Combined effects of mild hypothermia and nitrous-oxide-induced narcosis on manual and cognitive performance.

Divers are at enhanced risk of suffering from acute cognitive deterioration because of the low ambient temperatures and the narcotic action of inert gases inspired at high pressures. Yet, the behavioral effects of cold and inert gas narcosis have commonly been assessed in isolation and during short-term provocations. We therefore evaluated the interactive influence of mild hypothermia and narcosis engendered by a subanesthetic dose of nitrous oxide (N2O; a normobaric intervention analog of hyperbaric nitrogen) on cognitive function during prolonged iterative exposure. Fourteen men partook in two ∼12-h sessions (separated by ≥4 days), wherein they performed sequentially three 120-min cold (20°C) water immersions (CWIs), while inhaling, in a single-blinded manner, either normal air or a normoxic gas mixture containing 30% N2O. CWIs were separated by a 120-min rewarming in room-air breathing conditions. Before the first CWI and during each CWI, subjects performed a finger dexterity test, and the Spaceflight Cognitive Assessment Tool for Windows (WinSCAT) test assessing aspects of attention, memory, learning, and visuospatial ability. Rectal and skin temperatures were, on average, reduced by ∼1.2 °C and ∼8 °C, respectively (P < 0.001). Cooling per se impaired (P ≤ 0.01) only short-term memory (∼37%) and learning (∼18%); the impairments were limited to the first CWI. N2O also attenuated (P ≤ 0.02) short-term memory (∼37%) and learning (∼35%), but the reductions occurred in all CWIs. Furthermore, N2O invariably compromised finger dexterity, attention, concentration, working memory, and spatial processing (P < 0.05). The present results demonstrate that inert gas narcosis aggravates, in a persistent manner, basic and higher-order cognitive abilities during protracted cold exposure.

Orbital infarction during drug abuse: tissues of the globe do not appear to recover function.

AIM: To describe the features of an orbital infarction syndrome arising after prolonged orbital pressure during drug-induced stupor in young people. PATIENTS AND METHODS: The clinical presentation and course for drug-induced orbital infarction is described, based on a retrospective review of clinical notes and imaging. RESULTS: Two cases of orbital infarction syndrome, due to prolonged orbital compression caused by sleeping with pressure on the orbit during drug-induced stupor, are described. Both patients presented with very poor vision and mydriasis, marked periorbital swelling with some pain, and complete external ophthalmoplegia. Whilst the orbital changes and eye movements recovered, the affected eyes had persistent wide mydriasis, and remained blind with marked optic atrophy. CONCLUSION: With a mechanism analogous to prolonged orbital pressure due to improper head positioning during neurosurgical procedures, drug-users appear to risk developing an orbital infarction syndrome if they rest with prolonged pressure on the orbit during a drug-induced stupor.

External Compressive Ischemic Orbitopathy: A Rising Clinical Entity.

PURPOSE: Saturday night retinopathy, the term coined by Jayam et al . in 1974, is a rare condition in which external compression of the orbit during a drug and alcohol stupor causes a unilateral orbitopathy with ophthalmoplegia and ischemic retinopathy. This condition has been increasingly reported in the last decade, correlating with an increasing burden of substance use. This condition mirrors a similar entity typically reported in patients following spinal surgery, where a headrest supporting the patient's face compresses the orbit. The current authors combine these 2 entities, entitled external compressive ischemic orbitopathy, and present a comprehensive literature review describing this entity. METHODS: A systematic review was carried out in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. All related publications of vision loss in the setting of orbital compression were reviewed. Data collected included patient demographics, precipitating circumstances of vision loss, presenting ocular symptoms, outcomes, and ancillary imaging. RESULTS: In total 31 articles were selected for inclusion, yielding 46 patients. A total of 10 patients suffered orbitopathy in the setting of a drug stupor, and 36 following prone-positioned surgery. However, 79% of patients presented with visual acuity of light perception or worse. Also, 86% of patients presented with ophthalmoplegia, 92% with proptosis and orbital edema, and 86% with varying degrees of retinal ischemia. When compared with iatrogenic cases, self-induced stuporous cases demonstrated worse presenting visual acuity, ophthalmoplegia, retinal and choroidal filling, and worse final outcomes. CONCLUSION: External compressive ischemic orbitopathy is a severe vision-threatening condition that has been increasingly reported in the last decade.

