Physical Rehabilitation for the Critically Injured Veterinary Patient

The critically injured veterinary patient can present a daunting challenge to the clinician trying to provide physical rehabilitation. Types of injuries sustained may range from single or multiple orthopedic injuries; soft tissue trauma to the chest, abdomen, or head; or a combination of these injuries. Burn injury or smoke inhalation can cause severe metabolic and cardiorespiratory dysfunction. The common thread in all of these patients is a debilitating injury that renders them partially or completely immobile for prolonged periods. Although bedrest is important to the recovery from critical injuries, prolonged inactivity can have deleterious effects on both injured and healthy body systems. The goals of providing physical rehabilitation to critically injured patients are to prevent complications stemming from injuries, prevent complications secondary to prolonged inactivity, maintain body condition, improve patient comfort, and hasten recovery. The purpose of this chapter is to discuss the effects of prolonged inactivity on traumatized and healthy body systems and to describe the application of basic physical rehabilitation techniques for specific critical injuries.

The Musculoskeletal System

Rarely do traumatized animals escape injury to the musculoskeletal system. Injuries can include single or multiple fractures of the appendicular or axial skeleton, hemorrhage into skin, muscle, and joint spaces, or injury to nerves supplying these structures. Patients with head, chest, or abdominal trauma may be unable to move because of decreased consciousness or pain. Disuse or injury to the musculoskeletal system may result in muscle weakness and muscle atrophy; skin, muscle, and joint contractures; and eventually may limit an animal’s ability to move, groom, eat, and ambulate. With these global implications maintenance of this body system is paramount.

The balance between collagen synthesis and degradation is abnormal in immobile patients. Trauma with bleeding into soft tissue and muscle and subsequent inflammation and degeneration can trigger increased collagen synthesis. Increased collagen synthesis in an inactive patient leads to tighter packing of collagen fibers and contributes to the development of contractures.

Muscle contracture is shortening of the muscle owing to either intrinsic or extrinsic causes. Intrinsic changes are structural and can result from inflammatory or traumatic processes. Trauma, inflammation, ischemia, and hemorrhage in injured patients can restructure muscle tissue components and result in fibrosis and the development of adhesions. Following hemorrhage into a muscle, fibrin deposition occurs. Within 2 to 3 days fibrin is replaced with reticular fibers that form a loose connective tissue network. If the affected muscle is kept immobile, the network becomes more dense and resistant to stretch.¹

Extrinsic muscle contracture is secondary to neurologic abnormalities or mechanical factors and is commonly associated with prolonged immobilization. Causes of extrinsic muscle contracture include paralytic or spastic muscle conditions. Paralyzed muscles cannot provide adequate resistance to opposing muscles across a joint. Eventually the antagonistic muscle will shorten. Carpal contracture in brachial plexus injuries illustrates this type of extrinsic contracture. To prevent contracture of the carpus in this situation, stretch must be applied to the normal muscle. Spastic muscle, which may exist in the pelvic limb musculature following trauma to the spinal cord between T3-L3, results from imbalance of muscle control. Increased muscle tone reduces the resting length of the spastic muscle and results in abnormal joint positioning. Treatment is aimed at stretching the abnormal muscle. Joint contracture is defined as an inability to move a joint through its full range of motion (ROM). Conditions that contribute to joint contracture include absence of mobility at the joint, immobilization of a joint in an inappropriate position, joint pain, paralysis, and muscle damage.

The position in which limbs are immobilized also contributes to the development of contractures. Muscle fibers lose up to 40% of the length of sarcomeres when immobilized in a shortened position. Therefore whenever possible joints should be kept in a neutral position to keep muscle fibers at equal length and tension to minimize contracture.² Additional factors that affect the rate of contracture development include the precipitating cause, duration and degree of immobilization, and preexisting joint restrictions. Edema, ischemia, and bleeding accelerate the development of muscle and joint contracture. Immobile, injured patients therefore require efforts directed at prevention and treatment of contracture development following soft tissue musculoskeletal injuries (Table 37-1).

Table 37-1

Treatment of Musculoskeletal Injuries

Technique	Benefits	Frequency
Cryotherapy	Reduces inflammation, swelling, and pain	Every 4-6 hr (after initial 24-72 hr)
Superficial or deep heating	Improves circulation, reduces muscle spasm, provides pain relief	Every 4-6 hr (after acute inflam. has subsided)
Massage	Increases circulation to paralyzed musculature, reduces/breaks down adhesions, provides pain relief, reduces edema	4-6 times/day
Range-of-Motion (ROM) Exercises
Passive	Maintains existing mobility of joints and soft tissue, minimizes contracture formation, prevents loss of ROM, maintains muscle elasticity, improves circulation, reduces edema	4-6 times/day
Active	Same as passive ROM exercise plus maintains physiologic muscle elasticity, maintains bone integrity, and may increase muscle strength	4-6 times/day
Splinting and casting	Corrects severe muscle and joint contracture by providing prolonged stretch to muscle and joint structures

Respiratory System

The respiratory complications of prolonged immobility and those resulting from primary injuries are numerous and potentially catastrophic in critically injured patients. Injuries to the head, chest, and abdomen often result in reduced respiratory function because of pain, inability to move, altered consciousness, or damage to thoracic structures. Impaired consciousness from head injury may lead to altered breathing patterns, diminished ability to cough, and inability to change body position. Rib fractures, pneumothorax, pulmonary contusions, and painful soft tissue injuries to the chest and abdomen may result in a restrictive breathing pattern characterized by shallow, rapid ventilation. This type of breathing pattern causes a reduction in tidal volume, functional residual capacity, and lung compliance. Altered respiratory patterns in conjunction with immobility may lead to atelectasis, accumulation of respiratory secretions, and pneumonia. It is important for the clinician to note any injuries that may compromise respiratory function and devise a physical rehabilitation plan to address those concerns. Chest physical rehabilitation is a term that describes the use of techniques aimed at improving lung volumes or facilitating the removal of airway secretions.³ The goals of chest physical rehabilitation are to maintain bronchial hygiene, eliminate secretions from the airways, re-expand atelectatic lung segments, improve oxygenation, and reduce the incidence of pneumonia (Table 37-2). These goals can be achieved through techniques such as stimulating the animal to cough, frequent repositioning, postural drainage, percussion, vibration, and exercise. Each of these techniques is reviewed in detail.

Table 37-2

Goals of Chest Physical Rehabilitation

Technique	Goals
Positioning	Reduce risk of atelectasis, improve ventilation/perfusion, improve gas exchange, reduce risk of pressure sores, minimize muscle and joint stiffness
Cough	Remove secretions from trachea to fourth-generation bronchi
Postural drainage	Increase mobilization and elimination of secretions from upper airways
Percussion	Dislodge bronchial secretions
Vibration	Move secretions into larger airways

Coughing is the most important defense mechanism to eliminate retained secretions. A cough can eliminate secretions from the trachea to the level of the fourth-generation segmental bronchi.⁴ An effective cough is initiated by a deep inspiration, followed by closure of the glottis and contraction of the chest wall and abdominal musculature to generate high intrathoracic pressure. After high intrathoracic pressure is attained, the glottis opens and is followed by rapid expulsion of air during exhalation. Critically injured patients may not be able to initiate a cough because of impaired consciousness, pain, weakness, or injuries to the chest or abdominal wall. These animals can be assisted to cough by applying gentle pressure to the trachea at the level of the third tracheal ring. Placing an animal in sternal recumbency may also improve an animal’s ability to cough. Animals should be assisted to cough after postural drainage, percussion, and vibration and before changes are made in the patient’s position.