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 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A young woman with acute intermittent porphyria is described. She was admitted in a prolonged attack and had developed a flaccid quadriplegia. During the course she showed various manifestations of the autonomic nervous system, including pupils, gastrointestinal tract, cardiovascular system and others. On admission her pupils were equally mydriatic, and reacted to light sluggishly. Dilation of the pupils was seen when cocaine was instilled, but not when adrenalin. It was suggested that the parasympathetic control of pupils was disturbed. She complained repeatedly abdominal pain, nausea, vomiting, and constipation. However, diarrhea was rarely found. Radiological examinations revealed that her bowel movements were markedly impaired. Sinus tachycardia and elevation of blood pressure were frequently observed with attacks, and they correlated with the clinical course. With tachycardia the coefficient variance of R-R interval was markedly decreased, and large dose of atropine failed to accelerate the heart rate. These indicate that the vagal function was markedly impaired with attacks. The effects of isoproterenol and of propranolol on the heart rate were normal. Phenylephrine and phentolamine changed the blood pressure normally. From these it was concluded that the sympathetic nervous function was not so impaired at the time examined. However, with the elevation of blood pressure plasma and urinary noradrenaline were markedly increased. Other autonomic and related manifestations observed during the course included disorders of sweating, loss of sphincter control, fever of unknown cause and amenorrhea.
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PMID:[Autonomic dysfunctions in acute intermittent porphyria]. 258 92

A total of 221 cases of deliberate acute overdose with fluvoxamine reported to the Paris Poison Centre, and 78 cases collected by the International Drug Safety Department of Duphar BV were analysed. Other agents, mainly benzodiazepines, neuroleptics, other antidepressants and alcohol, were also taken in 77% of the cases. The acute toxicity that could be attributed to fluvoxamine alone was rarely severe. The symptoms observed were always benign when the dose of fluvoxamine was below 1000 mg and included drowsiness, tremor, nausea, vomiting, abdominal pain, bradycardia and/or anticholinergic effects (dry mouth, mydriasis, sinus tachycardia, urinary retention). Seizures occurred in a few cases after high doses (generally > 1500 mg). Cardiotoxicity was not a serious problem; sinus bradycardia was noted with doses of less than 1000 mg, but was always moderate and required no treatment. Conduction abnormalities were rare.
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PMID:Acute fluvoxamine poisoning. 790 58

Pneumatic tourniquet and hone cement are often applied in orthopaedic surgery. In lower limb surgery, deep vein thrombosis may occur after release of tourniquet, causing embolism of lungs and vital organs. Paradoxical embolism may develop if the patients present extracardiac or intracardiac right to left shunt, such as atrial septum defect, etc. A 60-year-old female patient suffered from osteoarthritis of both knees was admitted for total knee replacement (TKR). Pneumatic tourniquet was inflated on the operated leg for the orthopaedic surgery which lasted for 2h. Dyspnea, sinus tachycardia and abdominal pain were noted after TKR. Blood gases analysis showed arterial hypoxemia and respiratory alkalosis. Chest X-ray revealed diffused bilateral pulmonary infiltration, pulmonary trunk engorgement, and decreased lung markings. Two days after TKR under the impression of peritonitis, she received exploratory laparotomy in which ischemic bowel and gall bladder were found. Pulmonary and paradoxical embolism were diagnosed, both of which were the well-known complications of TKR with tourniquet and bone cement application. The patient finally succumbed because of multiple organ failures.
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PMID:[Pulmonary and paradoxical embolism after total knee replacement--a case report]. 908 31

