Period Of Paralysis Research Articles

Sedative use in patients receiving neuromuscular blocking agents from a helicopter flight team

Introduction Cognitive awareness under general anesthetic may occur in up to 0.2% of patients, with approximately twice the risk in chemically paralyzed patients. Patients in emergency and critical care areas frequently receive neuromuscular blocking agents (NMBA), but a recent survey indicated that only 90% to 96% of critical care nurses routinely provide concurrent sedative medications to those patients. We sought to determine the potential for awake paralysis in patients transported by helicopter critical care transport teams and to evaluate for associations with clinical factors. Methods A retrospective review was performed of the rotor-wing transport records of 103 consecutive patients receiving NMBAs and without cardiac arrest during their care. Using hospital-approved pharmacological references, independent reviewers determined whether individual patients were likely to be under the effects of sedative medications during their period of neuromuscular blockade. Descriptive statistics are reported, and the chi-square test was used to evaluate relationships. Results The sample population was 70.9% male, 89.3% adult, 53.4% trauma/surgical, 66% interhospital, and 88.3% normotensive (SBP > 90 mm Hg). Clinically, 91.3% of patients were judged as probably to have been under the effects of some sedative during their period of paralysis. There was not a significant association between the use of sedatives and any of the factors studied: sex, age, diagnosis, site of origin, flight nurse experience, or systolic blood pressure. Patients most commonly received benzodiazepine alone (70.2%), followed by benzodiazepine + opioid (23.4%), opioid alone (5.3%), and propofol (1.1%). Medication choice was also unrelated to any of the clinical factors studied. Discussion Awake paralysis is difficult to detect but is a serious practice complication. In anesthesia practice, 96% of such cases were considered substandard care, even with prompt recognition and management. Flight nurses administer sedatives at rates similar to other critical care nurses but not to all chemically paralyzed patients. We were unable to identify clinical correlations with medication use or omission. Additional phenomenological and quantifiable evaluations of consciousness during the transport of chemically paralyzed patients would be valuable studies. Conclusion Patients receiving NMBAs during transport by helicopter flight teams are at risk for awareness during paralysis. Both practice development and research efforts in this area would be useful.

Osteoporosis in the disabled

Osteoporosis is a well-known complication of paralytic diseases. We investigated 11 patients with chronic spinal cord injury who have been paralyzed for 20 years or more. History of fracture was searched in these 11 patients. Mineral density in the lower limbs was measured, and the bone metabolism was examined. Of the total of 8 fractures, 87.5% occurred in the relatively low muscle tonus group. Patients showed decreased bone mineral density of the femoral neck, and this was negatively correlated with period of paralysis. One female patient showed an abnormal rise in bone absorption markers. In this case, bisphosphonates can be effective to increase the bone mineral density. To prevent fracture in patients with paralysis, particular care should be taken in wheelchair operation and handling of the lower limbs.

Soft tissue body composition differences in monozygotic twins discordant for spinal cord injury.

To determine the effect of paralysis on body composition, eight pairs of male monozygotic twins, one twin in each pair with paraplegia, were studied by dual-energy X-ray absorptiometry. Significant loss of total body lean tissue mass was found in the paralyzed twins compared with their able-bodied co-twins: 47.5 +/- 6. 7 vs. 60.1 +/- 7.8 (SD) kg (P < 0.005). Regionally, arm lean tissue mass was not different between the twin pairs, whereas trunk and leg lean tissue masses were significantly lower in the paralyzed twins: -3.0 +/- 3.3 kg (P < 0.05) and -10.1 +/- 4.0 kg (P < 0.0005), respectively. Bone mineral content of the total body and legs was significantly related to lean tissue mass in the able-bodied twins (R = 0.88 and 0.98, respectively) but not in the paralyzed twins. However, the intrapair difference scores for bone and lean tissue mass were significantly related (R = 0.80 and 0.81, respectively). The paralyzed twins had significantly more total body fat mass and percent fat per unit body mass index than the able-bodied twins: 4.8 kg (P < 0.05) and 7 +/- 2% (P < 0.01). In the paralyzed twins, total body lean tissue was significantly lost (mostly from the trunk and legs), independent of age, at a rate of 3.9 +/- 0.2 kg per 5-yr period of paralysis (R = 0.87, P < 0.005). Extreme disuse from paralysis appears to contribute to a parallel loss of bone with loss of lean tissue in the legs. The continuous lean tissue loss may represent a form of sarcopenia that is progressive and accelerated compared with that in ambulatory individuals.

