Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To ascertain the impact of intrauterine methamphetamine exposure on the overall health of newborn infants at Siriraj Hospital, Bangkok, Thailand, birth records of somatic growth parameters and neonatal withdrawal symptoms of 47 infants born to methamphetamine-abusing women during January 2001 to December 2001 were compared to 49 newborns whose mothers did not use methamphetamines during pregnancy. The data on somatic growth was analyzed using linear regression and multiple linear regression. The association between methamphetamine use and withdrawal symptoms was analyzed using the chi-square. Home visitation and maternal interview records were reviewed in order to assess for child-rearing attitude, and psychosocial parameters. Infants of methamphetamine-abusing mothers were found to have a significantly smaller gestational age-adjusted head circumference (regression coefficient = -1.458, p < 0.001) and birth weight (regression coefficient = -217.9, p < or = 0.001) measurements. Methamphetamine exposure was also associated with symptoms of agitation (5/47), vomiting (11/47) and tachypnea (12/47) when compared to the non-exposed group (p < 0r =0.001). Maternal interviews were conducted in 23 cases and showed that: 96% of the cases had inadequate prenatal care (<5 visits), 48% had at least one parent involved in prostitution, 39% of the mothers were unwilling to take their children home, and government or non-government support were provided in only 30% of the cases. In-utero methamphetamine exposure has been shown to adversely effect somatic growth of newborns and cause a variety of withdrawal-like symptoms. These infants are also psychosocially disadvantaged and are at greater risk for abuse and neglect.
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PMID:Methamphetamine abuse during pregnancy and its health impact on neonates born at Siriraj Hospital, Bangkok, Thailand. 1527 73

Gastric dilatation-volvulus (GDV) is a disease in which there is gross distension of the stomach with fluid or gas and gastric malpositioning. It causes pathology of multiple organ systems and is rapidly fatal. It is common in large- and giant-breed dogs. The disease appears to have a familial predisposition. Thoracic depth/width ratio also appears to predispose dogs to GDV. Implicated dietary factors include dietary particle size, frequency of feeding, speed of eating, aerophagia and an elevated feed bowl. A fearful temperament and stressful events may also predispose dogs to GDV. Abdominal distension, non-productive retching, restlessness, signs of shock, tachypnoea and dyspnoea are possible clinical signs. Initial treatment includes treatment of shock and gastric decompression. Surgical treatment should be performed promptly. There are no studies comparing the use of different anaesthetic agents in the anaesthetic management of GDV. Pre-medication with an opioid/benzodiazepine combination has been recommended. Induction agents that cause minimal cardiovascular changes such as opioids, neuroactive steroidal agents and etomidate are recommended. Anaesthesia should be maintained with an inhalational agent. Surgical therapy involves decompression, correction of gastric malpositioning, debridement of necrotic tissue, and gastropexy. Options for gastropexy include incisional, tube, circumcostal, belt-loop, incorporating, and laparoscopic gastropexy. Expected mortality with surgical therapy is 15-24%. Prognostic factors include mental status on presentation, presence of gastric necrosis, presence of cardiac arrhythmia and plasma lactate levels. Prophylactic gastropexy should be considered in dogs identified as being at high risk.
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PMID:Gastric dilatation-volvulus in dogs. 1603 41

Shock remains a significant cause of morbidity and potential mortality in the pediatric population. It is defined as a impaired perfusion with a too high oxygen demand in comparison to oxygen delivery. The cause of hypoxia may be found in a hypovolemic condition due to hemorrhage or loss of gastro-intestinal fluids, a disorder in volume distribution or a cardiac dysfunction. Less frequent are patients with an obstruction in the outflow tract of the heart or disorders in binding oxygen to hemoglobin. Hypoxia leads to lactat-acidosis with the clinical signs of tachypnoea, tachycardia and restlessness. It is of greatest importance to recognize the ongoing dysfunction early, in spite of mechanism of compensation with a high cardiac output, warm periphery and dry skin (warm shock). Is there no adequate therapy decompensation will occur with vasoconstriction, cold periphery and low cardiac output. This will lead to multiple organ dysfunction syndrome with neurological, renal, further cardiac, pulmonary and metabolic disorders. If this point of no return is reached, cell death will continue to occur and the patient will die. Early and aggressive volume therapy is indicated, filling the cardiac system with crystalloids or colloids. Later on under clinical conditions inotropic drugs will improve cardiac output and oxygen delivery. Only by recognizing these patients as early as possible we will be able to reduce morbidity and mortality of this potentially dangerous syndrome.
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PMID:[Pediatric shock--pathophysiology, diagnosis and treatment]. 1613 17