Possible causes of narcosis-like symptoms in freedivers.

During deep-sea freediving, many freedivers describe symptoms fairly similar to what has been related to inert gas narcosis in scuba divers. This manuscript aims to present the potential mechanisms underlying these symptoms. First, known mechanisms of narcosis are summarized while scuba diving. Then, potential underlying mechanisms involving the toxicity of gases (nitrogen, carbon dioxide and oxygen) are presented in freedivers. As the symptoms are felt during ascent, nitrogen is likely not the only gas involved. Since freedivers are frequently exposed to hypercapnic hypoxia toward the end of the dive, it is proposed that carbon dioxide and oxygen gases both play a major role. Finally, a new "hemodynamic hypothesis" based on the diving reflex is proposed in freedivers. The underlying mechanisms are undoubtedly multifactorial and therefore require further research and a new descriptive name. We propose a new term for these types of symptoms: freediving transient cognitive impairment.

Catatonia associated with prolonged stupor after general anesthesia in a patient with multiple neuropsychiatric disorders -a case report.

BACKGROUND: Delayed emergence after general anesthesia may significantly affect a patient's condition. We present the case of a patient who experienced prolonged delayed recovery of consciousness, language, and motor response due to catatonia after eight hours of total elbow arthroplasty under general anesthesia. CASE: A 68-year-old woman with neuropsychiatric disorders and Parkinson's disease did not respond adequately during recovery after more than eight hours of general anesthesia. Following the operation, the patient was semi-comatose and appeared to have nonconvulsive status epilepticus upon awakening from anesthesia. However, subsequent examinations did not reveal any organic causes. The patient was subsequently diagnosed with catatonia, treated, and discharged following gradual improvement. CONCLUSIONS: Although rare, patients taking psychiatric drugs for an extended period may experience delayed emergence after prolonged general anesthesia without identifiable causes. Catatonia should be considered in the differential diagnoses of these patients.

EEG functional connectivity is sensitive for nitrogen narcosis at 608 kPa.

Divers commonly breathe air, containing nitrogen. Nitrogen under hyperbaric conditions is a narcotic gas. In dives beyond a notional threshold of 30 m depth (405 kPa) this can cause cognitive impairment, culminating in accidents due to poor decision making. Helium is known to have no narcotic effect. This study explored potential approaches to developing an electroencephalogram (EEG) functional connectivity metric to measure narcosis produced by nitrogen at hyperbaric pressures. Twelve human participants (five female) breathed air and heliox (in random order) at 284 and 608 kPa while recording 32-channel EEG and psychometric function. The degree of spatial functional connectivity, estimated using mutual information, was summarized with global efficiency. Air-breathing at 608 kPa (experienced as mild narcosis) caused a 35% increase in global efficiency compared to surface air-breathing (mean increase = 0.17, 95% CI [0.09-0.25], p = 0.001). Air-breathing at 284 kPa trended in a similar direction. Functional connectivity was modestly associated with psychometric impairment (mixed-effects model r2 = 0.60, receiver-operating-characteristic area, 0.67 [0.51-0.84], p = 0.02). Heliox breathing did not cause a significant change in functional connectivity. In conclusion, functional connectivity increased during hyperbaric air-breathing in a dose-dependent manner, but not while heliox-breathing. This suggests sensitivity to nitrogen narcosis specifically.

Catatonic Stupor in Schizophrenic Disorders and Subsequent Medical Complications and Mortality.

