Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroglossal cysts are one of the most common midline neck masses. They usually present as midline painless cystic neck mass in the first three decades of life. These anomalies are very rare in elderly patients and may pose difficult diagnostic and therapeutic challenges. Here, we report a case of giant thyroglossal cyst in a 72-year-female patient who presented with stridor, hoarseness of voice, and vocal cord paresis with gross distortion of normal airway anatomy secondary to pressure effect of the mass. The gross distortion and displacement of airway along with respiratory distress in this patient posed a difficult situation in securing the airway. The airway was secured by a unique way of orotracheal intubation with the help of a ventilating airway exchange catheter. The cyst was excised in toto under general anaesthesia. The stridor completely resolved after surgery and tracheostomy was avoided.
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PMID:Stridor in an elderly woman: an unusual presentation of a giant thyroglossal cyst. 2399 73

Neuromuscular blocking agents and corticosteroids are widely used in medicine and in particular in the intensive care unit (ICU). Neuromuscular blockade is commonly used to ease tracheal intubation, to optimize mechanical ventilation and oxygenation in acute respiratory disorders such as status asthmaticus and acute respiratory distress syndrome (ARDS), to prevent shivering during therapeutic hypothermia, and also in patients with elevated intracranial pressure. In the ICU, patients with sepsis, ARDS, community-acquired pneumonia, exacerbation of chronic obstructive pulmonary disease, severe asthma, or trauma may receive corticosteroids. It is not rare that ICU patients receive concomitantly neuromuscular blocking drugs and corticosteroids. Among the various serious adverse reactions to these drugs, secondary infection and ICU-acquired weakness may place a burden to the health-care system by resulting in substantial cost and long-term morbidity. Both superinfections and ICU-acquired paresis are more likely when high doses of fluorinated corticosteroids are combined with prolonged treatment with a long-acting non-depolarizing neuromuscular blocker. Modern ICU practices favor lower dose of corticosteroids and very short course of short-acting curare for the management of sepsis or ARDS. Recent trials provided no evidence for increased risk of secondary infections or critical illness neuromyopathy in patients with sepsis or ARDS with the use of corticosteroids or neuromuscular blockers.
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PMID:What Is the Evidence for Harm of Neuromuscular Blockade and Corticosteroid Use in the Intensive Care Unit? 2682 Feb 74

In this article, we discuss the emerging role of lung point-of-care ultrasonography for regional anesthesiologists and pain management specialists. Lung ultrasonography is a well-established clinical tool that is used on a routine basis in emergency rooms and critical care units internationally to evaluate patients with respiratory distress; however, its benefits to the regional anesthesiologist and pain specialist are not as well known and are practiced less frequently. This review article covers the clinical evidence in support of lung point-of-care ultrasonography as a rapid and superior tool to traditional imaging modalities such as chest radiography and fluoroscopy. As anesthesiologists routinely perform nerve blocks that put patients at potential risk of complications such as pneumothorax or diaphragmatic paresis, it is important to understand how to use lung ultrasonography to evaluate for these conditions, as well as to differentiate between other potential causes of respiratory distress, such as interstitial syndrome and pleural effusions. This article describes the normal and pathological findings that can be used to quickly and confidently evaluate a patient for these conditions.
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PMID:Lung Ultrasound for the Regional Anesthesiologist and Acute Pain Specialist. 2926 6

Cerebral malaria (CM) is the most severe manifestation of human malaria yet is still poorly understood. Mouse models have been developed to address the subject. However, their relevance to mimic human pathogenesis is largely debated. Here we study an alternative cerebral malaria model with an experimental Plasmodium berghei Keyberg 173 (K173) infection in Sprague Dawley rats. As in Human, not all infected subjects showed cerebral malaria, with 45% of the rats exhibiting Experimental Cerebral Malaria (ECM) symptoms while the majority (55%) of the remaining rats developed severe anemia and hyperparasitemia (NoECM). These results allow, within the same population, a comparison of the noxious effects of the infection between ECM and severe malaria without ECM. Among the ECM rats, 77.8% died between day 5 and day 12 post-infection, while the remaining rats were spontaneously cured of neurological signs within 24-48 hours. The clinical ECM signs observed were paresis quickly evolving to limb paralysis, global paralysis associated with respiratory distress, and coma. The red blood cell (RBC) count remained normal but a drastic decrease of platelet count and an increase of white blood cell numbers were noted. ECM rats also showed a decrease of glucose and total CO2 levels and an increase of creatinine levels compared to control rats or rats with no ECM. Assessment of the blood-brain barrier revealed loss of integrity, and interestingly histopathological analysis highlighted cyto-adherence and sequestration of infected RBCs in brain vessels from ECM rats only. Overall, this ECM rat model showed numerous clinical and histopathological features similar to Human CM and appears to be a promising model to achieve further understanding the CM pathophysiology in Humans and to evaluate the activity of specific antimalarial drugs in avoiding/limiting cerebral damages from malaria.
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PMID:Young Sprague Dawley rats infected by Plasmodium berghei: A relevant experimental model to study cerebral malaria. 2874 9

