Non-cardiogenic pulmonary edema and life-threatening shock due to calcium channel blocker overdose and its management: a case report and a clinical review.

May 2013

Siddiqi TA, Hill J, Huckleberry Y, Parthasarathy S.

Source

Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, University of Arizona Medical Center, Tucson, Arizona.

Abstract

Calcium channel blockers (CCB) overdose can be life-threatening when manifest as catastrophic shock and non-cardiogenic pulmonary edema. We describe a case of massive overdose of multiple medications, including sustained-release verapamil that was resistant to conventional support. Initial treatment for CCB overdose is primarily supportive and includes fluid resuscitation. The mechanism of non-cardiogenic pulmonary edema is not well known and reported cases in the literature were successfully treated with mechanical ventilation. Circulatory shock may fail to respond to atropine, glucagon and calcium in severely poisoned patients, and vasopressors are usually required. Attempts to overcome calcium-channel antagonism with the use of supratherapeutic doses of calcium salts are clinically indicated to reverse hypotension and bradycardia. There is evidence that hyperinsulinemia-euglycemia (HIE) therapy is superior to other therapies for CCB poisoning, and the potential mechanism is thought to be the insulin-mediated active transport of glucose into the cells that counters the CCBinduced intra-cellular carbohydrate-deficient state. Conventional decontamination measures are ineffective in accelerating clearance of CCB. Experience with intravenous lipid emulsion for lipophilic drug overdose, such as verapamil, is limited but has been proposed as a rescue therapy with improvements in cardiac inotropy through intravascular sequestration of the lipophilic CCB.

Keywords

ARDS, Calcium Channel Blockers, Hyperinsulinemia-euglycemiatherapy, Intravenous lipid emulsion, Overdose, Pulmonary edema, Shock, Toxicology, Verapamil

PubMed

http://www.ncbi.nlm.nih.gov/pubmed/23674813

(or)   Respiratory Care

http://rc.rcjournal.com/content/early/2013/05/14/respcare.02244.short

Drug-Induced Macular Edema.

May 3, 2013

Makri OE, Georgalas I, Georgakopoulos CD.

Source

Department of Ophthalmology, Medical School, University of Patras, Rio, 26504, Patras, Greece.

Abstract

Macular edema constitutes a serious pathologic entity of ophthalmology resulting in vision loss with a remarkable impact on the quality of life of patients. It is the final common pathway of various systemic diseases and underlying intraocular conditions, with diabetes mellitus being the most frequent cause. Other causes include venous occlusive disease, intraocular surgery, and inflammatory conditions of the posterior segment of the eye. Macular edema is a recognized side effect of various systemic and local medications and requires special consideration among ophthalmologists and other clinicians. Recently, antidiabetic thiazolidinediones have been implicated in the development of macular edema, and a review of the English literature revealed that other systemically administered drugs like fingolimod, recently approved for relapsing forms of multiple sclerosis, the anticancer agents tamoxifen and the taxanes, as well as niacin and interferons have been reported to cause macular edema. Ophthalmologic pharmaceutical agents, like prostaglandin analogs, epinephrine, timolol, and ophthalmic preparation preservatives have also been reported to cause macular edema as an adverse event. The purpose of this article is to provide a short, balanced overview of the available evidence in this regard. The available data and the possible pathophysiologic mechanisms leading to the development of macular edema are discussed. Possible therapeutic strategies for drug-induced macular edema are also proposed.

PubMed

I have not been well as soon as I am I will again be posting 04/10/13

Effects of ginseng total saponin on traumatic brain edema of rats.

Dec 2012

[Article in Chinese]

Xia L, Chen Q, Cheng GL.

Source

Department of Neurology, Huai' an First People's Hospital, Nanjing Medical University, Jiangsu 223300.

Abstract

OBJECTIVE:

To observe the effects of ginseng total saponin (GTS) on the water content in the brain tissue, the activity of superoxide dismutase (SOD), the content of malondialdehyde (MDA), the expression levels of tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta), and the neurological function in rats with traumatic brain injury (TBI), and to explore the roles of GTS in treating traumatic brain edema rats and its possible mechanisms.