Suppression of murine chronic relapsing experimental autoimmune encephalomyelitis by the oral administration of myelin basic protein.

Chronic relapsing experimental autoimmune encephalomyelitis (EAE), induced in mice by the injection of myelin basic protein (MBP), is a T cell-mediated autoimmune disease characterized by periods of paralysis and remission. We have shown previously that the oral administration of MBP or MBP peptides renders Lewis rats refractory to EAE. This study was undertaken to examine the conditions necessary to produce oral tolerance in a chronic relapsing model of EAE in B10.PL mice. The optimal tolerizing regimen for the mouse was found to be a single feeding of 20 mg of MBP suspended in PBS. To determine the ability to suppress chronic disease, a range of doses (0.4-100 mg) was administered orally in a single dose before challenge. Larger oral doses (20 or 100 mg) of MBP provided the best protection from EAE, while 0.4 mg exacerbated the clinical course of disease. Secretion of the proinflammatory cytokines, IL-2 and IFN-gamma, were lowest in the group fed 20 mg. A single feeding of MBP before challenge or as late as the first day of clinical signs showed significant protection over the relapsing disease course. Once relapsing EAE was established, multiple oral doses of MBP were required to achieve suppression of clinical signs of disease. These findings suggest that vehicle, dosage, and timing are important considerations in the successful application of oral tolerance strategies for suppression of chronic disease processes.

Masseter muscle rigidity after administration of succinylcholine during rapid sequence induction

Case Report A 79-year-old, 8Wlogram woman with a medical history of asthma, atria1 fibrillation, Type-I diabetes, congestive heart failure and hypertension, presented to an outlying emergency department complaining of shortness of breath. She had been seen two days earlier for similar complaints, which were diagnosed and treated as an exacerbation of her asthma. On the day of transfer, the patient arrived in florid pulmonary edema. This diagnosis was confirmed by physical exam and chest X-ray. Initial arterial blood gases (ABGs) showed a pH of 7.08, PaCOz of 73 torr, PaOz of 50 tot-r, and a bicarbonate of 21 mEq. The electrocardiogram demonstrated atria1 fibrillation with a ventricular rate of 120 and evidence of anteroseptal ischemia. Her initial treatment included 120 mg of intravenous furosemide, 3 mg of intravenous bumetanide and initiation of a nitroglycerine drip at 50 mcg/min. Ventilation was assisted with 100% oxygen via bag-valve-mask (BVM) device. Repeat ABGs, following this treatment, showed a pH of 7.29, PaC02 of 43 torr, PaOa of 98 torr and a bicarbonate of 20 mEq. Electrolytes were reported to be within normal limits. On arrival of the flight crew, this patient was ashen and diaphoretic. Ventilation was being assisted via BVM at a rate of 44 breaths/min. Rales were audible in all lung fields. The patient’s blood pressure was 132/96 mmHg, and her heart rate was 130 and irregular. Three attempts at nasotracheal intubation were unsuccessful. Therefore, rapid sequence induction for orotracheal intubation was undertaken. As per protocol, an initial 50 mcg dose of fentanyl citrate was followed by 120 mg of succinylcholine. These were given intravenously while cricoid pressure was applied. Flaccid paralysis of the extremities was obtained in approximately 40 seconds. Difficulty was encountered in attempting to insert the laryngoscope because of limited motility of this patient’s mandible, which effectively reduced her mouth opening to approximately 4 cm. This lack of motility initially was felt to be related to arthritic changes in the temporomandibular joint. Visualization of the epiglottis was achieved with difficulty, but the poor motility of the mandible rendered visualization of the vocal cords impossible. Multiple attempts at orotracheal intubation by two experienced providers were unsuccessful. Hyperventilation between intubation attempts with 100% oxygen via BVh4 enabled maintenance of oxygen saturation between 89% and 95%. Cricoid pressure was maintained throughout the periods of paralysis. Two

Paralytic strabismus: the role of botulinum toxin.

