Abstract. The mechanism of death in patients struggling against restraints remains a topic of debate. This article presents a series of five patients with restraint-associated cardiac arrest and profound metabolic acidosis. The lowest recorded pH was 6.25; this patient and three others died despite aggressive resuscitation. The survivor's pH was 6.46; this patient subsequently made a good recovery. Struggling against restraints may produce a lactic acidosis. Stimulant drugs such as cocaine may promote further metabolic acidosis and impair normal behavioral regulatory responses. Restrictive positioning of combative patients may impede appropriate respiratory compensation for this acidemia. Public safety personnel and emergency providers must be aware of the life threat to combative patients and be careful with restraint techniques. Further investigation of sedative agents and buffering therapy for this select patient group is suggested. Key words: metabolic acidosis; restraint -physical; heart arrest; cardiac arrest. AC-ADEMIC EMERGENCY MEDICINE 1999; 6:239 -243 M ANAGEMENT of violent and agitated patients is a significant problem for public safety and emergency medical agencies, and death occasionally occurs during restraint of these patients. The cause of death in these circumstances has not been elucidated. Speculation has focused on autonomic reflexes, restraint stress, 1 agitated delirium from stimulant drugs, 1 and positional asphyxia due to use of the hobble (or ''hog-tie'') position as potential contributing factors.2 -4 Acidosis has not been cited as a contributing factor in restraint-associated death. Severe metabolic acidosis has, however, been noted with stimulant drug use (notably cocaine), 5 and when exertion and stimulant drug use are combined.6 -8 Profound metabolic acidosis can have significant negative cardiovascular effects, including promotion of dysrhythmias and autonomic instability, which may contribute to cardiovascular collapse.We present five cases of cardiovascular collapse occurring in ED patients who were struggling despite maximal restraint techniques. They were all profoundly acidotic. Our experience with these cases led to institution of an aggressive proactive CASE 1A 36-year-old man was acting extremely agitated and belligerent on a downtown sidewalk. When approached, he attacked a police officer and ran. He was subsequently subdued by several officers. He was transported to the ED, where he continued to fight vigorously while lying prone with his hands cuffed behind him. Breath analysis was negative for ethanol. Shortly thereafter, the patient had a witnessed respiratory arrest. He was intubated within 4 minutes of his apnea. Shortly after intubation, a 15-second episode of asystole was noted; he recovered a sinus rhythm at a rate of 140 beats/ min after epinephrine, atropine, and hyperventilation. His initial arterial blood gas (ABG) obtained 5 minutes after intubation was pH 6.46, pCO 2 49 mm Hg, pO 2 523 mm Hg, and a bicarbonate (HCO 3 ) of 4 mEq/L. Aggressive fluid resus...

A. Elevated plasma free fatty acid concentrations in patients with pheochromocytoma-change with therapy and correlations with basal metabolic rate. N Engl J Med. 1964; 270:865-70. 9. Bethke RA, Gratton M, Watson WA. Severe hyperlactemia and metabolic acidosis following cocaine use and exertion.

No abstract

The intraoral approach to the infraorbital nerve block after adjunctive topical anesthesia appeared at least as effective in producing upper-lip anesthesia as the percutaneous approach without adjunctive topical anesthesia. Although the volunteers subjectively preferred the intraoral approach and visual-analog pain scores were lower for this approach, these differences did not achieve statistical significance. The intraoral approach was associated with a longer duration of upper-lip anesthesia.

No abstract