Cardiopulmonary arrest following cervical epidural injection.

Epidural steroid injection is a common treatment for the management of pain in a wide variety of patients. It is generally well tolerated and perceived to have few side effects, with a low risk of serious complications. Only a handful of reports exist that describe life-threatening complications such as subdural hematoma, respiratory depression, vasovagal response, and pneumocephalus. This is a case report of a 67-year-old woman with a relatively unremarkable past medical history, other than rheumatoid arthritis, osteoarthritis, and hypertension, who suffered from chronic neck pain treated with cervical epidural steroid injection at the C6-C7 level. She went into immediate cardiopulmonary arrest following the injection. She was brought to the emergency department by ambulance and resuscitated, and was found to have pneumocephalus. Ultimately, she made a relatively full recovery over the following weeks. Cardiopulmonary arrest is a rare but potentially deadly side effect of epidural steroid injection. To the best of our knowledge, this is the first report of such an arrest following a steroid injection in the cervical spinal region. There are several possible mechanisms for the immediate arrest, including cardioacceleratory center blockade, severe vasovagal response, iatrogenic pneumocephalus, and involvement of the phrenic nerve followed by apnea. Our conclusion in this case is that the most likely scenario was injection of the C6-C7 level led to a blockade of the cardiac accelerator fibers located just below in the T1-T4 spinal level, causing a sympathetic blockade and profound bradycardia, leading to cardiopulmonary arrest.

Differential roles of cardiomyocyte and macrophage peroxisome proliferator-activated receptor gamma in cardiac fibrosis.

OBJECTIVE: Cardiac fibrosis is an important component of diabetic cardiomyopathy. Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands repress proinflammatory gene expression, including that of osteopontin, a known contributor to the development of myocardial fibrosis. We thus investigated the hypothesis that PPARgamma ligands could attenuate cardiac fibrosis. RESEARCH DESIGN AND METHODS: Wild-type cardiomyocyte- and macrophage-specific PPARgamma(-/-) mice were infused with angiotensin II (AngII) to promote cardiac fibrosis and treated with the PPARgamma ligand pioglitazone to determine the roles of cardiomyocyte and macrophage PPARgamma in cardiac fibrosis. RESULTS: Cardiomyocyte-specific PPARgamma(-/-) mice (cPPARgamma(-/-)) developed spontaneous cardiac hypertrophy with increased ventricular osteopontin expression and macrophage content, which were exacerbated by AngII infusion. Pioglitazone attenuated AngII-induced fibrosis, macrophage accumulation, and osteopontin expression in both wild-type and cPPARgamma(-/-) mice but induced hypertrophy in a PPARgamma-dependent manner. We pursued two mechanisms to explain the antifibrotic cardiomyocyte-PPARgamma-independent effects of pioglitazone: increased adiponectin expression and attenuation of proinflammatory macrophage activity. Adenovirus-expressed adiponectin had no effect on cardiac fibrosis and the PPARgamma ligand pioglitazone did not attenuate AngII-induced cardiac fibrosis, osteopontin expression, or macrophage accumulation in monocyte-specific PPARgamma(-/-) mice. CONCLUSIONS: We arrived at the following conclusions: 1) both cardiomyocyte-specific PPARgamma deficiency and activation promote cardiac hypertrophy, 2) both cardiomyocyte and monocyte PPARgamma regulate cardiac macrophage infiltration, 3) inflammation is a key mediator of AngII-induced cardiac fibrosis, 4) macrophage PPARgamma activation prevents myocardial macrophage accumulation, and 5) PPARgamma ligands attenuate AngII-induced cardiac fibrosis by inhibiting myocardial macrophage infiltration. These observations have important implications for potential interventions to prevent cardiac fibrosis.