The pharmacology and history of neuromuscular blockade in clinical care are complex, with multiple theoretical and observed potential benefits and potential harms. Past studies raised concern for long-term paresis, but more recent studies have not found evidence for harm, possibly due to changes in background care, neuromuscular blocking agent, and duration of blockade. Current use is highly variable, likely due to limited evidence for efficacy beyond short-term physiologic improvement and lingering concerns for harm. A recently completed large multicenter trial will provide further information on the role of pharmacologic paralysis in acute respiratory distress syndrome.
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PMID:Role of Pharmacologic Paralysis in Acute Respiratory Distress Syndrome. 3167 53

Neurologic complications following acute respiratory distress syndrome (ARDS) are well described, however, information on the neurologic outcome regarding peripheral nervous system complications in critically ill ARDS patients, especially those who received extracorporeal membrane oxygenation (ECMO) are lacking. In this prospective observational study 28 ARDS patients who survived after ECMO or conventional nonECMO treatment were examined for neurological findings. Nine patients had findings related to cranial nerve innervation, which differed between ECMO and nonECMO patients (p = 0.031). ECMO patients had severely increased patella tendon reflex (PTR) reflex levels (p = 0.027 vs. p = 0.125) as well as gastrocnemius tendon reflex (GTR) (p = 0.041 right, p = 0.149 left) were affected on the right, but not on the left side presumably associated with ECMO cannulation. Paresis (14.3% of patients) was only found in the ECMO group (p = 0.067). Paresthesia was frequent (nonECMO 53.8%, ECMO 62.5%; p = 0.064), in nonECMO most frequently due to initial trauma and polyneuropathy, in the ECMO group mainly due to impairments of N. cutaneus femoris lateralis (4 vs. 0; p = 0.031). Besides well-known central neurologic complications, more subtle complications were detected by thorough clinical examination. These findings are sufficient to hamper activities of daily living and impair quality of life and psychological health and are presumably directly related to ECMO therapy.
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PMID:Longtime Neurologic Outcome of Extracorporeal Membrane Oxygenation and Non Extracorporeal Membrane Oxygenation Acute Respiratory Distress Syndrome Survivors. 3133 27

COVID-19 is frequently accompanied by a hypercoagulable inflammatory state with microangiopathic pulmonary changes that can precede the diffuse alveolar damage characteristic of typical acute respiratory distress syndrome (ARDS) seen in other severe pathogenic infections. Parallels with systemic inflammatory disorders such as atypical hemolytic uremic syndrome (aHUS) have implicated the complement pathway in the pathogenesis of COVID-19, and particularly the anaphylatoxins C3a and C5a released from cleavage of C3 and C5, respectively. C5a is a potent cell signalling protein that activates a cytokine storm-a hyper-inflammatory phenomenon-within hours of infection and the innate immune response. However, excess C5a can result in a pro-inflammatory environment orchestrated through a plethora of mechanisms that propagate lung injury, lymphocyte exhaustion, and an immune paresis. Furthermore, disruption of the homeostatic interactions between complement and extrinsic and intrinsic coagulation pathways contributes to a net pro-coagulant state in the microvasculature of critical organs. Fatal COVID-19 has been associated with a systemic inflammatory response accompanied by a pro-coagulant state and organ damage, particularly microvascular thrombi in the lungs and kidneys. Pathologic studies report strong evidence of complement activation. C5 blockade reduces inflammatory cytokines and their manifestations in animal studies, and has shown benefits in patients with aHUS, prompting investigation of this approach in the treatment of COVID-19. This review describes the role of the complement pathway and particularly C5a and its aberrations in highly pathogenic virus infections, and therefore its potential as a therapeutic target in COVID-19.
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PMID:COVID-19: A collision of complement, coagulation and inflammatory pathways. 3260 59

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has become a global pandemic. This disease has been shown to affect various organ systems, including the cerebrovascular system with sequelae still not completely uncovered. We present an unusual case of extensive brainstem intraparenchymal hemorrhage in a patient with COVID-19 to caution readers of this possible complication in patients positive for COVID-19. In this report, we outline the clinical presentation of a 40-year-old male who developed severe coughing and sneezing before presenting to the emergency department with confusion, somnolence, and respiratory distress. CT head without contrast revealed extensive pontine and midbrain hemorrhage with intraventricular extension and early hydrocephalus. Neurological examination revealed pinpoint, minimally reactive pupils, withdrawal to painful stimuli in the right hemibody, left hemibody paresis, and intact left corneal, cough, and gag reflexes. MRI and MRA brain revealed no evidence of an underlying vascular lesion. Over the next two days, the patient had worsening multiorgan failure and hypoxemia without intracranial hypertension. He remained too unstable to undergo cerebral angiogram. On hospital day four, his neurological examination deteriorated to quadriparesis and only cough and gag reflexes remaining intact after which his family opted for comfort measures only. In summary, a potential increased risk of intracerebral hemorrhage adds to the complexity of management of patients with COVID-19. This is especially true in those who have violent sneezing or coughing, or those who are on anticoagulation or antiplatelet therapy.
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PMID:Spontaneous Brainstem Hemorrhagic Stroke in the Setting of Novel Coronavirus Disease 2019 - A Case Report. 3316 13


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