Management of the Upper Limb in the Acute Phase

Original Editor - Dr. Jennifer Dunne

Top Contributors - Naomi O'Reilly and Kim Jackson  

Introduction[edit | edit source]

The main aim of management of the upper limb in the acute phase is to prevent secondary complications such as swelling and contractures from occurring in addition to developing tenodesis function.  

In the first days following injury, immobilization results in structural changes to the muscle characterized by:

  • Shortening of muscles fibre length
  • Disorganization and loss of sarcomere
  • Increase in connective perimysium
  • Accumulation of intramuscular collagenous connected tissue
  • Atrophy, increased changes at the myotendinous junction. [1][2]

Awareness of these structural changes, along with imbalances of joint biomechanics due to paralysis of key muscles is of paramount importance should treatment of the upper limb should commence early following injury to prevent secondary complications.  

Diagnosis of Upper and Lower Motor Neuron Damage[edit | edit source]

As discussed above, following a spinal cord injury damage occurs to the upper motor neurons, preserving the lower motor neurons below the level of injury. At the level of the injury, the lower motor neurons are not viable and muscle atrophy from loss of neuromuscular junctions is seen.  Below the level of injury, as the anterior horn cells are viable, the neuromuscular junctions are intact, the muscle is viable and a reflex arc is present. Functional Electrical Stimulation (FES) can be used diagnostically to distinguish between paralyzed muscles with intact versus damaged lower motor neurons with a weak or absent response of a paralyzed muscle recorded at least eight days following injury indicating, with 100% certainty, that the peripheral motor nerve has undergone irrecoverable damage. [3] There is also evidence that lower motor lesions can predict both contracture development and the development of the tenodesis function. [4] Knowledge of the presence of lower motor neuron damage is also important for those considering nerve transfer surgery. Therefore, there may be value in the use of surface FES to assess tetraplegic upper limbs to determine functional denervation and assist in identifying appropriate interventions for maximizing function in the acute phase.  

Oedema Prevention and Treatment[edit | edit source]

Due to the loss of muscle pump activity due to paralysis combined with the dependent position of the upper limb, there is reduced capacity for venous and lymphatic return, which, left unmanaged, will result in oedema. The hand can contain up to 50ml of additional fluid before oedema is visible. [5] If this is left and becomes persistent, the proteins in the fluid increases and oedema becomes viscous and fibrotic.  Untreated, this can result in loss of tenodesis grip due to loss of range of motion especially around the MCP joints (Figure 3). Prevention of oedema is a primary goal of upper limb management and can consist of elevation, activity, orthoses and compression. [6]

Positioning of the hand in elevation, especially in the acute phase assists venous return and reduces arterial hydrostatic pressure.[5] Elevation usually provided by pillows or slings attached to the bed (Figure XX) can be used in conjunction with positioning to maintain length and prevent contracture as discussed later in the chapter. 

In sitting, if the individual does not have sufficient movement to activate the muscle pump, the arm needs to be fully supported with a well-fitting armrest or the wrist braced into extension.  Wrist positioning is especially important as extended periods of flexion can obstruct the venous and lymphatic return on the dorsum of the hand and encourage the development of oedema.  

Hand Orthoses have been used to manage the tetraplegic hand for many years.  However, there is variability between clinicians/centres on the purpose, positioning and treatment prescription of orthoses and minimal research on the effectiveness of this intervention. [7] Consensus does however, endorse the use of static splinting, either custom-made or off-the-shelf, depending on the need of the patient.  Ideally, static splinting should begin immediately following injury with the aims to:

  • Facilitate conditions for venous return
  • Maintain range of motion of structures of the hand, and
  • Encourage slight shortening of the finger flexors for optimal tenodesis function. [8]

Compared to passive or active movements, orthoses aim for low-load prolonged stretch. [9] In the acute phase the primary purpose of the orthosis is to prevent oedema and protect the structures of the hand. Therefore the orthosis should ensure the hand is resting in a position of safety with the wrist extended approximately 20° to maintain length of the finger extensors, MCP’s flexed 70° to maintain MCP collateral ligament length and balance finger flexors/extensors and intrinsics, IP joints of the fingers straight to balance the intrinsics and the thumb CMC joint abducted 30°, MCP and IP joints straight or slightly flexed to position the thumb for opening and key pinch (Figure 6).  To facilitate the transport of fluid to the dorsum of the hand, where the majority of venous return occurs, the orthosis should provide firm volar pressure.  If required additional compression by bandaging or elastic bands over the dorsum of the hand and forearm may be used in conjunction with the orthosis if oedema is problematic.  Ideally, during the bedrest stage, the orthosis should be worn for 3 hours on/3 hours off during the 24 hour period.  

Once the patient mobilises and becomes more active the risk of oedema reduces due to the use of the muscle pump.  Thus the need for splinting to prevent oedema is decreased and such splints interfere with function.  Thus the aims of splinting changes and should be individually assessed for each patient.  If the hand demonstrates spasticity, stretching of the involved muscles using orthoses overnight is indicated and constant assessment and evaluation of the balance of the hand and positioning are essential.  

