Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Esophageal necrosis with perforation secondary to traumatic aortic transection is extremely rare but usually fatal. A 47-year-old man complained of sudden swallowing difficulty 6 days after blunt trauma. Computed tomography showed a ruptured aorta and the midesophagus shifted to the right side with luminal obliteration because of the ruptured aorta. After primary repair of the partially transected aorta, unexpected mediastinitis because of esophageal perforation was noted. Upper endoscopy showed midesophageal ulceration, necrosis, and perforation. Biopsy samples were consistent with ischemia. The possibility of direct esophageal trauma or intraoperative esophageal injury was ruled out. Esophageal exclusion with thoracoscopic decortication and multiple antibiotics were ineffective, and the patient eventually died. Ischemic esophageal necrosis caused by mechanical compression can occur in a traumatic aortic transection. Dysphagia, when present with radiologic signs, indicates a displaced and compressed esophagus. In spite of aggressive surgical and medical treatment for a perforated esophagus, the prognosis remains poor.
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PMID:Ischemic esophageal necrosis secondary to traumatic aortic transection. 1556 Oct 68

We report a severe unilateral recurrent laryngeal nerve neuropraxia following use of the ProSeal laryngeal mask airway (PLMA) in a 71-year-old female patient with CREST syndrome. She required amputation of the 5th phalanx of foot because of gangrene due to Raynaud's syndrome. Anesthesia was induced with propofol, and a size 3 PLMA was inserted. Anesthesia was maintained with sevoflurane and nitrous oxide for 2 h and the operation was performed uneventfully. On removal of PLMA, the cuff volume was measured to 40 ml. The patient did not complain of respiratory discomfort shortly after PLMA removal. However, the next day she developed dysphagia and hoarseness. Laryngoscopic examination revealed unilateral vocal cord paralysis. Cricothyrotomy was required because of suspected silent aspiration pneumonia. The pharyngolaryngeal complications improved with a mobile vocal cord but slight hoarseness after 2 months. We considered the patient's CREST syndrome with a potential of tissue ischemia, and the high intracuff pressure of the PLMA due to nitrous oxide influx, to be the cause of severe recurrent laryngeal nerve neuropraxia in this case.
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PMID:Unilateral recurrent laryngeal nerve neuropraxia following placement of a ProSeal laryngeal mask airway in a patient with CREST syndrome. 1577 10

C1 inhibitor (C1-INH) is a serine protease inhibitor (serpins) that inactivates several different proteases in the complement, contact, coagulation, and fibrinolytic systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds, and blocks the activity of its target proteases. The N-terminal end (nonserpin domain) confers to C1-INH the capacity to bind lipopolysaccharides and E-selectin. Owing to this moiety, C1-INH intervenes in regulation of the inflammatory reaction. The heterozygous deficiency of C1-INH results in hereditary angioedema (HAE). The clinical picture of HAE is characterized by bouts of local increase in vascular permeability. Depending on the affected site, patients suffer from disfiguring subcutaneous edema, abdominal pain, vomiting and/or diarrhoea for edema of the gastrointestinal mucosa, dysphagia, and dysphonia up to asphyxia for edema of the pharynx and larynx. Apart from its genetic deficiency, there are several pathological conditions such as ischemia-reperfusion, septic shock, capillary leak syndrome, and pancreatitis, in which C1-INH has been reported to either play a pathogenic role or be a potential therapeutic tool. These potential applications were identified long ago, but controlled studies have not been performed to confirm pilot experiences. Recombinant C1-INH, produced in transgenic animals, has recently been produced for treatment of HAE, and clinical trials are in progress. We can expect that the introduction of this new product, along with the existing plasma derivative, will renew interest in exploiting C1-INH as a therapeutic agent.
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PMID:C1 inhibitor: molecular and clinical aspects. 1626 49