A 39-year-old white female underwent an uneventful vaginal hysterectomy for dysfunctional bleeding. Evaluating a mild aortic insufficiency murmur preoperatively an echocardiogram revealed normal left ventricular wall motion and function. Postoperatively the patient developed severe abdominal pain, acute hypertension (200/100 mmHg), and sinus tachycardia. Within minutes she decompensated into acute pulmonary edema. ECG demonstrated acute ST segment elevation in the precordial leads consistent with acute infarction. Emergency left heart catheterization showed normal coronary vessels with severe left ventricular dysfunction. An abdominal ultrasound was obtained, revealing a right adrenal mass. Plasma epinephrine was 334, norepinephrine 34,543 pg/ml; urine epinephrine 45, urine norepinephrine 2,137 micrograms/24 hours. She was started on prazosin and nifedipine sustained release with good blood pressure control. Four days later, an echocardiogram demonstrated the left ventricular wall motion reverting to normal. The adrenal tumor was subsequently resected successfully. Acute pulmonary edema causing dilated cardiomyopathy is a rare complication of pheochromocytoma that has been seldomly reported. A progressive fatal course is common: reversibility and survival depend on identifying and removing the pheochromocytoma.
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PMID:Postoperative acute pulmonary edema: a rare presentation of pheochromocytoma. 928 51

A 42-year-old man came to our emergency room hyperthermic (oral temperature, 42.4 degrees C), diaphoretic, and delirious. Other findings included labile blood pressure, sinus tachycardia (heart rate, 138/min), tachypnea (respiratory rate 34/min), muscle rigidity, and incontinence. Two days earlier, he had gone to a local clinic with complaints of abdominal pain, nausea, and vomiting. Promethazine was prescribed, and this was the patient's only medication on admission. Laboratory studies showed leukocytosis, hypernatremia, metabolic acidosis, elevated creatinine phosphokinase level, elevated transaminase levels, azotemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobulinuria. The clinical and laboratory findings were characteristic of the neuroleptic malignant syndrome, with promethazine as the offending agent.
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PMID:Neuroleptic malignant syndrome due to promethazine. 1054 78

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

Pseudoaneurysm of the infrarenal aorta due to Behcet s disease is very rare. We report a case of pseudoaneurysm associated with Behcet s disease in a 17-year-old boy with a recurrent right ventricular thrombus successfully treated with revascularization using arterial homograft patch. Echocardiography examination revealed a right ventricular mass, thought to be a thrombus in an unusual location. Postoperatively, the findings of the pathologic examination confirmed the mass as a thrombus. When the patient was subsequently re-admitted to the emergency unit with complaints of severe abdominal pain, fever, fatigue, sinus tachycardia, and a pulsating and tender abdominal mass, a right ventricular thrombus and a large pseudoaneurysm of the abdominal aorta were found on echocardiography and angiography. The patient underwent resection of the aortic aneurysm and aortoplasty, using arterial homograft patch, and received immunosuppressive and anticoagulation therapy. The thrombus of the right ventricle disappeared 4 months later. This case indicates that a right ventricular thrombosis in Behcet s disease may be managed by medical therapy.
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PMID:Arterial homograft and medical therapy in pseudoaneurysm of infrarenal aorta concomitant with recurrent right ventricular thrombus in Behcet's disease. 1695 82

We report the case of a 28-year-old woman who presented simultaneously with superior sagittal sinus thrombosis and thyroid crisis, and was subsequently found to have protein C deficiency. February 3, 2003, she admitted complaining of abdominal pain. The diagnosis of appendicitis was made, and she was operated on under lumbar anaesthesia. Day 7, she developed acute headache and distal weakness of the left lower limb. On examination she was alert, with a temperature of 38 degrees C, a sinus tachycardia of 124/min and blood pressure 164/84 mmHg. Neurological examination revealed neck stiffness and left hemiparesis, predominantly in her lower limb. Gadlinium-enhanced brain MRI revealed extensive superior sagittal sinus thrombosis. CT scan demonstrated infarction in the right frontal cortex, and subarachnoid hemorrhage adjacent to the right cerebellar tentorium. The patient was treated with a free radical scavenger edarabon, and glycerin. No anticoagulant therapy was instituted. Over the next 24 hours, her condition worsened. She became comatose, as well as developing a generalized tonic-clonic seizure. Day 12, laboratory examinations revealed an undetectable TSH-level CTSH (thyroid stimulating hormone) <0.005 mcIU/ml), with a level of free thyroxin 7.77 ng/dl (0.9-1.7), free triiodothyronin 29.6 pg/ml (2.3-4.3), and positive anti-TSH receptor antibodies determined subsequently. Coagulation factor VIII activity was 155% (normal range 60-150). Protein C deficiency (antigen 59%, activity 49%) was also present, suggesting a congenital type I heterozygous deficiency. A diagnosis of thyroid crisis on the basis of Graves' disease was made. The patient remained comatose and died on Day 16, with renal failure. The patient had protein C deficiency, a well-established risk factor for cerebral venous thrombosis (CVT). However, additional risk factors are required in most cases to precipitate CVT. In our case, this trigger was most likely thyroid crisis, suggesting that thyrotoxicosis, probably through hypercoagulability, may be a predisposing factor for the development of CVT.
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PMID:[Thyroid crisis and protein C deficiency in a case of superior sagittal sinus thrombosis]. 1737 Jun 53