OBJECTIVE: Although catatonia can occur secondary to a general medical condition, catatonia itself has been known to lead to various medical compolications. Although case reports on the association of catatonia with subsequent medical complications have been documented, no comprehensive large-scale study has been performed. To investigate specific medical complications after catatonia, we conducted a retrospective cohort study of specific medical complications of schizophrenia patients with catatonia. METHODS: The 1719 schizophrenia inpatients in our study were categorized into two groups: the catatonia group, i.e., those who exhibited catatonic stupor while they were hospitalized, and the noncatatonia group, i.e., those who never exhibited catatonic stupor. Differences between the two groups in the occurrence of subsequent medical complications were examined using linear and logistic regression analyses, and models were adjusted for potentially confounding factors. RESULTS: The catatonia group had an increased risk for mortality (odds ratio = 4.8, 95% confidence interval = 2.0-10.6, p < .01) and certain specific medical complications, i.e., pneumonia, urinary tract infection, sepsis, disseminated intravascular coagulation, rhabdomyolysis, dehydration, deep venous thrombosis, pulmonary embolism, urinary retention, decubitus, arrhythmia, renal failure, neuroleptic malignant syndrome, hypernatremia, and liver dysfunction (all p values < .01, except for deep venous thrombosis, p = .04 in the multiple linear regression analysis). CONCLUSIONS: Catatonic stupor in schizophrenia substantially raises the risk for specific medical complications and mortality. Hyperactivity of the sympathetic nervous system, dehydration, and immobility, which are frequently involved in catatonia, might contribute to these specific medical complications. In catatonia, meticulous care for both mental and medical conditions should be taken to reduce the risk of adverse medical consequences.

Early post-transplant hyperbilirubinemia is a possible predictive factor for developing neurological complications in pediatric living donor liver transplant patients receiving tacrolimus.

The cause of post-transplant CNI-NCs is multifactorial and not ascribed solely to CNI toxicity. A total of 90 children (aged <20 years) who underwent LDLT were evaluated to investigate the predictive factors associated with CNI-NCs. Twelve patients (13.3%) developed CNI-NCs after LDLT (age range, 2-15 years). The symptoms of CNI-NCs were seizures, VD, and stupor. The median onset of CNI-NCs was 10 days (range, 5-30 days) post-transplant. In the univariate analysis, higher recipient age at LDLT, donor age and recipient's BW, lower actual GV/SLV and TAC dosage/BW, and higher mean T-Bil and sodium level for 7 days after transplantation were independently significantly associated with TAC-NCs. Multivariate analysis showed that the T-Bil level in the first week after LDLT was the only significant independent predictive factor for TAC-NCs (HR, 1.588; 95% CI, 1.042-2.358; P=.031). In conclusion, CNI-NCs occurred most frequently in children over 5 years and were associated with hyperbilirubinemia for 7 days post-transplant, regardless of TAC levels. The transplant team should refer to a neurologist to define the diagnosis and to collaborate to resolve the neurological problems.

Refractory status epilepticus: new insights in presentation, treatment, and outcome.

Refractory status epilepticus (RSE), defined as status epilepticus that fails to respond to the acute administration of two antiepileptic medications, occurs in approximately a third of patients with status epilepticus, and is associated with increased hospital length of stay, mortality, and functional disability. Common presentations include: (1) generalized convulsive status epilepticus or complex partial status epilepticus that continue despite initial therapies; (2) stupor or coma following a generalized convulsive or complex partial seizure; or (3) stupor or coma following brain surgery or acute brain injury. When status epilepticus continues or recurs 24 hours or more after the initiation of anesthetic therapy, or recurs on the reduction or withdrawal of anesthesia, it is termed super RSE. Published evidence on optimal management of RSE consists largely of case reports or small series. The mainstay of treatment is the administration of anesthetic agents titrated to electrographic seizure control. Adjunctive therapies include hypothermia and immunosuppression and less commonly, surgery, electrical stimulation therapies, and induction of ketosis. Patients with cardiopulmonary complications and prolonged duration of drug-induced coma tend to have worse post-treatment functional outcomes. However, significant improvement over time can occur in survivors, and thus treatment is justified even in patients who require prolonged anesthetic coma. The strongest predictors of outcome are duration of anesthetic coma, etiology, and development of cardiopulmonary complications.

