Massive arm edema following arteriovenous dialysis shunt creation in a patient with ipsilateral permanent pacemaker.

Massive arm edema following arteriovenous dialysis shunt creation in a patient with ipsilateral permanent pacemaker.

J Clin Ultrasound. 2007

Maher J, Rivero A, Zaim S, Pappas PJ, Labropoulos N, Klapholz M, Saric M.
Department of Medicine, New Jersey Medical School, University of Medicine and Dentistry (UMDNJ), 185 South Orange Avenue, Newark, NJ 07103.

Asymptomatic subclavian vein occlusion following insertion of a permanent pacemaker (PPM) or implantable cardioverter-defibrillator (ICD) is not uncommon. We report a case of a dual-chamber PPM in a patient with an unrecognized left subclavian vein occlusion who developed massive left arm edema following ipsilateral implantation of an arteriovenous (AV) hemodialysis graft. We recommend that patients with pre-existing PPM or ICD leads who are in need of vascular access for hemodialysis should have the AV shunts placed in the contralateral arm. If this is unavoidable, then preoperative subclavian vein screening for patency should be mandatory, even in asymptomatic patients. Sonography is an appropriate initial test in such a situation.

(2007 Wiley Periodicals, Inc. J Clin Ultrasound, 2007.

A Case of Negative-Pressure Pulmonary Edema After Electroconvulsive Therapy.

A Case of Negative-Pressure Pulmonary Edema After Electroconvulsive Therapy.

J ECT. 2007 Dec

Myers CL, Gopalka A, Glick D, Goldman MB, Dinwiddie SH.
From the *Departments of Psychiatry and †Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, IL.

Pulmonary edema after electroconvulsive therapy (ECT) is a rarely reported condition that can result in serious morbidity and even death if not promptly recognized and treated. We report the case of 21-year-old man with FG syndrome and schizophrenia who developed negative-pressure pulmonary edema after his 28th ECT. The patient developed acute hypoxemia requiring positive-pressure ventilation and was observed overnight in the intensive care unit. He recovered fully and received 43 subsequent ECT treatments without complication. This case illustrates the importance of taking steps to prevent airway obstruction as well as recognizing this rare but serious complication.

PMID: 18090704 [PubMed - as supplied by publisher]

Pulmonary edema after electroconvulsive therapy in a patient treated for long-standing asthma with a beta2 stimulant.

2007

Case Reports Journal of ECT. 23(1):26-27, March 2007.Hatta, Kotaro MD, PhD; Kitajima, Akiyoshi MD, PhD; Ito, Masanobu MD; Usui, Chie MD, PhD; Arai, Heii MD, PhD

Abstract: A 68-year-old man was scheduled to receive 8 treatments of electroconvulsive therapy (ECT) for severe depression. He was being treated for long-standing asthma with a [beta]2 stimulant, clenbuterol hydrochloride, and had experienced no asthma attack for 9 years. Although he experienced no adverse consequence in his 7 treatments, pulmonary edema ensued from his eighth treatment despite no change in anesthesia and in the technical parameters of ECT. He was treated with oxygen and intravenous hydrocortisone, after which he quickly recovered. Transient eosinophilia was observed, but clinical symptoms of asthma did not appear. Although the association between pulmonary edema and well-controlled asthma was unclear, thiopental as induction of anesthesia or esmolol as poststimulus delivery might have played a role in the event. There may be a possibility of pulmonary edema even after several uneventful ECT treatments in a patient with asthma.

Lippincott Williams & Wilkins, Inc.

An investigation of cerebral edema and injury volume assessments for controlled cortical impact injury.

An investigation of cerebral edema and injury volume assessments for controlled cortical impact injury.

J Neurosci Methods. 2007 Nov

Elliott MB, Jallo JJ, Tuma RF.
Department of Physical Therapy, Temple University, 3307 North Broad Street, Philadelphia, PA 19140, United States.

Using the controlled cortical impact (CCI) model, our laboratory compared edema in contralateral and ipsilateral regions to help clarify conflicting reports of contralateral edema and for enhanced assessment and interpretation of CCI injury pathophysiology. This investigation examined regional edema in response to graded injury severities over time with regards to tissue damage. Prior to injury rats were anesthetized with ketamine and xylazine (1:1). CCI injury parameters were set at 4.0m/s and 120 to 130ms. Rats were randomized to receive moderate or severe injuries set at 2.0 and 3.0mm depths, respectively. Cerebral edema and injury volume were examined separately following euthanasia with pentobarbital. Cerebral edema was measured using the wet-dry weight technique at 24 or 48h after injury. Sham animals underwent all surgical procedures except the impact injury. Injury volume was quantified using 2,3,5-triphenyltetrazolium chloride staining at 24h or 7 days after injury. The results of this investigation confirm that cerebral edema is absent in the uninjured, contralateral hemisphere after moderate and severe CCI injury. There were regional differences in cerebral edema formation in the hemisphere ipsilateral to injury that were dependent on injury severity and the length of time after injury. Tissue damage was reduced over 7 days following moderate CCI injury. Conclusions: (1) the absence of edema in the contralateral hemisphere allows it to serve as a valid control for edema formation, (2) misrepresenting injury volume because of edema continues to be a problem for evaluating CCI injury and treatment efficacy, and (3) reduced injury volume over 7 days following CCI injury suggests tissue recovery after initial dysfunction.

PMID: 18076998 [PubMed - as supplied by publisher]