventilation without respirator with high-frequency spinal cord stimulation (HF-SCS) of the intercostal muscles. DiMarco and Kowalski110, in a study conducted on dogs, achieved periods of up to 6 hours without a respirator preventing muscle fatigue.
In some groups, approximately 40% of the patients are supported at all times with these devices. It is important to note that diaphragmatic pacemakers only supplement the inspiratory function and do not replace the expiratory functions such as coughing or the removal of secretions. It is here where rehabilitation and external mechanical assistance have considerable importance.
It is known that patients with cervical SCI have increased resistance in the airways due to a loss of sympathetic control.
Tracheostomy is a common procedure in patients with traumatic SCI, especially in cervical SCI or thoracic level with associated injuries.
The literature has suggested that early insertion of a tracheostomy facilitates pulmonary management and an earlier discharge from the intensive care unit (ICU).
Both surgical and percutaneous tracheostomies (PTs) can be safely performed in the ICU.
Tracheostomy appears to facilitate weaning by decreasing the work of breathing, especially in patients with limited respiratory reserve.92 Compared to the native airway, the tracheotomy cannula constitutes an additional resistive component.
Respiratory complications are the main cause of morbidity and mortality in the acute phase of SCI, with an incidence of 36% to 83%.1,2 Although pulmonary complications are a common and well-known problem in SCI, there is little information about their management. Current practice is mainly based on clinical experience and expert opinion.7
The pillars of early treatment of respiratory dysfunction in SCI are intensive management of secretions and atelectasis, which has been shown to improve the outcomes in patients with SCI.71 The most important objective of treatment is the expansion of the lungs and the clearing of secretions. The techniques commonly used to help remove secretions include:
Increasing ventilation in patients on mechanical ventilation include133:
Interventions for mobilizing secretions are essential for preventing mucus plugs, atelectasis, pneumonia, and respiratory failure and should be started early after the injury.
To optimize results when using respiratory therapy techniques, it is essential to have:
The goal of postural drainage and passive positioning techniques if the patient is immobilized is to use gravity to facilitate the movement of secretions from the most peripheral regions of the lungs to the main airway, where the secretions can be more easily removed using coughing or other methods of aspiration.
Percussion and Vibration
Percussion and vibration consist of external manipulations of the chest to mobilize secretions.
The goal of assisted coughing techniques is to help generate effective cough strength. They are often used with postural drainage, intermittent positive-pressure breathing (IPPB), and insufflator. Several techniques which may be used include:
There is no clear evidence of the benefit of RMT in patients with SCI.
IMT consists of the use of resistance during inspiration to improve the strength and resistance of the inspiratory musculature that is unaffected (or partially affected) by the SCI.
With regard to the expiratory musculature, the strengthening of the pectoralis major muscle may be useful (C5–C7 innervation, its function may be partially preserved), because the clavicular part helps expiration.
Although there is scant evidence from the physiological point of view, it does make sense to use RMT, at least in the ventilator weaning phase. The treatment is started only when the patient is able to tolerate periods of spontaneous respiration.
Noninvasive ventilatory support is used to provide positive pressure in the airway during expiration and/or inspiration. There are various types of positive-pressure support but the most widely used include:
Noninvasive ventilation can also be supplied through negative-pressure body ventilators such as the iron lung, the pneumobelt, and other devices.143 They are very rarely used but may provide some advantage as an option for temporary or permanent ventilation of patients with high quadriplegia/tetraplegia, as well as, facilitating speech, mobility, and so forth.144
Per EMS (1900): 18-year old Thomas Hutton dove face first, at approximately 1800, into the 3 foot end of a cement swimming pool after drinking beer all afternoon with his friends. He hit his forehead on the bottom of the pool. His friends pulled him out of the pool while calling 911. He has not regained consciousness since.
Upon arrival in the emergency department, EMS reports:
HR: 140-160, sinus tachycardia
RR: 40-50, rapid, shallow
You observe: Patient is on a backboard with a semi-rigid cervical collar in place.
20 gauge peripheral IV placed in left antecubital with 1000ml Normal Saline infusing at 100ml/hr. Patient on 100% rebreather mask with oral airway inserted.
Continue backboard and semi-rigid collar.
Continue monitoring GCS.
Place EKG leads to cardiac monitoring.
Place pulse oximetry.
Place BP cuff.
Insert another 20 gauge IV into right antecubital while drawing stat Hgb/Hct, blood ETOH levels, serum electrolytes, coagulation studies, cell blood counts: send to lab.
Bedside fingerstick for blood glucose level.
Draw ABG for stat results.
Insert urinary catheter and send stat urine drug screen to lab.