Aspiration pneumonia caused by inadvertent insertion of gastric tube in an obtunded patient postoperatively.

A nasogastric feeding tube is commonly inserted to facilitate patient meeting nutritional needs after oral surgery. But sometimes incorrect position may cause a severe iatrogenic damage. The authors present a case of an aspiration pneumonia complication with the result of malposition of nasogastric tube while the patient was intubated postoperatively. He recovered 3 weeks later with antibody therapy.

Prolonged catatonic stupor successfully treated with aripiprazole in an adolescent male with schizophrenia: a case report.

We present the case of a fifteen-year-old adolescent male with schizophrenia who had long-term catatonic stupor and was successfully treated with aripiprazole. The onset of his stupor manifested rapidly after experiencing prodromal symptoms for two months. He was left untreated without adequate food ingestion for three weeks because of his parents' religious faith, and was severely dehydrated and malnourished upon admission to our hospital. After his physical recovery, treatment with risperidone (0.5-2.0 mg, 5 weeks) was started. However, hypersedation occurred, and the risperidone was switched to aripiprazole, with dose increases up to 18 mg/day (5 months). As a result, he recovered from his totally noncommunicative state. Aripiprazole, which has a unique pharmacological mechanism of action distinct from other atypical antipsychotics and an excellent safety profile, may be effective in the treatment of some schizophrenic patients with stupor, which sometimes carries a risk of physical debilitation and requires special attention due to the risk of adverse drug reactions.

[Combined spinal-epidural anesthesia for abdominal surgery in a patient with chronic obstructive pulmonary disease].

A 69-year-old man (150 cm, 57 kg)who had been diagnosed as having COPD, was admitted to our hospital because of abdominal pain and drowsiness. He was diagnosed as CO2 narcosis and perforation of appendix. When he recovered from CO2 narcosis, he was scheduled for elective ilectomy. Because his pulmonary function was impaired, combined spinal and epidural anesthesia was selected. With the patient in the right lateral position, an epidural catheter was inserted at T12-L1 interspace, and spinal anesthesia was performed at L3-4 interspace with 0.5% isobaric bupivacaine 4 ml. When the patient was positioned laterally, SpO2 decreased from 82% to 77%. After completion of injection, the patient was returned to the supine position, and SpO2 immediately recovered. Spinal block level was not satisfactory, and fentanyl 0.1 mg and 2% mepivacaine 4 ml were administered through epidural catheter to achieve a T4 level of block. Because severe intraperitoneal inflammation was observed, ilectomy was changed to drainage of intra-abdominal abscess. The patient did not complain of dyspnea, pain, or nausea, intraoperatively. SpO2 was 85-93% with O2 inhalation at 1l x min(-1) during the operation. Post-operative course was uneventful. Although lateral position is popular in performing epidural and spinal anesthesia, sitting position could be suitable for this patient. Decrease in SpO2 may have occurred due to ventilation-perfusion mismatch. Since combined spinal and epidural anesthesia can preserve spontaneous respiration and it is possible to titrate anesthetic level, it would be preferable for abdominal surgery in patients with COPD.

Opioid-related narcosis in a woman with myopathy receiving magnesium.

An Asian multiparous woman weighing 47 kg, who suffered from a rare myopathy, congenital fibre type disproportion, was given morphine 10 mg intramuscularly for labour analgesia. After delivery, she had diastolic hypertension and proteinuria and was prescribed magnesium sulphate. Some hours later she became unresponsive with little respiratory effort. Blood gas analysis revealed a respiratory acidosis. Naloxone administration reversed the symptoms. Further doses were required as the respiratory depression recurred. Opioid-related narcosis is the most likely diagnosis in this case. Other possible differential diagnoses were magnesium overdose or a post-ictal state. The presence of a myopathy could render this patient susceptible to the respiratory effects of opioids. Other explanations for an exaggerated and delayed response to opioids include co-administration of other respiratory depressant drugs such as magnesium sulphate, co-morbidity such as renal impairment and genetic variability in the metabolism of morphine. Robust guidelines and highlighting patients with risk factors are required to prevent this complication from recurring.