Acute Disturbance Of Consciousness Research Articles

Delirium in ICU patients is associated with increased temperature variability

Delirium is an acute disturbance of consciousness and cognition. It is a common disorder in the ICU and associated with impaired long-term outcome [1,2]. Despite its frequency and impact, delirium is poorly recognized by ICU physicians and nurses using delirium screening tools [3]. A completely new approach to detect delirium is to use monitoring of physiological alterations. Temperature variability, a measure for temperature regulation, could be an interesting parameter for monitoring of ICU delirium, but this has never been investigated before. The aim of this study was to investigate whether temperature variability is affected during ICU delirium.

Acute Disturbance of Consciousness as the First Clinical Manifestation of an Elderly Patient with Acute Transverse Myelitis

Acute transverse myelitis (ATM) is a rare entity in the elderly. This case report summarizes the clinical features and treatment of an elderly patient with ATM. The aim is to be expected to benefit the diagnosis and treatment of ATM in the elderly. A 68-year-old mail presented with a 5-hour history of acute loss of consciousness and high fever for one day. The examination showed that pin sensation disappeared below the level of the 8th thoracic spinal segment. The patient had paraplegia, muscle hypotonia, urinary incontinence and the disappearance of limb tendon reflexes. Magnetic resonance image (MRI) scan showed extensive increased T2 signal in the spinal cord from medulla oblongata to the first thoracic spine level. The combination treatment was used with 500mg methylprednisone and immunoglobulin (1g/kg) intravenously. On the10 days of hospitalization, the muscle strength of limbs was significantly improved. Methylprednisone was taken orally for one month (80 mg/d) and the amount of oral medications was gradually reduced, maintaining for two months after hospital discharge. After three months from hospital discharge, the patient could walk independently and had no sensory disturbances and urinary incontinence. This case highlights the rare presentation of an elderly patient with ATM which experienced acute disturbance of consciousness as the first clinical manifestation. This case also highlights that the prognosis is better under the acute ATM occurrence in the elderly if treated timely.

Outcome and quality of life in patients with postoperative delirium during an ICU stay following major surgery

IntroductionDelirium is an acute disturbance of consciousness and cognition that has been shown to be associated with poor outcomes, including increased mortality. We aimed to evaluate outcome after postoperative delirium in a cohort of surgical intensive care unit (SICU) patients.MethodsThis prospective study was conducted over a 10-month period in a SICU. Postoperative delirium was diagnosed in accordance with the Intensive Care Delirium Screening Checklist (ICDSC). The primary outcome was mortality at 6-month follow-up. Hospital mortality and becoming dependent were considered as secondary outcomes, on the basis of the evaluation of the patient’s ability to undertake both personal and instrumental activities of daily living (ADL) before surgery and 6 months after discharge from the SICU. For each dichotomous outcome - hospital mortality, mortality at 6-month follow-up, and becoming dependent - a separate multiple logistic regression analysis was performed, which included delirium as an independent variable. Another outcome analyzed was changes in health-related quality of life, as determined using short-form 36 (SF-36), which was administered before and 6 months after discharge from the SICU. Additionally, for each SF-36 domain, a separate multiple linear regression model was used for each SF-36 domain, with changes in the SF-36 domain as a dependent variable and delirium as an independent variable.ResultsOf 775 SICU-admitted adults, 562 were enrolled in the study, of which 89 (16%) experienced postoperative delirium. Delirium was an independent risk factor for mortality at the 6-month follow-up (OR = 2.562, P <0.001) and also for hospital mortality (OR = 2.673, P <0.001). Delirium was also an independent risk factor for becoming dependent for personal ADL (P-ADL) after SICU discharge (OR = 2.188, P <0.046). Moreover, patients who experienced postoperative delirium showed a greater decline in SF-36 domains after discharge, particularly in physical function, vitality, and social function, as compared to patients without postoperative delirium.ConclusionsPostoperative delirium was an independent risk factor for 6-month follow-up mortality, hospital mortality, and becoming independent in P-ADL after SICU discharge. It was also significantly associated with a worsening in the quality of life after surgery.

