A small compilation of nurse anesthesia care plans
These anesthesia care plans are meant to inspire nurse anesthesia residents when they are making their care plans. Always make sure you fully understand and "own" your care plan. Your plan must be specific for your patient and should always be with the most up-to-date information.
Paroxysmal Autonomic Instability with Dystonia (PAID)
Paroxysmal autonomic instability with dystonia (PAID) syndrome is a complication of severe brain injury, regardless of etiology. The syndrome is manifested by marked agitation, diaphoresis, hyperthermia, hypertension, tachycardia, and tachypnea accompanied by hypertonia and extensor posturing. Usually episodic, it first appears in the intensive care setting but may persist in the rehabilitation phase for weeks to months after injury in individuals who remain in a low-response state. The syndrome engenders alarm because it may be difficult to distinguish from life-threatening conditions such as sepsis, impending herniation, or epileptic seizure. These manifestations could lead to secondary hypertensive or hyperthermic encephalopathy and even death.
The pathophysiology of PAID can be best explained by the dysfunction of autonomic centers in the diencephalon (thalamus or hypothalamus) or their connections to cortical, subcortical, and brainstem loci that mediate autonomic function. Rigidity and decerebrate posturing are seen experimentally and clinically with lesions in the midbrain, blocking normal inhibitory signals to pontine and vestibular nuclei. This allows these nuclei to become tonically active, transmitting facilitatory signals to the spinal cord control circuits. Spinal reflexes become hyperexcitable, evoked by sensory input signals that are usually below the threshold for excitation of a motor response.
Opioid receptors are found in the brain, cardiovascular nuclei, the heart, and blood vessels. Opiates such as morphine, when peripherally injected into healthy animals, produce hypotension. Morphine induces analgesia, respiratory depression, and bradycardia. Its analgesic properties may interfere with pain as an inciting factor, and its sedative effects may counter the tachycardia and tachypnea. Constipation is a problematic adverse effect of morphine and narcotic dependency. Withdrawal from opiate therapy may provoke signs that falsely suggest PAID.
The use of dopamine antagonists or the withdrawal of dopamine agonist therapy may also result in neuroleptic malignant syndrome (NMS), which generally presents with muscle rigidity, fever, autonomic instability, and cognitive changes such as delirium and is associated with elevated creatine phosphokinase (CPK). The clinical features of NMS suggest PAID. Thus, it is not surprising that the use of bromocriptine, a dopamine agonist, has been found to be helpful in PAID.
Because excitation of the sympathetic nervous system appears to be a major feature of PAID, beta-adrenergic blockades, such as propranolol (nonselective -adrenergic blockade) or labetalol hydrochloride (nonselective—plus alpha1-adrenergic blockade), are logical choices and have proven clinically useful in ameliorating some of the most important clinical signs (eg, hypertension) but not cholinergic signs (eg, diaphoresis) of PAID.
Clonidine, an alpha2-adrenergic agonist, reduces blood pressure, has a behavior-stabilizing effect, and causes sedation. These features treat the sympathetic signs and may interrupt feedback into the system that otherwise would perpetuate the cycle of autonomic dysregulation.
The benzodiazepines, such as lorazepam, have anxiolytic and sedating effects and muscle relaxant properties that may account for benefits observed in the treatment of PAID.
In addition to its direct muscle relaxant properties, dantrolene may diminish fever due to prolonged muscle contraction and reduce the somatosympathetic spinal reflexes that contribute to sympathetic excitation.