Early postoperative dysphagia after anterior cervical surgery is a well-known phenomenon with so far unknown etiology. We hypothesised that direct pressure induced by the medial retractor blade on pharynx/esophagus mucosal wall leads to local ischemia. Subsequently postoperative hyperemia and swelling of the pharynx/esophagus may result in swallowing disturbance. To prove the hypothesis local blood flow inside the pharynx/esophagus wall during anterior cervical surgery was measured using a laser Doppler (LD) perfusion monitor unit. Fifteen patients underwent standard anterior cervical discectomy and fusion (ACDF). The LD probe was placed underneath the medial retractor blade in order to gain information at the maximum point of pressure applied onto the pharynx/esophagus wall. Local perfusion was measured prior to retractor opening (5 min), during spreading of the retractor and after its closure (5 min). Perfusion was measured semiquantitatively in perfusion units (PU). Local perfusion ranged from 30 to 210 PU (mean 107) prior to retractor opening, from 7 to 60 PU (mean 30) with open retractor and from 15 to 280 PU (mean 117) after retractor closure. In all 15 patients the open retractor led to hypoperfusion ranging from 21 to 93% compared to the baseline level. In seven patients a reactive hyperemia at the end of the procedure was detected (32-89% compared to baseline level). In four patients after hypoperfusion during spreading of the retractor the baseline levels were reached again and in four patients perfusion remained diminished even after retractor closure. To best of our knowledge, this is the first report on intraoperative measurement of local perfusion of the pharynx/esophagus wall during anterior cervical surgery. Diminished local perfusion was observed in all patients during spreading of the retractor and post-procedure hyperemia was recorded in 46% of the patients. The local ischemia of the pharynx/esophagus wall may be a crucial step in the development of postoperative dysphagia.
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PMID:Intraoperative measurement of pharynx/esophagus retraction during anterior cervical surgery. Part II: perfusion. 1647 47

Effective swallowing is an essential part of life and is performed thousands of times per day, often without conscious consideration. Difficulty in swallowing (dysphagia) commonly arises in stroke patients following ischemia of the cerebral cortex. However, whereas this tends to resolve spontaneously in the majority of patients, a small percentage will be left with a persistent dysphagia, which predisposes to airway compromise and aspiration pneumonia. This article reviews the recent research into ways of restoring swallowing function in these patients through promoting plasticity and reorganisation of the remaining, viable cerebral cortex.
Dysphagia 2009 Mar
PMID:Role of cerebral cortex plasticity in the recovery of swallowing function following dysphagic stroke. 1871 38

Arteria lusoria, an aberrant or anomalous right subclavian artery, is the most common anomaly of the aortic arch. It may be associated with other congenital anomalies of the heart and great vessels-including, rarely, truncus bicaroticus (a common trunk of both common carotid arteries), and, even more rarely, aneurysmal formation.Herein, we report the case of a 72-year-old man who had both an atherosclerotic aneurysm of an aberrant right subclavian artery and truncus bicaroticus. We resected the aneurysm through a posterolateral thoracotomy and did not restore the distal pulsatile blood supply to the right arm. During long-term clinical follow-up, the patient experienced no arm ischemia or cerebrovascular insufficiency.Aneurysm of arteria lusoria should be suspected in the presence of a right superior mediastinal mass on chest radiographs and should be considered as a cause of new-onset dyspnea, chest pain, or dysphagia. Symptomatic right arteria lusoria aneurysm should be removed promptly after diagnosis. Despite disagreement among investigators regarding the need to restore pulsatile blood flow to the right arm, we recommend reconstructing that flow, when possible.
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PMID:Arteria lusoria aneurysm with truncus bicaroticus: surgical resection without restoring blood supply to the right arm. 2097 81

Demyelination is characterized by the loss of myelin with the preservation of axons. Demyelinating diseases can be classified into several categories: demyelination due to inflammation, viral infection, osmotic derangements and hypoxic ischemia. In particular, osmotic myelinolysis is representative, and is associated with hyperosmolality, hypokalemia or rapid correction of hyponatremia. Osmotic myelinolysis was reported to be associated with underlying conditions, such as alcoholism, diuretics and malnutrition. A 67-year-old woman with hypertension was scheduled to undergo both total knee replacements (TKR). She was observed to be lethargic with dysphagia and quadriplegia after the second TKR. She had been taking diuretics for a long time, and did not have an adequate amount of food intake due to patient controlled analgesia and a gastric ulcer after the first TKR. A laboratory examination revealed hypokalemia but normonatremia. T2 weighted-MRI revealed abnormal high signal intensity in the basal ganglia and periventricular area. This case was diagnosed with osmotic myelinolysis associated with hypokalemia without an apparent sodium imbalance.
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PMID:Extensive demyelinating change in cerebrum after a total knee replacement -A case report-. 2128 40

