Muscle Rigidity
Opioids can increase muscle tone and may cause muscle rigidity.
The incidence of rigidity noted with opioid anesthetic techniques varies greatly
because of the following: differences in dose and speed of opioid administration,
the concomitant use of N2
O, the presence or absence of muscle relaxants,
and patient age. Opioid-induced rigidity is characterized by increased muscle tone
progressing sometimes to severe stiffness, leading to serious problems ( Table
11-5
). Clinically significant opioid-induced rigidity usually begins just
as, or after, a patient loses consciousness. Mild manifestations of rigidity, such
as hoarseness, can occur in conscious patients. Rigidity can decrease pulmonary
compliance and functional residual capacity, may diminish or preclude adequate ventilation,
and may cause hypercarbia, hypoxia, and an elevated ICP.[119]
[120]
Opioid-induced rigidity also increases pulmonary
artery and central venous pressures and pulmonary vascular resistance.[121]
[122]
It has been demonstrated that vocal cord
closure
is primarily responsible for difficult ventilation with bag and mask that follows
opioid administration. Rigidity may rarely occur hours after the last dose of opioid
has been administered.[123]
Delayed or postoperative
rigidity probably is related to second peaks that can occur in plasma opioid concentrations,
as may occur in the case of recurrence of respiratory depression. Abnormal muscle
movements ranging from extremity flexion to single or multiple extremity tonic-clonic
movements or global tonic-clonic motions can also occur after the use of opioids.
[124]
The precise mechanism by which opioids may cause muscle rigidity
is not clearly understood. Muscle rigidity is not due to a direct action on muscle
fibers, because it can be decreased or prevented by pretreatment with muscle relaxants.
Mechanisms for opioid-induced muscle rigidity have been sought for in the CNS.
The nucleus pontis raphae is reported to be an integral central site concerning
TABLE 11-5 -- Potential problems associated with opioid-induced rigidity
|
System |
Problem |
|
Hemodynamic |
↑ CVP, ↑ PAP, ↑ PVR |
|
Respiratory |
↓ Compliance, ↓ FRC, ↓ ventilation |
|
Hypercarbia |
|
Hypoxemia |
|
Miscellaneous |
↑ Oxygen consumption |
|
↑ Intracranial pressure |
|
↑ Fentanyl plasma levels |
|
CVP, central venous pressure; FRC, functional residual capacity;
PAP, pulmonary artery pressure; PVR, pulmonary vascular resistance. |
|
Modified from Bailey PL, Egan TD, Stanley TH: Intravenous
opioid anesthetics. In Miller RD (ed): Anesthesia,
5th ed. New York, Churchill Livingstone, 2000, p 291. |
opioid-induced rigidity.[120]
A pharmacologic investigation
using selective agonists and antagonists suggested that systemic opioid-induced muscle
rigidity is primarily due to the activation of central μ-receptors, whereas supraspinal
δ1
and κ1
receptors may attenuate this effect.
[125]
Some aspects of opioid-induced catatonia
and
rigidity (increased incidence with age, muscle movements resembling extrapyramidal
side effects) are similar to Parkinson's disease and suggest similarities in neurochemical
mechanisms. Parkinsonian patients, particularly if inadequately treated, may experience
reactions like dystonia following opioid administration.[126]
Pretreatment or concomitant use of nondepolarizing muscle relaxants
significantly decreases the incidence and severity of rigidity.[124]
Induction doses of sodium thiopental and less than anesthetic doses of diazepam
and midazolam have also been reported to prevent, attenuate, or successfully treat
rigidity. Persisting in an attempt to ventilate a patient with opioid-induced rigidity
by mask will likely result in gastric insufflation and inadequate ventilation or
oxygenation until a muscle relaxant is administered. Anesthesiologists should anticipate
the need for rapid neuromuscular blockade, when doses of opioids are administered
that produce rigidity, in order to minimize its occurrence and to allow effective
ventilation and airway management.