Negative-pressure pulmonary edema (NPPE) is a clinical entity of anaesthesiologic relevance, perioperatively caused by obstruction of the conductive airways (upper airway obstruction, UAO) due to laryngospasm in approx. 50% of the cases, its early recognition and treatment by the anaesthesist is mandatory. NPPE, also addressed as post-obstructive pulmonary edema (POPE) presents in most cases as a complex of symptoms with rapid onset, consisting of acute respiratory failure with dyspnea, tachypnea, and strained respiratory efforts. Additional signs are paradoxe ventilation, pink frothy sputum, stridor, and severe agitation. UAO produce extreme reduction of intrathoracic pressure during spontaneous ventilation, consecutively causing increase in venous return to the right ventricle and in intrathoracic blood volume, resulting in elevated hydrostatic pressures and interstitial transudation of fluids. Partially due to largely differing criteria used for diagnosis, opinions about incidence and prevalence of NPPE are unhomogenous in medical literature. It has been shown that generation of NPPE is not only limited to patients being intubated and ventilated, but occurs also in patients requiring higher fractions of oxygen.
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PMID:[Negative-pressure pulmonary edema (NPPE)]. 1649 58

The typical symptoms and signs of neuroleptic malignant syndrome (NMS) consist of fever muscle rigidity (stiffness, myoclonus, rod-like), alterations of consciousness (confusion, agitation, aggression, or catatonia), autonomic nervous system disturbances (i.e., hypertension, tachycardia, tachypnea, profuse sweating, and urine incontinence), abnormal blood tests such as low serum electrolytes, elevated serum creatinine phosphokinase (CPK) level, and leukocytosis. Muscle rigidity is often associated with myonecrosis, myoglobinuria, and elevated serum CPK. The mortality among NMS cases is in the 10 to 70% range depending on the severity of the symptoms and time of therapeutic approach. Mandatory therapy should include removal of causative agents, correction of body fluid and electrolytes, administration of benzodiazepine, clonazepam and bromocriptine (dopamine agonist), proved life-saving medications. The authors reported herein six cases with unusual clinical features of NMS. Four of them had been on antipsychotic for a year before becoming anorexic, dehydrated, agitated, and violent with paranoid delusion. One instance with underlying delirium tremens developed NMS after receiving haloperidol (30 mg IV) in addition to diazepam (200 mg IV) within 24 hours. Another patient was found to suffer from severe NMS after receiving bupropion (Dopamine inhibitor antidepressant) 300 mg/day. All patients displayed cardinal signs and symptoms of NMS in addition to dehydration and pallor. They were treated in the psychiatric ward and recovered rapidly from NMS after receiving clonazepam and bromocriptine and removal of the offending agents.
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PMID:Neuroleptic malignant syndrome: a review and report of six cases. 1721 72

Intractable fever in cancer patients is problematic and the causes of this fever can be diverse. Paroxysmal persistent hyperthermia after sudden mental change or neurologic deficit can develop via autonomic dysregulation without infection or any other causes of fever. Paroxysmal hyperthermic autonomic dysregulation is a rare disease entity. It manifests as a form of paroxysmal hypertension, fever, tachycardia, tachypnea, pupillary dilation, agitation and extensor posturing after traumatic brain injury, hydrocephalus, brain hemorrhage or brain neoplasm. We recently experienced a case of paroxysmal hyperthermia following intracerebral hemorrhage along with brain neoplasm. Extensive fever workups failed to show an infectious or inflammatory source and/or hormonal abnormality. Empirical treatments with antibiotics, antipyretics, morphine, steroid and antiepileptic agents were also ineffective. However, Propranolol, a lipophilic beta-blocker, successfully controlled the fever and stabilized the patient. Fever in cancer patients is a common phenomenon, but a central origin should be considered when the fever is intractable. Propranolol is one of the most effective drugs for treating paroxysmal hyperthermia that is due to autonomic dysregulation.
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PMID:Paroxysmal autonomic dysregulation with fever that was controlled by propranolol in a brain neoplasm patient. 1742 48