In this review of the gastrointestinal (GI) and hepatic manifestations of systemic lupus erythematosus (SLE), 180 articles from the English literature, found using a medline search from January 1965 to December 2010, were examined. Vasculitis may cause ulcerations, bleeding, stricture formation, and perforation from ischemia and infarction. Otherwise, GI symptoms, occurring in about 50% of patients, are usually mild. Esophageal dysmotility may result in heartburn, regurgitation, and dysphagia. Occasionally, pneumatosis cystoides intestinalis may develop, sometimes associated with benign pneumoperitoneum. Patients are prone to salmonella bacteremia, presenting more commonly with fever and abdominal pain than with diarrhea. Intestinal pseudoobstruction usually is found with active lupus serology, preferentially involving small rather than the large bowel. Protein-losing enteropathy, characterized by diarrhea, edema, and hypoalbuminemia, can be the initial presentation of SLE. Malabsorption with a prevalence of 9.5% is occasionally associated with celiac disease. Pancreatitis, with an annual incidence of 0.4 to 1/1000, has an overall mortality of 27% that is decreased with corticosteroid therapy. Acute and chronic ascites may be due to lupus peritonitis or to associated diseases, such as pancreatitis, nephrotic syndrome, heart failure, or infections. Abnormal liver function tests may be due to steatosis from lupus or from corticosteroid therapy. Only about 10% of patients with autoimmune hepatitis have lupus. Up to 4.7% of patients with SLE have chronic active hepatitis correlating strongly with the presence of antibody to ribosomal P protein. SLE can involve the entire GI tract and the liver. Treatment with corticosteroids, cytotoxic agents, and/or immunosuppressants is often successful.
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PMID:Gastrointestinal and hepatic manifestations of systemic lupus erythematosus. 2142 47

Acute gastrointestinal obstruction occurs when the normal flow of intestinal contents is interrupted. The blockage can occur at any level throughout the gastrointestinal tract. The clinical symptoms depend on the level and extent of obstruction. Various benign and malignant processes can produce acute gastrointestinal obstruction, which often represents a medical emergency because of the potential for bowel ischemia leading to perforation and peritonitis. Early recognition and appropriate treatment are thus essential. The typical clinical symptoms associated with obstruction include nausea, vomiting, dysphagia, abdominal pain and failure to pass bowel movements. Abdominal distention, tympany due to an air-filled stomach and high-pitched bowel sounds suggest the diagnosis. The diagnostic process involves imaging including radiography, ultrasonography, contrast fluoroscopy and computer tomography in less certain cases. In patients with uncomplicated obstruction, management is conservative, including fluid resuscitation, electrolyte replacement, intestinal decompression and bowel rest. In many cases, endoscopy may aid in both the diagnostic process and in therapy. Endoscopy can be used for bowel decompression, dilation of strictures or placement of self-expandable metal stents to restore the luminal flow either as a final treatment or to allow for a delay until elective surgical therapy. When gastrointestinal obstruction results in ischemia, perforation or peritonitis, emergency surgery is required.
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PMID:Acute GI obstruction. 2416 Sep 28

Stroke is a public health problem of the first order. In developed countries is one of the leading causes of death, along with cardiovascular disease and cancer. In addition, stroke is the leading cause of permanent disability in adulthood. Many of the patients who survive do so with significant sequelae that limit them in their activities of daily living. Most strokes (80-85%) are due to ischemia, while the rest are hemorrhagic. We have identified many modifiable risk factors, some with an important relationship with dietary factors or comorbidities in wich the diet has a significant impact. The incidence of malnutrition in stroke patients is not well known, but most likely impacts on patient prognosis. Furthermore, the nutritional status of patients admitted for stroke often deteriorates during hospitalization. It is necessary to perform a nutritional assessment of the patient in the early hours of admission, to determine both the nutritional status and the presence of dysphagia. Dysphagia, through alteration of the safety and efficacy of swallowing, is a complication that has an implication for nutritional support, and must be treated to prevent aspiration pneumonia, which is the leading cause of mortality in the stroke patient. Nutritional support should begin in the early hours. In patients with no or mild dysphagia that can be controlled by modifying the texture of the diet, they will start oral diet and oral nutritional supplementation will be used if the patient does not meet their nutritional requirements. There is no evidence to support the use of nutritional supplements routinely. Patients with severe dysphagia, or decreased level of consciousness will require enteral nutrition. Current evidence indicates that early nutrition should be initiated through a nasogastric tube, with any advantages of early feeding gastrostomy. Gastrostomy will be planned when the enteral nutrition support will be expected for long-term (4 weeks). Much evidence points to the importance of glycemic control during hospitalization for stroke. Hyperglycemia at diagnosis and during the first hours of admission impact on patient prognosis. The goal of glycemic control necessary to modify this bad prognosis without adding risk by iatrogenic hypoglycemia is still matter of debate.
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PMID:[Nutritional support in stroke patients]. 2507 46


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