Clinical Characteristics of Pediatric Patients With Carbon Monoxide Poisoning.

OBJECTIVES: Carbon monoxide (CO) poisoning is a common and deadly form of poisoning that is often treated with hyperbaric oxygen. The characteristics of children exposed to CO and then treated with hyperbaric oxygen have not been delineated. The purpose of this study was to describe the clinical characteristics of children treated with hyperbaric oxygen therapy for CO poisoning at a regional hyperbaric referral center. METHODS: The study is based on a retrospective review of data extracted from the medical records of children (age <19 years) who were referred to our center for hyperbaric oxygen therapy for CO poisoning between 2008 and 2013. Inferential analyses were used to compare demographic characteristics, serum carboxyhemoglobin (COHb) levels, and presenting symptoms. RESULTS: Forty-seven children met our study criteria. Their mean age was 8.9 years, and their mean COHb level was 14.3% (range, 3.4%-30.1%). Severity of symptoms did not correlate with serum COHb levels; however, neurologic symptoms at presentation were more common in patients with a COHb level greater than 25%. There was a correlation between increasing age and higher COHb levels and between COHb and lactate levels. CONCLUSIONS: Our retrospective review of patients' records showed no correlation of serum COHb levels with symptoms on presentation; however, a correlation was found between increasing age and COHb level as well as lactate level and COHb level.

Carbon monoxide and ST-elevation myocardial infarction: case reports.

We describe two cases of myocardial infarction with ST-segment elevation on electrocardiogram associated with carbon monoxide (CO) poisoning, a condition rarely reported in the literature. The first was a 62-year-old woman who experienced chest pain in the emergency department (ED) while being assessed for exposure to carbon monoxide in her home. The second was an 80-year-old man who fainted at home and was found to have ST elevation during the ED workup. After hospitalization, he returned home and soon thereafter had difficulty walking and speaking. The responding paramedics detected a very high CO level in the home. Both patients received hyperbaric oxygen therapy within the first several hours of presentation. For this combination of conditions, it is difficult to derive evidence-based management recommendations, given the paucity of cases reported to date. We conclude that rapid consultation with interventional cardiology and consideration of angioplasty or stenting are appropriate, especially when electrocardiographic findings and echocardiography point to a specific coronary distribution. Hyperbaric oxygen therapy might have a role in the treatment, based on its effects on myocardial ischemia and injury in other models.

Doxorubicin and BAY 12-9566 for the treatment of osteosarcoma in dogs: a randomized, double-blind, placebo-controlled study.

BACKGROUND: This study was designed to assess the efficacy of a matrix metalloproteinase inhibitor in prolonging posttreatment survival for dogs with appendicular osteosarcoma after treatment with amputation and doxorubicin chemotherapy. HYPOTHESIS: Survival will be prolonged in dogs receiving BAY 12-9566. ANIMALS: The study included 303 dogs with appendicular osteosarcoma. METHODS: Dogs were treated with doxorubicin (30 mg/m2) every 2 weeks for 5 treatments starting 2 weeks after amputation. Dogs were randomly allocated to receive a novel nonpeptidic biphenyl inhibitor of matrix metalloproteinases (MMPs, BAY 12-9566; 4-[4-4-(chlorophenyl)phenyl]-4-oxo-2S-(phenylthiomethyl) butanoic acid) or placebo after doxorubicin chemotherapy. RESULTS: Median survival for all 303 dogs was 8 months; and 1-year, 2-year, and 3-year survival rates were 35%, 17%, and 9%, respectively. Treatment with BAY 12-9566 did not influence survival. Multivariate analysis revealed that increasing age (P = .004), increasing weight (P = .006), high serum alkaline phosphatase (ALP) (P = .012) and high bone ALP (P < .001) were independently associated with shorter median survival times. Additional analyses on available data indicated that as the number of mitotic figures in the biopsy increased (P = .013), and as plasma active MMP-2 concentrations increased (P = .027), the risk of dying increased. CONCLUSIONS AND CLINICAL IMPORTANCE: Doxorubicin is an effective adjuvant to amputation in prolonging survival for dogs with appendicular osteosarcoma.

The effect of hyperbaric oxygen therapy on composite graft survival.