METHODS:

The TBI rat model was established using modified Feeney's method. Rats were randomly divided into 3 groups, i.e., the sham-operation group, the TBI group, and the GTS-treated group. All rats were sacrificed after their neurological behavior was scored at day 1, 3, 5, and 7 of TBI. The brain tissue was taken out to measure the brain water content with wet-dry weight method. The activity of SOD in the brain tissue and the content of MDA were determined using biochemistry method. The expression levels of TNF-alpha and IL-1beta in the brain tissue were detected using ELISA.

RESULTS:

Compared with the TBI group at the same time point, the brain water content and the content of MDA decreased, the activity of SOD increased, the expression levels of TNF-alpha and IL-1beta obviously decreased, and the neurological functions were obviously improved in the GTS-treated group.  

CONCLUSIONS:

GTS could obviously alleviate the degree of traumatic brain edema after TBI, and attenuate the deleted neurological behavioral symptoms. The underlying mechanisms might be achieved through reducing the production of MDA, decreasing the expression levels of TNF-alpha and IL-1beta, elevating the activity of SOD, inhibiting free radical reaction, and alleviating inflammatory reactions.

PubMed

Protective effect of melatonin on reexpansion pulmonary edema in rats model.

Protective effect of melatonin on reexpansion pulmonary edema in rats model.

Feb 2013

Zhong M, Xue ZG, Cang J, Wu W, Huang JF, Zhu DM.

Source

Department of Anesthesiology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

Abstract

BACKGROUND:

Rapid reexpansion of collapsed lungs leads to reexpansion pulmonary edema (RPE). We aimed to investigate the effect of melatonin in the prevention of RPE formation.

METHODS:

We used a Wistar rat model in which the left lung was collapsed by ligating the left bronchus for 48 hours and then reexpanded and ventilated for an additional 2 hours. Thirty minutes before reexpansion, we injected melatonin (10 mg/kg) or vehicle intraperitoneally. We compared the wet/dry ratio, oxygenation index, myeloperoxidase (MPO) activity, nitric oxide (NO), malondialdehyde (MDA) and interleukin 8 (IL-8) levels in the reexpanded lungs between untreated and treated animals.

RESULTS:

We found that the wet/dry ratio of the melatonin group was significantly lower than that of the vehicle group, and the oxygenation index was higher in the melatonin group. Compared with the control, melatonin pretreatment significantly decreased the activities of IL-8, NO, MDA levels and MPO in lung tissues. Histopathology of reexpanded lungs showed that the melatonin pretreatment group had less pulmonary edema and less inflammatory cell infiltration.

CONCLUSION:

Melatonin decreases pulmonary edema and improves oxygenation after reexpansion by attenuating oxidative stress and inhibiting pro-inflammatory cytokines.

PubMed

Scalp edema: don't forget sunburn in children.

2012

Shah B, Yavuz ST, Tekşam O.

Source

Department of Pediatrics, Hacettepe University Faculty of Medicine, Ankara, Turkey.

Abstract

Scalp edema is an uncommon and striking finding in children that may alarm both parents and physicians. The objectives of this case report were to raise awareness among pediatric emergency physicians of the unusual presentation of sunburn as scalp edema. We present the case of an eight-year-old boy with sunburn of the head, presenting with scalp and face edema. Pitting edema and erythema were dominant on the forehead. Shaving of the boy's head the day before the symptoms was the most striking issue, and the sunburn healed gradually without any complications. Healthcare professionals should be aware of this condition, and the diagnosis of sunburn must be kept in mind in otherwise healthy-looking patients with a unique history.

PubMed

Antibiotic treatment in patients with chronic low back pain and vertebral bone edema (Modic type 1 changes): a double-blind randomized clinical controlled trial of efficacy.

Feb 2013

Albert HB, Sorensen JS, Christensen BS, Manniche C.