フィンゴリモド投与10日後に多巣性白質病変を呈し急性増悪を示した視神経脊髄炎関連疾患（NMOSD）の1例

A 49-year-old female neuromyelitis optica spectrum disorder (NMOSD) patient with positive anti-aquaporin 4 (AQP4) antibody was treated with fingolimod (FTY720). Ten days later, she developed acute disturbance of consciousness, aphasia, right hemi-spatial neglect, and right hemiparesis. Brain MRI showed multiple white-matter lesions with slight Gadolinium enhancement. She was diagnosed of acute exacerbation of NMOSD. Thus, fingolimod may be associated with the development of a fulminant course in NMOSD patients with positive anti-AQP4 antibody.

A Case of a Primary Radiation-Induced Malignant Peripheral Nerve Sheath Tumor in the Cauda Equina in a Patient with Neurofibromatosis Type 2

Abstract Background: Radiation-induced malignant peripheral nerve sheath tumors (MPNSTs) may occur in any irradiated area of the body where primary malignant lesions existed. However, there have been isolated reports regarding the radiation-induced transformation of spinal schwannomas into MPNSTs in patients with neurofibromatosis type 2 (NF2). Case material: A 47-year-old woman presented with gradually progressive paraparesis, bowel-bladder dysfunction, and acute consciousness disturbance. Fifteen years previously, she had undergone radical hysterectomy with adjuvant intraoperative para-aortic radiotherapy for the treatment of uterine cervical cancer. Magnetic resonance (MR) images of the brain revealed hydrocephalus and multiple intracranial tumors in bilateral oculomotor and vestibular nerves. Spinal MR images revealed numerous tumors in the cervical cord and cauda equina. Signal alteration in the lumbosacral vertebral bodies on MR images, which implies fatty degeneration, suggested that the cauda equina was included in the previous radiation field. Because the patient complained of severe pain in the lower back region and lower extremities, we partially resected the lumbosacral tumors to achieve pain control. Histological examination of the resected tumors revealed the lesions to be MPNSTs. Despite postoperative radiation therapy, the residual tumor regrew. The patient is now under palliative care. Conclusion: We report a rare case of a primary MPNST in the cauda equina occurring 15 years after the administration of intraoperative irradiation for uterine cancer. In patients with NF2 who undergo irradiation for malignancies, long-term observation is mandatory because tardive malignant transformation may occur in pre-existing schwannomas in the irradiated field.

Delirium and multiple electrolyte abnormalities associated with high dose paroxetine exposure