Inspect, palpate, percuss and auscultate the following systems where feasible: neurologic, integumentary, pulmonic, cardiovascular, abdominal, urinary.
Chest x-ray: AP and lateral
Cervical spine x-rays: AP, lateral and odontoid
Head and neck CT
Continue to try to locate family to ascertain information pertaining to allergies, current medication and immunization status, past medical and surgical history.
Discussion of Outcomes
GCS continues at 3.
Chest x-rays show pulmonary infiltrates.
Cervical spine x-rays indicate an extension teardrop fracture at C2 with neck CT confirming the diagnosis.
Head CT shows fracture of frontal bone with hematoma at base of occiput.
All laboratory tests WNL except blood alcohol level 0.42, ABG’s show acute respiratory acidosis: pH 7.26, PaO2 75, PaCO2 56, HCO3 24, BE -4.
Strengths and Weaknesses
Continuing GCS of 3 with imaging studies indicative of a severe head injury and an extension teardrop fracture at C2: a neurologist and neurosurgeon should be consulted.
Chest x-ray indicating pulmonary infiltrates and respiratory acidosis coupled with continuing hypertension, rapid, shallow respirations, and lower than expected SaO2 per oximetry: emergent intubation indicated.
Pulmonary physiologic changes due to SCI are related to the extent of neurological impairment. The American Spinal Injury Association Impairment Scale (AIS) is used to classify the degree of impairment that is based on strength in key muscles and on a sensory examination.
Immediately after SCI, flaccid paralysis affects all muscles caudal to the level of injury (i.e. spinal shock). Subsequent improvements in pulmonary function are due primarily to functional descent of the neurologic injury level as spinal cord inflammation resolves, enhanced recruitment of accessory ventilatory muscles, retraining of deconditioned muscles, and the evolution from flaccid to spastic paralysis.
The extent of ventilatory muscle impairment depends upon the degree and location of the injury, as well as, the duration of time since the injury. The higher the level and more complete the injury, the more likely that there will be respiratory muscle dysfunction. Complete injury above C3 produces near total ventilatory muscle paralysis because the phrenic nerve, which innervates the diaphragm, arises from the third to fifth cervical roots.
When obtaining spirometry, American Thoracic Society (ATS) standards may need to be modified to accept expiratory efforts less than six seconds in duration, as long as a 0.5 second plateau is achieved (presumably at residual volume), and a greater degree of back-extrapolated volume (e.g., ~7.5% of forced vital capacity), when volume-time curves and flow volume loops are otherwise acceptable.
Among individuals with chronic cervical cord injury, spirometry typically shows a restrictive ventilatory defect with FVC and FEV1 values approximately 55% of the values predicted for able-bodied subjects.
SCIs often lead to restrictive respiratory changes. VC is an indicator of overall pulmonary function. Patients with severely impaired VC may require assisted ventilation. It is best to proceed with intubation under controlled circumstances rather than waiting until the condition becomes an emergency.
Lung volumes following complete cervical cord injury show a marked reduction in ERV, a mild to moderate reduction in TLC and FRC, and preservation of RV. The main lung volume abnormality after incomplete cervical or thoracic SCI is a moderate reduction in ERV.
f supine length is preferred over arm-span or recalled standing height for use in the calculation of predicted pulmonary function values for individuals with SCI.
Posture has a significant impact upon lung mechanics in the majority of patients with SCI. Typically, individuals with SCI have an increase in VC when changing from a seated to supine position, whereas the normal response to recumbency is a slight decrease in VC.
Greater lifetime cigarette smoking (pack years) is associated with lower values for FVC and FEV1 both initially after SCI and during long-term follow-up.
f SCI is below C5 and thus spares the phrenic nerve, maximal expiratory force is impaired more than maximal inspiratory pressure, which remains near or within the normal range.
quadriplegia/tetraplegia may demonstrate mild expiratory airflow limitation, which only becomes apparent during reversibility testing with inhaled bronchodilators such as beta2-agonists and the anticholinergic agent ipratropium bromide. However, the clinical benefit regarding the routine use of bronchodilators in quadriplegia/tetraplegia for purposes of maximizing pulmonary function has not been established.
Mechanical ventilation can adversely affect the structure and function of the diaphragm. Early tracheostomy following short orotracheal intubation is probably beneficial in selected patients.
Weaning should start as soon as possible, and the best modality is progressive ventilation-free breathing (PVFB/t-tube), due to its efficacy and ease of performance. Appropriate candidates can sometimes be freed from mechanical ventilation by electrical stimulation. The conservative management of respiratory dysfunction in SCI patients can be used to help remove secretions by various techniques and to increase ventilation by respiratory exercises and noninvasive positive air pressure support.