Background: Critical illness polyneuropathy (CIN) and critical illness myopathy (CIM), together “ICU-Acquired weakness (ICUAW),” occur frequently in septic patients. One of the proposed mechanisms for ICUAW includes prolonged inactivation of sodium channels. Propofol, used commonly in patients with acute respiratory failure (ARF), primarily acts via enhancement of GABAergic transmission but may also increase sodium channel inactivation, suggesting a potential interaction. Methods: Electronic medical records and EMG reports of patients with ICUAW and a diagnosis of either sepsis, septicaemia, severe sepsis, or septic shock, concurrent with a diagnosis of acute respiratory failure (ARF), were retrospectively analyzed in a single center university hospital. Results: 74 cases were identified (50.0% men, age 58±14 years), and compared to age- and sex-matched controls. Of these, 51 (69%) had CIN, 19 (26%) had CIM, and 4 (5%) had both. Propofol exposure was significantly higher in patients with ICUAW compared to controls (63.5% vs. 33.8%, p<0.001). The odds ratio of developing ICUAW with propofol exposure was 3.4 (95% CI:1.7-6.7, p<0.001). Patients with ICUAW had significantly more days in hospital (59±44 vs. 30±23) and ICU (38±26 vs. 17±13), days dependent on mechanical ventilation (27±21 vs. 13±16), and rates of tracheostomy (79.7% vs. 36.5%) and gastrostomy (75.7% vs. 25.7%) (all p<0.001). They also received a significantly higher number of distinct intravenous antibiotics, cumulative days of antibiotic therapy, and exposure to vasopressors and paralytics. Conclusions: Propofol exposure may increase the risk of ICUAW in septic patients. An interaction through sodium channel inactivation is hypothesized.

Hypokalemic periodic paralysis is the most common form of periodic paralysis and is characterized by attacks of muscle paralysis associated with a low serum potassium (K+) level due to an acute intracellular shifting. Thyrotoxic periodic paralysis (TPP), characterized by the triad of muscle paralysis, acute hypokalemia, and hyperthyroidism, is one cause of hypokalemic periodic paralysis. The triggering of an attack of undiagnosed TPP by β2-adrenergic bronchodilators has, to our knowledge, not been reported previously. We describe two young men who presented to the emergency department with the sudden onset of muscle paralysis after administration of inhaled β2-adrenergic bronchodilators for asthma. In both cases, the physical examination revealed an enlarged thyroid gland and symmetrical flaccid paralysis with areflexia of lower extremities. Hypokalemia with low urine K+ excretion and normal blood acid-base status was found on laboratory testing, suggestive of an intracellular shift of K+, and the patients' muscle strength recovered at serum K+ concentrations of 3.0 and 3.3 mmol/L. One patient developed hyperkalemia after a total potassium chloride supplementation of 110mmol. Thyroid function testing was diagnostic of primary hyperthyroidism due to Graves disease in both cases. These cases illustrate that β2-adrenergic bronchodilators should be considered a potential precipitant of TPP.

Case 1: A previously healthy 15-year-old boy was brought by paramedics to the emergency department (ED) after suffering multiple penetrating gunshot wounds (GSWs) to the lower extremities and a single entry to the left suprascapular region. Vital signs were within normal limits upon presentation.

Case 2: A previously healthy 19-year-old man was brought by paramedics to the ED after suffering multiple stab wounds to the back. The patient was hypoxic and in severe respiratory distress upon arrival. A left thoracostomy tube was placed. Clinically the patient improved and vital signs returned to normal.

The relationship between varicella-zoster virus and idiopathic associated laryngeal paralysis was examined in five patients, using complement fixation or enzyme immunoassay testing. In all cases, significant changes in serum levels of varicella-zoster virus antibody were observed. Videofluoroscopy was useful in assessing the severity of the dysphagia and in making an accurate diagnosis; both laryngeal elevation and weakness of pharyngeal wall contraction were also observed. In two cases in which antiviral therapy was delayed, the outcome was poor, with increased levels of varicella-zoster virus immunoglobulin M found on enzyme immunoassay. The outcome of the condition may thus depend both on the speed of antiviral therapy commencement following onset of symptoms, and on the levels of varicella-zoster virus immunoglobulin M antibody (measured by enzyme immunoassay). Our study suggests that varicella-zoster virus should be considered in the differential diagnosis of patients with idiopathic associated laryngeal paralysis, and rapid antiviral therapy should be initiated when necessary.