The authors describe a 57-year-old male patient who suffered from acute delirium after 3 days usage of paroxetine 60 mg/day. Besides hyponatremia, hypokalemia and hypophosphatemia were also noted concurrently. Paroxetine related syndrome of inappropriate antidiuretic hormone secretion (SIADH) and concurrent renal loss of potassium and phosphate were suspected. All the electrolyte abnormalities recovered quickly after discontinuation of the drug and electrolyte supply. The 57-year-old man with myelodysplastic syndrome had received a successful bone marrow transplant 10 years earlier. Although his hematological disease condition was stable, he developed major depression 5 years ago after a severe pneumonia episode. He has been on paroxetine 20 mg/d since, without any other regular medications. The patient discontinued paroxetine of his own accord 2 months before the present admission. Depressed mood and insomnia recurred, so he took paroxetine again. He took paroxetine 60 mg/d for 3 days. Unfortunately, acute consciousness disturbance was noted, and he was brought to the emergency department of the National Taiwan University Hospital, Taipei, Taiwan. Blood examinations showed serum sodium 113 mmol/L, potassium 3.2 mmol/L, phosphate 1.3 mg/dL, chloride 92 mmol/L (normal range, 98–108), calcium 1.98 mmol/L (normal range, 2.02–2.60), and magnesium 0.77 mmol/L (normal range, 0.78–1.03). There was no vomiting, anorexia, diarrhea, or other identifiable causes for electrolyte abnormalities. His renal function was normal. The transtubular potassium gradient was >4, and other urinary studies also revealed renal wasting of phosphate and magnesium. A room air arterial blood sampling revealed mild acute respiratory alkalosis. His blood pressure was 158/89 mmHg and heart rate was 90/min. Paroxetine was discontinued and he was admitted. Subsequent laboratory studies showed that thyroid and adrenal function examinations, plasma aldosterone and renin activity were all within normal limits. After electrolyte supplementation, his consciousness level improved and all electrolyte abnormalities disappeared quickly. During the entire time of hospitalization he didn’t receive any other medication besides electrolyte supplementation. Paroxetine associated hyponatremia has been well reported in the literature and the underlying mechanism was assumed to be SIADH. The incidence of hyponatremia related to paroxetine varied greatly from 3.5/1000 to 12%1, 2 in different patient populations. However, there had been no report regarding delirium and multiple electrolyte imbalances besides hyponatremia in association with paroxetine usage. The normovolemic hypotonic hyponatremia without evidence of hepatic, cardiac, renal, thyroid, or adrenal dysfunction indicated SIADH, but in this case, the cause of multiple electrolyte disturbances was less clear. Serotonin, acting through 5-HT2 receptors, can stimulate the rennin–angiotensin–aldosterone system and may cause hyperaldosteronism.3 However, normal plasma aldosterone level and absence of metabolic alkalosis made hyperaldosteronism unlikely. Reviewing the literature, only one case report associating SIADH with multiple electrolyte disturbances was found.4 The authors speculated that the multiple electrolyte depletion was related to increased renal excretion as a result of relative volume expansion, but the cause of SIADH was not specified in that case report. For other selective serotonin reuptake inhibitor (SSRI), only venlafaxine had been reported to be associated with hypokalemia in a patient with underlying Gitelman syndrome.5 In the present patient, increased urinary excretion of potassium, phosphate and magnesium may suggest paroxetine’s effect on renal tubular cells since there was no evidence of hyperaldosteronism and no solid association between SIADH and multiple electrolyte imbalances previously published. However, the authors think further pharmacological studies on SSRI are necessary to prove this observation. The patient remained well at the dose of 20 mg/d, but multiple electrolyte abnormalities developed at the dose of 60 mg/d, indicating a dose–response relationship. According to Naranjo probability scale,6 the association is likely. Since the present patient had an abrupt high dose paroxetine exposure, it’s conceivable that paroxetine may not cause these electrolyte abnormalities if the dosage was escalated gradually and slowly. The authors, therefore, suggest that careful clinical monitoring of electrolytes, especially during an escalation of dosage, may be necessary in patients using SSRI.

Acute disseminated encephalomyelitis in children: one medical center experience.

Acute disseminated encephalomyelitis (ADEM) is a rare inflammatory demyelinating disease of the central nervous system. The experience in children is limited. We retrospectively reviewed our experience with 20 ADEM patients (10 females, 10 males) with age of onset before 18 years old in Taiwan to clarify the clinical manifestations, neuroimaging findings, and the relationship between ADEM and multiple sclerosis (MS). The age at onset ranged from 4 months to 15 years. Seventeen (85%) children had a recent infectious prodrome. Children presented most often with acute consciousness disturbance (70%) and motor deficits (55%). Seizures occurred in 10 (50%), but only one child developed epilepsy in follow-up. Brain magnetic resonance imaging (MRI) evaluations done in all patients revealed multifocal lesions, mainly in subcortical white matter (80%), brainstem (65%), basal ganglia (55%), cerebellum (45%), thalamus (40%), and periventricular white matter (35%). Spinal cord MRI was performed in 9 patients and all of them showed abnormal lesions. Eleven patients were treated with high-dose intravenous methylprednisolone pulse therapy, and only one had mild long-term neurological sequelae. Among the 20 patients, five had long-term neurological sequelae and one died. Three patients fit the criteria of multiphasic disseminated encephalomyelitis, in which two developed MS in follow-up. Another patient with ADEM turned out to be MS two years later. We concluded that seizures are not uncommon in ADEM, but the subsequent development of epilepsy is rare. Long-term prognosis of ADEM is generally good. Because recurrence of ADEM is not uncommon, long-term follow-up of those children with ADEM is needed to distinguish between ADEM and MS.