Five adults with acute extraocular muscle palsies followed by limited recovery of muscle function were treated with injections of botulinum toxin A to the ipsilateral antagonist of the affected muscle. Three were cases of unilateral sixth nerve palsy, one of bilateral sixth nerve palsy, and one of third nerve palsy. After a period of paralysis, during which the strabismus was overcorrected, the injected muscle recovered and binocular sensory and motor functions were restored and have been maintained for periods of up to 21 months. The treatment is a safe and effective alternative to surgery, particularly in cases in which a general anaesthetic is not advisable.

Contribution of the Na+‐K+ pump to membrane potential in familial periodic paralysis

The possibility has been raised that in familial periodic paralysis, the relatively large depolarization of the muscle fiber membrane seen during periods of paralysis might be attributable to a reduction in activity of the electrogenic Na(+)-K+ pump. The theoretical analysis presented here shows that although such hypotheses are qualitatively correct, the quantitative contribution of the electrogenic pump is too small to account entirely for the changes in membrane potential observed between the paralytic and interictal states.

Chronic, relapsing myelitis in hamsters associated with experimental measles virus infection.

Chronic, relapsing myelitis has been induced in golden Syrian hamsters by the intracerebral inoculation of measles virus when the animals were less than 1 day old. No acute illness was seen in animals that developed myelitis, and the onset of the myelitis was at 5 to 50 weeks after infection. In most animals the illness was slowly progressive, with hindquarter myoclonus being the most common clinical sign. Occasionally the disease involved episodic limb paresis with nearly total recovery of limb function between periods of paralysis. In most animals pathologic changes were confined to the spinal cord and involved mononuclear cell infiltration, marked gliosis, widespread demyelination, and necrosis. Virus could not be isolated from nervous tissue by cocultivation techniques, and virus-specific immunofluorescence could not be detected. The strain of virus used was distinctive in that it contained high levels of a naturally occurring viral variant that differs from typical measles virus in several distinctive ways.

The effect of prolonged, reversible block of nerve impulses on the elimination of polyneuronal innervation of new-born rat skeletal muscle fibers

The soleus muscle was reversibly paralyzed in 9- and 10-day-old rats by implantation of a plastic plug containing slowly releasable tetrodotoxin under the epineurium of the sciatic nerve. After different periods of paralysis we determined the frequency of polyneuronally innervated fibers in the muscle by intracellular recording of end-plate potentials to nerve stimulation. During the first 2–4 days of nerve block the elimination of polyneuronal innervation, occurring in rat muscles of this age, proceeded nearly as normally. After longer periods of block there was an increased frequency of polyneuronally innervated muscle fibers presumably due to motor nerve sprouting induced by the paralyzed muscle.

Morphological observations on motor end-plates in rabbits with experimental myasthenia

The morphology of motor end-plates in rabbits immunized with Torpedo nicotinic acetylcholine receptor (nAChR) has been studied by light and electron microscopy. Rabbits were studied either after one period of paralysis, some in parallel with electrophysiological recordings of MEPPs and EPPs and of Naja naja α-neurotoxin binding properties or after recovery followed by a second paralysis. Changes in the subneural apparatus were noted after cholinesterase staining only in the latter group. Ultrastructurally, however, most end-plates in both groups contained a wide range of abnormalities. Many were similar in appearance to those observed in human myasthenia gravis (MG). This further supports the theory that immunized rabbits can be used as a model for myasthenia gravis. In the rabbits with 1 period of paralysis an acute stage of influence on the neuromuscular junction seemed to be present while simplified motor end-plates typical for human MG were mostly found in rabbits with 2 periods of paralysis. Short post-synaptic folds in conjugation with thickened membrane-bound vesicles at their tops, inside the basement membrane, were frequently observed. These were interpreted as if the crests of the folds containing nAChR had degenerated and had been budded off. If so, a large number of receptor sites had been lost which would be one possible explanation for the lowered capacity of the muscles to bind Naja naja α-neurotoxin. Membrane thickenings with projections and striations were interpreted as reflecting ACh receptors and were observed in the post-junctional membrane without proximity to the nerve terminal. The degeneration of the top of the post-synaptic folds and the occurrence of receptors at other locations within the motor end-plate will result in a widened distance between the nerve terminal and the receptors, which can explain previous interpretations of a presynaptic defect in MG.