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Results for “Respiratory Paralysis”

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At least 19 recordsLinked to original sources
PubMed1988

GABA involvement in naloxone induced reversal of respiratory paralysis produced by thiopental.

No agent is yet available to reverse respiratory paralysis produced by CNS depressants, such as general anesthetics. In this study naloxone reversed respiratory paralysis induced by thiopental in rats. 25 mg/kg, i.v. thiopental produced anesthesia without altering respiratory rate, increased GABA, decreased glutamate, and had no effect on aspartate or glycine levels compared to controls in rat cortex and brain stem. Pretreatment of rats with thiosemicarbazide for 30 minutes abolished the anesthetic action as well as the respiratory depressant action of thiopental. 50 mg/kg, i.v. thiopental produced respiratory arrest with further increase in GABA and decrease in glutamate again in cortex and brain stem without affecting any of the amino acids studied in four regions of rat brain. Naloxone (2.5 mg/kg, i.v.) reversed respiratory paralysis, glutamate and GABA levels to control values in brain stem and cortex with no changes in caudate or cerebellum. These data suggest naloxone reverses respiratory paralysis produced by thiopental and involves GABA in its action.

Animals↗
PubMed1986

Respiratory paralysis secondary to epidural anesthesia in a dog.

Transient respiratory paralysis developed in a 12-year-old spayed female Cocker Spaniel that received an anesthetic epidurally for excisional biopsy of perianal masses. Paralysis developed almost immediately after injection of 2.5 ml of 2% lidocaine (1 ml/4.9 kg), and was managed by mechanical ventilation and appropriate fluid therapy IV until spontaneous respiration returned. The respiratory paralysis was attributed to the excessive cranial extent of the anesthetic block.

Anesthesia, Epidural↗
PubMed1989

Respiratory paralysis as a presenting symptom in Japanese encephalitis--a case report.

In the literature there are rare reports on Japanese encephalitis (JE) mimicking poliomyelitis or presenting as respiratory paralysis. A case of JE presenting as respiratory paralysis is described. The 22-year-old male was well until five days earlier, when he experienced the acute onset of headache and fever. Four days after onset he developed dysphagia and respiratory difficulty, and a tracheotomy was performed. The following day he lapsed into semicoma and the respiration had to be maintained by an artificial ventilator. He regained consciousness by the 10th day after onset. He became able to comprehend questions and express himself by gestures. But the respiration was still paralytic, and assisted ventilation via a tracheotomy had to be continued. The case was clinically diagnosed as encephalitis. Bulbar poliomyelitis was initially considered due to the clinical features of aseptic meningitis, respiratory paralysis, pharyngeal paralysis with pooling secretions in the pharynx, tachycardia and elevated blood pressure. But poliovirus culture obtained from stool and appropriate serological studies were negative. The diagnosis of encephalitis due to JE virus was confirmed by hemagglutination inhibition test (acute phase HI titer 1:320; convalescent phase HI titer 1.1280).

Adult↗
PubMed1988

The treatment of acute polyradiculoneuritis with respiratory paralysis.

This paper reports 504 cases admitted with acute polyradiculoneuritis (AP) to Beijing Children's Hospital from 1975 through 1984. 343 of the 504 cases (68.1%) with AP had respiratory paralysis and in 198/504 (39.3%), tracheotomy was performed. In this study, none of the patients received steroids. We attempted to assess the grades of respiratory paralysis and established the criteria for tracheotomy. We also must perform the following procedures: 1) Artificial ventilation must be used correctly, 2) The secretion should be aspirated regularly in order to maintain a clear airway, 3) Sterilization must be strictly conducted to prevent cross infection. As a result, of 504 cases with AP 9 died, the mortality rate being 1.79%. The study suggests tracheotomy should be performed early and it is one of the most important procedures in the treatment of AP with respiratory paralysis.

Acute Disease↗
PubMed1979

Prolonged respiratory paralysis in wound botulism.

Two patients had wound botulism with longer duration of respiratory paralysis than previously described. Each sustained extensive trauma to soft tissues and grossly contaminated wounds when thrown from a vehicle in a rural area. Progressive muscular weakness and respiratory distress occurred 8 and 13 days after injury, in the presence of infected wounds and clinical and laboratory findings characteristic of botulism. Spontaneous vital capacity and inspiratory effort served as bedside indicators of ventilatory function throughout 11 weeks of ventilatory support in each case and paralleled other clinical assessments of progress and recovery. Wound botulism may result in neuromuscular paralysis for a prolonged period. These cases illustrate the primary role of scrupulous nursing and respiratory care throughout such a period of ventilatory insufficiency.