Spasticity and Contracture[edit | edit source]

Cervical spinal cord injury is commonly associated with hypertonia, which is characterized by spasticity and dystonia that can involve both the upper and lower limb.  Splinting of the upper extremity can be used to prevent soft tissue shortening and contracture.  It has been demonstrated that an elbow flexion contracture greater than 25 degrees has a significant impact on the independence of a person with tetraplegia.[10] Consideration of splints to assist with positioning the elbow in extension for those patients who lack triceps innervation and who have increased tone and spasticity is recommended.[10] Once present, contracture is difficult to reduce, thus emphasis is placed on prevention. [11] Prediction of contracture is an essential task of the therapist, and factors such as innervation pattern, spasticity, pain, oedema and long term position of the body are important to observe and analyse. [12] Prevention is a team approach and can include medication, including pain relief, anti-spasmodics, botulinum toxin, in conjunction to passive movement and regular positioning of the upper limb at end ranges throughout the day.  

Passive Movement[edit | edit source]

The rationale and the use of passive movement and stretching are mostly justified by old animal studies. [13] The intensity of passive movements necessary to reach therapeutic benefit is unknown despite strong clinical confidence in the effect.  However, daily assessment of the upper limb in the acute phase can be combined with passive movements performed by a therapist, providing ongoing monitoring of the limb. Passive movements are important to prevent adhesions of tendons and lubricate joints. Therefore joint-by-joint passive ranging is vital.  Stretching of the joints is performed slowly and joints should never be forced. As it is difficult to reduce contractures once developed, stretch is most likely to be effective if started before the onset of contracture thus rehabilitation and treatments of the upper-limb should be initiated as soon as possible after injury. [12] Soft tissues, such as muscles, ligaments and joint capsules, most at risk should be targeted, particularly if contracture is likely to impose functionally important limitations including loss of passive elbow extension (due to tight biceps), loss of pronation (due to biceps contracture), loss of external rotation (due to tight pectoralis muscle); shoulder pain (due to increased tone in innervated muscles and poor positioning of arm due to tightness. Orthoses and positioning of the limbs are important compliments to twice-daily passive movement.

To promote tenodesis function in the hands, it is important to avoid stretching the finger- and thumb flexor tendons when the wrist is extended.  Finger extension should only be performed with the wrist flexed (figure XX). Emphasis should be on flexion and extension of the wrist, flexion of the MCP joints of the fingers, extension of finger PIP joints and thumb adduction - the same movements that are lost if prolonged oedema is present. If any tightness occurs, specific attention should be focused on the affected joint.

The length of time required to perform passive movements for therapeutic benefit is unknown but could be as long as 15 minutes per joint daily, dependent upon such factors as age, presence or absence of spasticity and pain.17 The individual should, therefore, be taught as early as possible good habits of stretching and managing passive movements and long term positioning. Stretching should be incorporated into everyday life activities.

References[edit | edit source]

  1. Lieber RL, Ward SR. Cellular mechanisms of tissue fibrosis. 4. Structural and functional consequences of skeletal muscle fibrosis. Am J Physiol Cell Physiol. 2013;305(3):C241-252.
  2. Williams PE, Goldspink G. Connective tissue changes in immobilised muscle. J Anat. 1984;138 ( Pt 2):343-350.
  3. Bryden AM, Hoyen HA, Keith MW, Mejia M, Kilgore KL, Nemunaitis GA. Upper Extremity Assessment in Tetraplegia: The Importance of Differentiating Between Upper and Lower Motor Neuron Paralysis. Arch Phys Med Rehabil. 
  4. Bersch I, Koch-Borner S, Friden J. Electrical stimulation-a mapping system for hand dysfunction in tetraplegia. Spinal Cord. 2018;56(5):516.
  5. 5.0 5.1 Vasudevan SV, Melvin JL. Upper extremity edema control: rationale of the techniques. The American journal of occupational therapy : official publication of the American Occupational Therapy Association. 1979;33(8):520-523.
  6. Miller LK, Jerosch-Herold C, Shepstone L. Effectiveness of edema management techniques for subacute hand edema: A systematic review. J Hand Ther. 2017;30(4):432-446.
  7. DiPasquale-Lehnerz P. Orthotic intervention for development of hand function with C-6 quadriplegia. American Journal of Occupational Therapy. 1994;48(2):138-144.
  8. Krajnik SR, Bridle MJ. Hand splinting in quadriplegia: current practice. The American journal of occupational therapy : official publication of the American Occupational Therapy Association. 1992;46(2):149-156.
  9. Glasgow C, Tooth LR, Fleming J. Mobilizing the stiff hand: combining theory and evidence to improve clinical outcomes. J Hand Ther. 2010;23(4):392-400; quiz 401.
  10. 10.0 10.1 Bryden AM, Kilgore KL, Lind BB, Yu DT. Triceps denervation as a predictor of elbow flexion contractures in C5 and C6 tetraplegia. Archives of Physical Medicine & Rehabilitation. 2004;85:1880-1885.
  11. Harvey L, Herbert R, Crosbie J. Does stretching induce lasting increases in joint ROM? A systematic review. Physiother Res Int. 2002;7(1):1-13.
  12. 12.0 12.1 Harvey LA, Herbert RD. Muscle stretching for treatment and prevention of contracture in people with spinal cord injury. Spinal cord. 2002;40(1):1-9.
  13. Tabary JC, Tabary C, Tardieu C, Tardieu G, Goldspink G. Physiological and structural changes in the cat's soleus muscle due to immobilization at different lengths by plaster casts. J Physiol. 1972;224(1):231-244.