Acute intermittent prophyria (AIP) is an autosomal dominant disease that results from a defect in the enzyme porphobilinogen deaminase. Acute intermittent porphyria is the most common of hepatic porphyrias and can tax the therapeutic capabilities of the physician to the limit. Motor weakness is a major feature of an acute attack, and flaccid paralysis of all extremities can occur rapidly, within a matter of days. The acute attacks may be life threatening. Hematin (Heme Arginate) should be given early during an acute attack to prevent neurologic sequel. Hemodialysis and hemoperfusion have been tried in the treatment of acute attacks of AIP with success. As hematin is not available in India, a severe acute attack of AIP in a patient was managed with hemodialysis successfully. Later, hematin was imported and provided to the patient. An 18-year-old girl was admitted to our hospital with recurrent abdominal pain and 2 episodes of convulsions. She had undergone an appendectomy earlier at another hospital for abdominal pain. On evaluation, she had hyponatremia, episodic abnormal behavior, generalized muscle pain, hypertension, and sinus tachycardia. In view of the above clinical picture, a clinical diagnosis of acute intermittent porphyria was made. Her 24-hr urinary porphobilinogen was 90.8 mg/day (<2 mg-normal) and alpha amino levalunic acid was 108.8 mg/day (1-7 mg-normal), consistent with the diagnosis. Her hyponatremia was corrected. Arrangements were made to import hematin and she was managed with dextrose infusion. Meanwhile, she developed flaccid quardriparesis with urinary incontinence and bulbar palsy. Her brain MRI was normal. Her nerve conduction study was suggestive of motor radiculoneuropathy. Specific treatment for severe porphyric crisis was planned. She failed to improve with dextrose infusion alone. As hematin was not readily available in the country, other therapeutic options were considered. As few case reports of AIP being successfully treated with hemodialysis were available, the option of dialytic support was explained to the family. After procuring informed consent, she was subjected to hemodialysis for 4 hr in the first day, increasing to 6 hr a day for the next 6 days. Her abdominal pain and myalgia subsided on the third day of dialysis. Her lower limb muscle power improved and she became ambulant by the fourth day. Urinary retention improved within 4 days. Hematin was imported by then from the United States. Later, 2 doses of hematin (4 mg/kg-160 mg in 20% albumin) were given via a central vein. She was maintained on physiotherapy. Repeat nerve conduction study revealed recovery. She has been provided with a list of drugs that have to be avoided. Currently, she is on outpatient follow-up with occasional abdominal pain, which subsides with intravenous dextrose therapy.
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PMID:Hemodialysis: a therapeutic option for severe attacks of acute intermittent porphyria in developing countries. 1827 38

Two males, 15 and 17 years old respectively, presented at the Emergency Department complaining of cramping abdominal pain, nausea and vomiting after ingestion of energy capsules. Physical examination revealed sinus tachycardia and slight abdominal pain. Laboratory examination showed substantial hypokalaemia and mild hyperglycaemia. Questioning revealed that they had taken 5 and 3 'herbal energy capsules' respectively and that these capsules supposedly contained 200 mg of caffeine each. Toxicological analysis showed a greatly increased serum caffeine concentration in both patients. The peak concentrations calculated were in the highly toxic range and could have led to severe acute complications such as convulsions. Pharmaceutical analysis demonstrated that these 'Supercap Xtreme'-capsules contained 700 mg caffeine or more. All symptoms presented were compatible with caffeine intoxication. The content of these capsules is not reliable and could lead to life-threatening intoxication.
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PMID:[Acute caffeine intoxication after intake of 'herbal energy capsules']. 1900 85


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