Adult↗
PubMed1979

Respiratory paralysis to improve oxygenation and mortality in large newborn infants with respiratory distress.

The nonsynchronous respiratory efforts of neonates with surgically correctable disorders may inhibit effective mechanical ventilation. The records of 25 infants treated with metocurine for muscular paralysis to improve mechanical ventilation were reviewed. All patients were greater than 35 (37.6 +/- 2.1) weeks gestation and 2.27 (2.98 +/- .47) kg. All required ventilatory support with an FiO2 of 100%. The mortality rate of this group of infants was 20% as compared with 73% (p < .001) in a similar group of 26 infants managed without paralysis. In 10 of the 25 infants treated with metocurine, pre- and 1 hr postparalysis paO2 values were available. The mean paO2 prior to paralysis was 62 (45--111) mm Hg and the mean post-paralysis paO2 was 144 (75--227) mm Hg, representing at 132% increase in paO2 (p < .001). The mean dosage for metocurine was 3.5 (1.45--6.79) mg/kg/day; however, those requiring paralysis for greater than 7 days showed a dramatically increasing requirement. These preliminary data suggest that respiratory paralysis reduces right-to-left shunting, improves paO2 and decreases mortality in large infants with severe respiratory distress requiring ventilatory support.

Diaphragm↗
PubMed1975

Complete respiratory paralysis caused by a large dose of streptomycin and its treatment with calcium chloride.

Several cases have been reported, in which a rather large dose of streptomycin given intraperitoneally at operation has produced respiratory paralysis. In these cases the treatment has usually consisted of respirator ventilation and administration of atropine and neostigmine. In animal experiments, in which a cessation of breathing has been produced, calcium salts have produced quick recovery. The authors present a case, in which appendicetomy was performed on a 10-year-old girl for a perforated appendix at the end of which, an overdose of intraperitoneal streptomycin was given, followed 10 minutes later by complete cessation of breathing. The patient had to be intubated again and put into a respirator. Neostigmine and atropine were used without noticeable effect. One and a half hours after the breathing had stopped 0.6 g calcium chloride was given intravenously and the girl recovered immediately and completely.

Calcium Chloride↗
PubMed1992

[Diaphragm pacing for the ventilatory support of the quadriplegic patients with respiratory paralysis].

Electrical stimulation of the phrenic nerve to pace the diaphragm in patients with chronic ventilatory insufficiency has been an established therapeutic modality since William W.L. Glenn first described using radiofrequency signals in 1978 to stimulate the phrenic nerves. Before this event, patients who were ventilator-dependent and thus bedridden because of respiratory paralysis associated with quadriplegia usually anticipated little chance for physical or psychosocial rehabilitation. Two cases of C1-C2 subluxtion with cord injury and chronic ventilatory insufficiency were implanted at VGH-Taipei with diaphragm pacemaker in 1988. Postoperative phrenic nerve stimulation was given according to individual training schedule. One case with total phrenic paralysis received bilateral phrenic nerve stimulation and became weaned from the ventilator 6 months later. The other case with partially active ventilatory function received unilateral phrenic nerve stimulation to compensate the ventilation. However, its final outcome still showed the necessity of a bilateral mode to achieve adequate ventilation irrespective of strenuous training for 2 years.

Adult↗
PubMed1976

Respiratory paralysis during treatment of hypertension with trimethaphan camsylate.

Four cases are reported in which respiratory arrest occured coincident with the intravenous administration of large doses of trimethaphan camsylate (Arfonad) to control hypertension. The mechanism of the respiratory depression is unknown, but it may have been related to a direct effect of trimethaphan on the respiratory center or to a curare-like effect of the drug. Close monitoring of ventilatory capacity should be maintained in all patients treated with trimethaphan.

Adult↗
PubMed1985

Phrenic nerve stimulation (diaphragm pacing) in respiratory paralysis.

Phrenic nerve stimulators (diaphragm pacers) were implanted in 16 patients with partial or total respiratory insufficiency due to high cervical medullary lesions and brain stem lesions (14 cases) or central hypoventilation syndrome (2 cases). At 5-72 months' follow-up (M = 35) 12 patients are entirely independent of conventional respirator, 2 of them after 8 years of total respirator dependency. Two patients are dead and the final 2 cases had limited help from diaphragm pacing.

Adolescent↗