Auricular composite grafts are a useful reconstructive option, particularly for nasal reconstruction. This study evaluates the effect of hyperbaric oxygen (HBO) therapy on auricular composite graft survival in rabbits. Circular chondrocutaneous composite grafts of 0.5, 1, or 2 cm in diameter were resected from the ears of rabbits. The grafts were sutured back into position. Half the rabbits in each group received HBO postoperatively, consisting of 90 minutes at 2.4 atm. Rabbits received 7 treatments in 5 days. Control rabbits did not receive HBO. On day 21 the percentage area of graft survival was calculated from gross and histologic examination. Two-centimeter grafts treated with HBO (n = 8) had a mean graft survival rate of 85.8 +/- 15.7% compared with a survival rate of 51.31 +/- 38.5% for the control group (n = 8; P = 0.0478). There was no such benefit in smaller grafts. HBO could prove clinically useful for larger composite grafts.

Hyperbaric oxygen reduces neuronal death and improves neurological outcome after canine cardiac arrest.

BACKGROUND AND PURPOSE: Studies suggest that hyperbaric oxygen (HBO) is neuroprotective after experimental cerebral ischemia, but the mechanism is unknown. This study tested the hypotheses that postischemic HBO affords clinical and histopathological neuroprotection after experimental cardiac arrest and resuscitation (A/R) and that this neuroprotection results from improved cerebral oxygen metabolism after A/R. METHODS: Anesthetized adult female beagles underwent A/R and randomization to HBO (2.7-atm absolute [ATA] for 60 minutes, 1 hour after A/R) or control (Po2=80 to 100 mm Hg; 1 ATA). Animals underwent neurological deficit scoring (NDS) 23 hours after A/R. After euthanasia at 24 hours, neuronal death (necrotic and apoptotic) in representative animals was determined stereologically in hippocampus and cerebral neocortex. In experiment 2, arterial and sagittal sinus oxygenation and cerebral blood flow (CBF) were measured. Cerebral oxygen extraction ratio (ERc), oxygen delivery (Do2c), and metabolic rate for oxygen (CMRo2) were calculated (baseline and 2, 30, 60, 120, 180, 240, 300, and 360 minutes after restoration of spontaneous circulation). RESULTS: NDS improved after A/R in HBO animals (HBO, 35+/-14; controls, 54+/-15; P=0.028). Histopathological examination revealed significantly fewer dying neurons in HBO animals; the magnitude of neuronal injury correlated well with NDS. HBO corrected elevations in ERc (peak, 60+/-14% for controls, 26+/-4% for HBO) but did not increase Do2c or CMRo2, which decreased approximately 50% after A/R in both groups. CONCLUSIONS: HBO inhibits neuronal death and improves neurological outcome after A/R; the mechanism of HBO neuroprotection is not due to stimulation of oxidative cerebral energy metabolism.

Neuroprotective effects of hyperbaric oxygen treatment in experimental focal cerebral ischemia are associated with reduced brain leukocyte myeloperoxidase activity.

OBJECTIVE: Hyperbaric oxygen (HBO) reduces cerebral infarct size after middle cerebral artery occlusion (MCAO) in rats through an unknown mechanism. In other forms of injury, cellular protection with HBO is associated with diminished infiltration of polymorphonuclear neutrophils (PMN). We hypothesized that HBO given prior to or after MCAO reduces PMN infiltration into the brain, and that decreased PMN infiltration is associated with improved functional and anatomic outcome. METHODS: Forty rats underwent MCAO and were randomized to pretreatment with HBO (3 ATA) immediately prior to (n=13), or posttreatment immediately after surgery (n=12), or to control (air 1 ATA) (n=15). Five rats underwent sham surgery. Neurologic outcome was measured at 24 h in all animals. Brain myeloperoxidase (MPO) activity (n=22) and infarct volume (n=23) were determined. RESULTS: MPO activity was significantly higher in controls (mean 0.28, 95% C.I. 0.17-0.38) than in the HBO pretreatment group (0.12, 0.08-0.16), HBO posttreatment group (0.16, 0.13-0.19), and the sham group (0.02, -0.02 to 0.05). HBO treated animals also had better neurologic outcomes (pretreatment 1.5, 0.9-2.1, posttreatment 2.6, 2.0-3.2) and smaller infarcts (pretreatment 27%, 18-37%, posttreatment 28%, 19-37%) than controls (neurologic outcome 3.7, 3.1-4.4, infarct volume 39%, 30-48%). Neurologic outcomes correlate better with MPO activity (R(2)=0.75) than with infarct volume (R(2)=0.25). CONCLUSION: These data confirm the neuroprotective effects of HBO in cerebral ischemia and suggest that the mechanism of this action may involve inhibition of PMN infiltration in the injured brain.