Source

Research Department, Spine Centre of Southern Denmark, Institute of Regional Health Services Research, Lillebaelt Hospital, University of Southern Denmark, Middelfart, Denmark, hanne.birgit.albert@slb.regionsyddanmark.dk.

Abstract

PURPOSE:

Modic type 1 changes/bone edema in the vertebrae are present in 6 % of the general population and 35-40 % of the low back pain population. It is strongly associated with low back pain. The aim was to test the efficacy of antibiotic treatment in patients with chronic low back pain (>6 months) and Modic type 1 changes (bone edema).

METHODS:

The study was a double-blind RCT with 162 patients whose only known illness was chronic LBP of greater than 6 months duration occurring after a previous disc herniation and who also had bone edema demonstrated as Modic type 1 changes in the vertebrae adjacent to the previous herniation. Patients were randomized to either 100 days of antibiotic treatment (Bioclavid) or placebo and were blindly evaluated at baseline, end of treatment and at 1-year follow-up.

OUTCOME MEASURES:

Primary outcome, disease-specific disability, lumbar pain. Secondary outcome leg pain, number of hours with pain last 4 weeks, global perceived health, EQ-5D thermometer, days with sick leave, bothersomeness, constant pain, magnetic resonance image (MRI).

RESULTS:

144 of the 162 original patients were evaluated at 1-year follow-up. The two groups were similar at baseline. The antibiotic group improved highly statistically significantly on all outcome measures and improvement continued from 100 days follow-up until 1-year follow-up. At baseline, 100 days follow-up, 1-year follow-up the disease-specific disability-RMDQ changed: antibiotic 15, 11, 5.7; placebo 15, 14, 14. Leg pain: antibiotics 5.3, 3.0, 1.4; placebo 4.0, 4.3, 4.3. Lumbar pain: antibiotics 6.7, 5.0, 3.7; placebo 6.3, 6.3, 6.3. For the outcome measures, where a clinically important effect size was defined, improvements exceeded the thresholds, and a trend towards a dose-response relationship with double dose antibiotics being more efficacious.

CONCLUSIONS:

The antibiotic protocol in this study was significantly more effective for this group of patients (CLBP associated with Modic I) than placebo in all the primary and secondary outcomes.

Springerlink

Continuous Positive Airway Pressure (CPAP) May Not Reduce Short-Term Mortality in Cardiogenic Pulmonary Edema: A Propensity-Based Analysis.

Feb 2013

Pirracchio R, Resche Rigon M, Mebazaa A, Zannad F, Alla F, Chevret S.

Source

Department of Biostatistics, Hôpital Saint Louis, Diderot, Paris, France; Department of Anesthesiology & Critical Care, Hôpital Européen Georges Pompidou, Paris, France. Electronic address: romain.pirracchio@gmail.com.

Abstract

INTRODUCTION:

Continuous positive airway pressure (CPAP) improves patients' condition in case of cardiogenic pulmonaryedema (CPE). However, the impact of CPAP on short-term mortality remains a matter of debate. We aimed at estimating the effect of CPAP on short-term mortality in patients treated for a CPE.

METHODS AND RESULTS:

We pooled the data from the Acute Heart Failure Global Registry of Standard Treatment and the Etude Francaise l'Innsuficiens Cardiaque Aigue observational cohorts to compare the estimations of the effect on short-term mortality of CPAP, before and after propensity score (PS) matching. A total of 2286 patients with a cardiogenic pulmonary edema were included in the analysis, of whom 321 (14%) received CPAP. Of these, 314 could be matched to a control patient (matched population: n = 628) and were included in the PS analysis. In naive analysis, CPAP application influenced neither short-term mortality (HR: 1.03, 95% CI: 0.73-1.46; P = .86) nor the need for tracheal intubation (OR: 1.04, 95% CI: 0.78-1.40; P = .78). After PS matching, CPAP was associated with a reduction in the need for tracheal intubation but it did not reduce short-term mortality. 

CONCLUSIONS:

Despite a reduction in the need for tracheal intubation, CPAP application may not reduce short-term mortality in patients suffering from cardiogenic pulmonary edema.

PubMed