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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We conducted a study to determine the type, incidence, and timing of complications that occur in patients who have a carbon monoxide (CO) exposure serious enough to require hyperbaric oxygen therapy (HBOT). Complication data were retrospectively collected from a ten-year period for 297 consecutive CO-poisoned emergency department patients who received HBOT. HBOT was indicated for 41% of the patients because of an elevated carboxyhemoglobin (COHb) level alone. Central nervous system dysfunction, including loss of consciousness, and/or cardiovascular dysfunction, was the criteria for HBOT in 59% of patients, regardless of their COHb level. The mean peak COHb level was 38 mg%, with 88% of patients having a peak COHb level greater than 25 mg%. The mortality rate was 6% in this case series. Cardiac arrest occurred in 8% of patients; all experienced their first arrest prior to HBOT. The 3% of patients who sustained an isolated respiratory arrest and those who had a myocardial infarction did so prior to HBOT. Several complications, however, occurred for the first time or as a recurrent event during HBOT. These included emesis (6%), seizures (5%), agitation requiring restraints or sedation (2%), cardiac dysrhythmias or arrests (2%), and arterial hypotension (2%). No patient's level of consciousness deteriorated subsequent to the initial resuscitation except for those who later had a generalized seizure. The most significant complication attributable to HBOT was tension pneumothorax, noted in three patients (1%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Complications and protocol considerations in carbon monoxide-poisoned patients who require hyperbaric oxygen therapy: report from a ten-year experience. 224 Jul 43

Adequate prehospital care of the severely traumatised patient is important to prevent or attenuate early as well as late life threatening complications, such as tissue hypoxia, ischemia/reperfusion injury and finally multiple organ failure. A mismatch of oxygen supply and oxygen demand is a hallmark in the pathophysiology of multiple trauma. Oxygen supply may be diminished by the following factors: shock-related decrease of cardiac output, anemia and hypoxia. On the other hand, oxygen demand may be increased by pain, panic, and agitation. Hence, it is a central point in prehospital care to reduce this supply-demand imbalance by identification and prompt reversal of the underlying causes. Most often, shock is caused by hypovolaemia and tissue injury ("traumatic-hemorrhagic shock"). However, shock may also be a result of central nervous system injury (neurogenic shock as a special form of distributive shock) or circulatory obstruction, e.g tension pneumothorax or cardiac tamponade (obstructive shock). Volume resuscitation by means of crystalloid or colloid solutions is an essential part in the therapy of the traumatic-haemorrhagic shock. In addition, catecholamines may be necessary in order to achieve an adequate arterial pressure. However, if bleeding cannot be controlled in the prehospital setting, only moderate volume support and permissive hypotension as well as rapid transportation into the next hospital may be preferable. This may be the case in penetrating thoracic or abdominal injuries as well as in traumatic amputations of the proximal limb. On the contrary, in patients with severe head injury, hypotension must be avoided by all means. Obstructive shock has to be treated urgently by insertion of a chest drain or drainage of the pericardium, respectively. Under all circumstances, it is an essential part of prehospital therapy to provide sufficient analgesia as soon as possible. Prehospital anesthesia, combined with artificial ventilation may be necessary for optimal patient management. Furthermore, ventilatory support is indicated when respiratory failure, loss of consciousness, or severe shock are present. Additional oxygen should be given whenever possible, even in the absence of an overt hypoxic state. Important additional measures are cervical spine immobilisation and reposition as well as splinting of long bone fractures or luxations, in order to avoid secondary injury of the spinal cord or ongoing tissue and vascular damage.
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PMID:[Emergency management of polytrauma patients]. 902 49

The lungs are surrounded by the pleural membranes. The visceral pleura directly covers the lung and is separated from the parietal pleura by a layer of surfactant, which reduces friction during respiratory movement. A potential space exists between these two layers, and they may become separated by fluid or air. A lung can collapse to the size of a fist under pressure from either. Standard treatment in the field for an open chest wound is an occlusive dressing. The first thing that can be used to occlude the wound is a gloved hand. After placing the dressing, evaluate the breath sounds and determine if they have improved. The dressing should be taped down on three sides, leaving one side open to relieve the pressure during exhalation (one-way valve). "Burping" the dressing involves lifting one side to make sure any pressure buildup is relieved, as occasionally the dressing can become adhered to the skin, which may lead to a tension pneumothorax. If, after ensuring the occlusive dressing is properly in place, the respiratory rate increases, distress level worsens, oxygen saturations fall and breath sounds decrease, then needle decompression is required. A neurovascular bundle is located underneath each rib, and it is important to avoid damage to that bundle by performing a decompression over the top of a rib. If the patient is intubated before the development of a tension pneumothorax, carefully evaluate the breath sounds (especially if the left-side sounds are diminished) to determine if the ET tube needs to be withdrawn a centimeter. The rescuer performing ventilation will usually recognize a tension pneumothorax by the difficulty in bagging the patient. Remember, when you perform a needle thoracentesis, you are creating an open chest wound. Early signs and symptoms of a tension pneumothorax include diminished or absent breath sounds, severe dyspnea, narrowing pulse pressure, tachycardia and restlessness. Neck veins may be distended, but this can be a normal finding in a supine patient. The classic sign is a deviated trachea; the trachea shifts toward the "good" lung as the buildup of pressure collapses the "bad" lung. This is a late sign and suggests the tension pneumothorax has been developing for some time. One sign that does not normally accompany a plain pneumothorax is hypotension. In this case, the persistent low BP, combined with cool, mottled skin and a delayed capillary refill time, led providers to suspect that a hemothorax was developing as well. With endotracheal intubation and pleural decompression, the positive-pressure ventilations allowed the affected right lung to inflate more fully, utilize more of the available alveolar space and "bag out" some of the blood pooling at the base. The patient's vital signs and saturation improved. He needed surgical treatment and removal of the blood in the pleural space before ventilation and oxygenation could normalize.
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PMID:An open question. 1475 Feb 94