Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0231807 (exertional dyspnea)
 3,402 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43-year-old man was admitted suffering from dyspnea on exertion and edema of the neck and face. Chest X-ray film and CT scan revealed a mediastinal tumor and a right pleural effusion. A biopsy of the tumor revealed poorly differentiated carcinoma. Severe snoring at night and excessive daytime sleepiness were noticed after admission. Nocturnal oxygen desaturation was documented with a pulse oximeter, and obstructive sleep apnea syndrome was diagnosed on the basis of results of respiratory inductive plethysmography. The severity of snoring and oxygen desaturation during sleep correlated well with the progression of facial swelling. Combination chemotherapy (carboplatin 300 mg/m2 day 1, vindesine sulfate 3 mg/m2 day 1 and 8) was started but no improvement was seen. An expandable metallic stent was inserted into the stenotic vena cava, and the facial swelling, snoring, and oxygen desaturation during sleep were promptly relieved. In this case, obstructive sleep apnea was caused by edema and vascular congestion in the upper airway, and by the decrease in pharyngeal inspiratory muscle function caused by superior vena cava syndrome.
 ...
PMID:[Obstructive sleep apnea syndrome associated with superior vena cava syndrome]. 773 76

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Assessment of ventilatory function in patients with neuromuscular disease. 786 89

The consumption of energy beverages is increasing, especially among young people. The increasing consumption of these drinks increases the data of side effects. Case report: A 26-year old male was admitted to Toxicology Department suspected of intoxication due to ethyl alcohol and unknown psychoactive substances. The patient lost consciousness during a party in which he drank an unknown amount of ethyl alcohol mixed with an energy beverage ("Red Bull"). The patient and his friends strongly denied the use of psychoactive substances. On admission, the patient was stable, but unconscious (GCS 8 points), pupils wide, symmetric with weak reaction to light, respiratory rate 15/min. Neurological examination did not reveal any abnormalities. During the hospitalization, somnolence slowly disappeared and the patient became restless, with recurrent episodes of seizures not reacting to diazepam, clonazepam and midazolam infusion. The seizures finally abated after administration of barbiturates (Thiopental). This, in turn, caused respiratory insufficiency, requiring patient intubation and mechanical ventilation. The patients mental status and respiratory status slowly improved. After regaining consciousness, the patient strongly denied the use of psychoactive substances or of chronic alcohol use. He confirmed the single use of high, but not clearly defined, caffeine dosage (in the form of "Red Bull") mixed with alcohol. He mentioned that eight months earlier in similar circumstances he was admitted to the neurology department due to an episode of seizures. Ultimately the origin was not established, despite broad diagnostic testing. Thus the origin of the seizures was suggested to be of a toxicological origin. The patient was released home in good condition, without any side effects of the poisoning. The psychological examination doe not reveal any symptoms of alcohol or psychoactive substances addiction. In our case, due to the unclear nature of the history, we preformed broad diagnostic testing on admission to the hospital, which do not reveal the presence of any toxic substances except ethanol; concentration in the blood was 2,41 gil. Unfortunately, serum caffeine levels were not measured. There was no identification of any other factors that could be responsible for the observed symptoms. It appears that based on the interview, clinical manifestation, and negative toxicology laboratory testing (excluding the presence of ethanol), it is possible to connect the seizure state with the consumption of a high dose of energy drinks, rich in caffeine and taurine.
 ...
PMID:[Energy drinks as a cause of seizures--real or possible danger? Case report]. 2607 78