Bickerstaff brainstem encephalitis after heat stroke

Sirs: Bickerstaff brainstem encephalitis (BBE) is characterized by acute onset of ophthalmoplegia and ataxia with symptoms and signs indicative of involvement of the central nervous system such as consciousness disturbance [1]. It has been proposed that BBE, Miller Fisher syndrome, and Guillain-Barre syndrome (GBS) are related disorders [8–10]. In fact, a considerable number of patients with BBE have overlapping GBS [8, 15]. A number of factors have been described as triggers of GBS [13]. Heat stroke produces a wide variety of neurological complications [6], but only one case of GBS after heat stroke has been reported [11]. We present a patient with overlapping BBE and GBS after heat stroke. To our knowledge, this is the first report of such a patient. A previously healthy 43-year-old man experienced generalized tonic seizure with loss of consciousness during hard physical work on a hot summer day. He was transferred to our intensive care unit. The core temperature was 42.8°C, heart rate 173 bpm, and blood pressure 66/36 mmHg. Deep coma and bilateral miotic pupils were observed. Laboratory tests showed a platelet count of 113.000/mm3, creatinine 2.73 mg/dL, creatine kinase 2833 U/L, and serum interleukin-6 8594 pg/ml (normal < 4). He was treated with surface cooling (35 °C), mechanical ventilation, intravenous dopamine, and continuous hemodiafiltration. His general status gradually improved. On day 8, he was weaned from mechanical ventilation. On day 9, he was fully conscious with no weakness in the limbs, normal external ocular movements, and normal tendon reflexes. The next day, he again showed consciousness disturbance and weakness in all four limbs. On day 11, he was drowsy, but he was able to respond to commands. His pupils were equal (3.0 mm) and pupillary light reflexes absent. There were complete external ophthalmoplegia, bilateral facial palsy, aphonia, tetraparesis (MRC grade 3 for the upper extremities, grade 2 for the lower ones), limb ataxia, and areflexia. Laboratory examinations on day 12 revealed near-normal blood cell count (white blood cell, 9.900/mm3), and normal serum electrolytes and vitamin B1 levels. Brain MRI found no obvious abnormalities responsible for his consciousness disturbance and muscle weakness. Serum antibodies against ganglioside GM1, GD1a, GT1a, or GQ1b were negative. Cerebrospinal fluid (CSF) contents on day 12 were normal (cell count, 0/mm3; protein level, 21 mg/dl), and a follow-up CSF examination on day 30 revealed the slightly increased protein level (43 mg/dl; normal < 40 mg/dl). Nerve conduction studies (NCS) showed slightly decreased compound muscle action potential (CMAP) amplitudes, normal nerve conduction velocities and distal latencies, and absent F-waves in all the nerves tested (the median, ulnar, peroneal, and tibial nerves). He underwent plasmapheresis 4 times, every other day from day 15. After this treatment, his neurological symptoms were gradually improved. On day 24, he could talk, but his speech was slurred and ataxic. On day 35, when his muscle strength was near-normal, NCS revealed restored F-waves and increased CMAP amplitudes. On day 60, he was discharged to a rehabilitation facility because he was still unable to stand independently due to ataxia. This patient was characterized by acute consciousness disturbance, ophthalmoplegia, facial palsy, tetraparesis, and ataxia, 7 days after heat stroke. After treatment with plasmapheresis, the signs gradually lessened, resulting in a monophasic course. Although several diseases including Wernicke’s encephalopathy, infectious brainstem encephalitis, and GBSlike syndrome by severe exertion [16] should be considered in the differential diagnosis, his clinical features met the criteria for BBE and overlapping GBS [8, 15], suggesting that the disorders may have been triggered by heat stroke. The absence of F-waves during tetraparesis and their restitution in the recovery phase are consistent with proximal conduction block [7]. Pfeiffer reported the only case of GBS after heat stroke, and speculated that heat stroke activates the immune system by cytokine release which opens the blood-nerve barrier and exposes peripheral nerve antigens, thereby inducing GBS [11]. In fact, various cytokines including tumor necrosis factoralpha and interleukin (IL)–6 are conjectured to function in the pathogenesis of heat stroke [2, 4], and also of GBS and related diseases [3, 5, 12, 14]. Elevated serum IL-6 was detected in our patient. Hypercytokinemia may be the key to the association of GBS and related diseases with heat stroke. LETTER TO THE EDITORS