We report the ameliorating effects of prazosin on the cardiovascular CV manifestations and pulmonary edema PE after treatment with antivenom AV failed to improve the conditions of scorpion stung patients. Three cases of scorpion envenoming, 2 children and one adult, were received at the Accident and Emergency Department of Al-Birk Hospital, Asir Region, Saudi Arabia. They presented to the hospital late with features of severe perspiration, tachypnea, restlessness, drooling of saliva, priapism, sinus tachycardia, PE, and shock like syndrome. When polyvalent scorpion PVS AV and intensive supportive treatment failed to show any improvement, prazosin was administered to the patients, which resulted in dramatic improvement in the conditions of the patients. We conclude that PVS AV may not be beneficial in all cases of scorpion envenomation, and prazosin may be an effective alternative for treating scorpion sting cases with CV manifestations and PE.
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PMID:Role of prazosin on cardiovascular manifestations and pulmonary edema following severe scorpion stings in Saudi Arabia. 1824 47

Serotonin syndrome is a potentially life-threatening adverse drug reaction caused by excessive serotonergic agonism in central and peripheral nervous system serotonergic receptors (Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352:1112-1120). Symptoms are characterized by a triad of neuron-excitatory features, which include (a) neuromuscular hyperactivity -- tremor, clonus, myoclonus, hyperreflexia and, in advanced stages, pyramidal rigidity; (b) autonomic hyperactivity -- diaphoresis, fever, tachycardia and tachypnea; (c) altered mental status -- agitation, excitement and, in advanced stages, confusion (Gillman PK. Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. Br J Anaesth 2005;95:434-441). It arises when pharmacological agents increase serotonin neurotransmission at postsynaptic 5-hydroxytryptamine 1A and 5-hydroxytryptamine 2A receptors through increased serotonin synthesis, decreased serotonin metabolism, increased serotonin release, inhibition of serotonin reuptake or direct agonism of the serotonin receptors (Houlihan D. Serotonin syndrome resulting from coadministration of tramodol, venlafaxine, and mirtazapine. Ann Pharmacother 2004;38:411-413). The etiology is often the result of therapeutic drug use, intentional overdosing of serotonergic agents or complex interactions between drugs that directly or indirectly modulate the serotonin system (Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352:1112-1120). Due to the increasing availability of agents with serotonergic activity, physicians need to more aware of serotonin syndrome. The following case highlights the complex nature in which serotonin syndrome can arise, as well as the proper recognition and treatment of a potentially life-threatening yet easily avoidable condition.
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PMID:Serotonin syndrome: a complex but easily avoidable condition. 1843 63

Staff may be reluctant to discuss end of life decisions in chronic lung disease (CLD) as it is usual for the disease to take a prolonged course and most infants recover to be discharged home without supplemental oxygen. A minority suffer a protracted and very severe illness in spite of treatments. Further intensive care may prolong a distressing death rather than offer any hope of survival. An end of life decision may be made after discussions with parents. Assisted ventilation may be withdrawn, or care redirected to withhold further episodes of assisted ventilation. A lingering death is a risk in infants who have not yet reached the point of dying but whose care has been redirected. Tachypnoea, rib retractions and agitation are distressing for the infant and parents. Palliative care must meet the needs of parents as well as their baby. It includes the legal use of drugs to relieve the infant's distress.
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PMID:End of life decisions in chronic lung disease. 1973 20

Forty patients of aluminum phosphide poisoning who were admitted to the ICU of Sir Sunder Lal Hospital, Banaras Hindu University, were studied. Restlessness, excessive thirst, shock, arrhythmias, tachypnoea, and severe metabolic acidosis were the common clinical findings. Only repeated and full correction with intravenous sodium bicarbonate was able to cope up with the severity and rapidity of acidosis. There was no significant change in blood pressure, pulse rate, and respiratory rate after full correction but gradually pulse and systolic blood pressure settled after ionotropic support in the survivors. There was significant improvement from 30.36% in the case when only half correction was done, as has been the common practice, to 57.5%, when full correction of metabolic acidosis was done.
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PMID:Aluminum phosphide poisoning: effect of correction of severe metabolic acidosis on patient outcome. 2004 Aug 19


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