Accepted concepts of the pathophysiology and treatment of laryngeal paralysis have changed over the years. It has long been observed that symptoms of laryngeal paralysis vary greatly, both between patients and over time. There have been various theories to explain these differences. This article reviews how these ideas have changed over time as research has produced new information. Currently, the most popular view is that the laryngeal nerve regenerates after injury, albeit incompletely and inconsistently, and that variations in symptoms and laryngeal posture can be accounted for by muscle activity.

We recorded continuously, with high precision, the positions of the eyes in anesthetized macaque monkeys prepared for physiological recording. Most recordings were made after the infusion of muscle relaxant to immobilize the eyes; in some cases we also were able to record eye position for periods before the eyes were immobilized. In all monkeys, the eyes moved continuously by as much as 0.5 deg over a 10-min sampling period. The average distance moved was proportional to the square root of the sampling period, as would be expected from a random walk. The movements had three distinct components: slow drifts, and two rhythms driven by the pulse and respiration. The rhythmic movements occurred only under paralysis: they were not discernible in measurements made before the infusion of muscle relaxant. The movements of the eye in the paralyzed animal can have substantial effects on the measured physiological characteristics of neurons. For excursions in the midrange of those we observed, a neuron's sensitivity to a spatial frequency of 10 cycle/deg might be underestimated by as much as a factor of three, depending on the method by which responses were averaged. We show how the effects of eye-movements can be mitigated by appropriate data analysis.

While tonsillectomy is the commonest operation performed by otolaryngologists, paralysis of the hypoglossal nerve following tonsillectomy is not well recognized in the otolaryngology text or literature.

We report a case of hypoglossal nerve paralysis following tonsillectomy and discuss the theories on the pathoaetiology as described in the predominantly anaesthetics literature. The likely causes of nerve injury are described and precautions are suggested to help avoid this problem.

Bilateral extracranial internal carotid aneurysms are very rare, though well documented. We report a case of bilateral extracranial internal carotid aneurysms presenting with vocal fold paralysis, which we believe to be the first.

Facial schwannoma is a relatively rare but well documented lesion, presenting either as a mass or with facial nerve symptoms. In this report, an extensive facial schwannoma, extending from the brain stem to the periphery with minimal facial nerve symptoms and normal facial function is presented.

Parathyroid tumours and cysts are rare and, when presenting as neck masses, can be clinically misdiagnosed as thyroid lesions. Symptoms may be caused by compression of the surrounding structures or hormonal overactivity. This paper describes a patient with recurrent hoarseness owing to the pressure effects of a parathyroid cyst on the recurrent laryngeal nerve.

We present a case of a 63-year-old diabetic male who developed malignant otitis externa following mastoidectomy. Extensive skull base osteomyelitis caused thrombosis of the jugular bulb and subsequent paralysis of cranial nerves VII, IX, X and XII. Hewas treated aggressively with intravenous antibiotics and debridement of granulation tissue in the mastoid bowl with full recovery of the cranial nerve palsies associated with recanalization of the jugular bulb. We believe this is the first reported case of malignant otitis externa to occur following mastoidectomy with complete recovery of the cranial nerve paresis.

Laryngeal obstruction due to bilateral vocal fold paralysis has been treated in many different ways. The CO2 laser or KTP-532 laser endoscopic cordectomy described in this report is a slight modification of the posterior partial cordectomy proposed by Dennis and Kashima. This technique was used in 18 patients (14 with the CO2 and four with the KTP-532 laser). Prophylactic tracheostomy was performed preoperatively. Post-operative results were excellent in nine cases, good in seven cases and poor in two cases who had to remain with a permanent tracheostomy tube with a speaking valve. The main complications noted were the formation of a granuloma (seven cases) and arytenoid oedema (six cases). Revision surgery was performed in the seven cases with granuloma formation and in the two with persistent oedema. The results and the post-operative findings from the use of the two lasers were similar.