Delirium en pacientes de una Unidad de cuidados intermedios: estudio prospectivo

Delirium or acute confusional state is defined as an acute disturbance of consciousness and attention. Its prevalence among hospitalized patients fluctuates between 25 and 60%. To assess the prevalence and features of delirium in an intermediate care unit. All patients admitted to intermediate care unit during a period of two months were assessed and followed. Delirium was assessed daily during the stay in the unit, using the Inouye Confusion Assessment Method. Delirium was classified as hyperactive if the patient required pharmacological or physical restraining methods. Sixty four patients, 32 female, aged 19 to 90 years old were assessed. Forty one percent had delirium. Of these, delirium started after admission in 46% and was hyperactive in 35%. Cognitive disturbances were ascertained by the health care team in 69% of patients with delirium. Age over 70 years old and a history of dementia were defined as predisposing factors for delirium. Serum albumin was > 3.5 g/dl in 14 of 18 patients with and in 11 of 27 patients without delirium (p = 0.04). The most frequent risk factors were systemic infections, metabolic disturbances and intracranial lesions. Physical restraining and neuroleptics were the most commonly used measures to deal with hyperactive patients. The prevalence of delirium found in this study is similar to that reported elsewhere, except for the high proportion of patients whose delirium started after admission.

Differential Diagnosis of Dementia, Delirium and Depression

Dementia, delirium and depression are the 3 most prevalent mental disorders in the elderly. While dementia and depression are prevalent in the community, hospitals and nursing homes, delirium is seen most often in acute care hospitals. Much of the management of these syndromes is undertaken by primary care physicians rather than psychiatrists. Therefore, it is imperative that generalist physicians be adept at recognising, evaluating and managing patients with these syndromes. Because no diagnostic tests are pathognomonic of these syndromes, the differential diagnosis hinges on a careful clinical evaluation. The first step is to recognise which of the syndromes is present. Dementia is defined by a chronic loss of intellectual or cognitive function of sufficient severity to interfere with social or occupational function. Delirium is an acute disturbance of consciousness marked by an attention deficit and a change in cognitive function. Depression is an affective disorder evidenced by a dysphoric mood, but the most pervasive symptom is a loss of ability to enjoy usual activities. It is important to recognise that these syndromes are not mutually exclusive, as dementia frequently coexists with delirium and depression. Furthermore, physical diagnoses, such as chronic obstructive lung disease, congestive heart failure, stroke and endocrine disorders, are frequently associated with depressive symptoms. Given this, a comprehensive evaluation is mandatory. Laboratory tests are necessary to exclude concurrent metabolic, endocrine and infectious disorders, and drug effects. Imaging studies should be obtained selectively in patients with signs and symptoms, such as focal neurological findings and gait disturbances, which are suggestive of structural lesions: stroke, subdural haematoma, normal pressure hydrocephalus and brain tumours. Appropriate management involving pharmacological and nonpharmacological measures will result in significant improvement in most patients with these syndromes. Potentially offending drugs should be discontinued. In delirious patients the underlying illness must be treated concomitantly with the use of psychotropics, if necessary. Although no current medications have been shown to have a significant effect on the functional status of patients with the 2 most common causes of dementia, Alzheimer's disease and multi-infarct dementia, the management of concomitant illness in these patients may result in improved function for as long as a year. Tacrine, an anticholinesterase inhibitor, improves cognitive function slightly in selected patients with Alzheimer's disease over short periods. Finally, the treatment of depression with medications or electroconvulsive therapy (ECT) results in significant reductions in mortality and morbidity.

Surgical Treatment of Intracranial Hematoma with Congenital Factor XIII Deficiency

A case of the intracranial hemorrhage due to the congenital factor XIII deficiency was experienced. The patient was a 27-year-old female, who had been diagnosed as congenital factor XIII deficiency at the age of 18. She presented acute consciousness disturbance and the left hemiplegia which was caused by a subcortical hemorrhage in the right frontal lobe. Removal of the hematoma through craniotomy was successfully carried out under a total of 1, 500 units of factor XIII concentrate derived from human placenta, was followed by complete recovery without rebleeding or delay in wound-healing. Clinical features of the congenital factor XIII deficiency with intracranial hemorrhage were discussed with analysis of 27 cases including this case. Whenever a patient with intracranial hemorrhage is encountered, especially in case with a past history such as umbilical bleeding, posttraumatic hematoma, and defective wound-healing, congenital factor XIII deficiency must be borne in mind. Although intracranial hemorrhage is the most fatal complication with deficiency of coagulation factor XIII, the surgical treatment may be safe under replacement therapy of factor XIII concentrate derived from human placenta.