44 research outputs found
Case Report Traumatic Page Kidney Induced Hypertension in Critical Care: Immediately Resolved or Long-Term Resistant Problem
Page kidney is a well-known phenomenon causing hypertension, due to compression of renal parenchyma by a subcapsular hematoma, of either traumatic or non-traumatic origin. The main therapeutic approach is based on surgical approach (nephrectomy or hematoma evacuation) and antihypertensive treatment. In this paper we present a post-traumatic case of Page Kidney in a Critical Care unit. We discuss different therapeutical opportunities to extremely elevated systemic blood pressure resistant to traditional drug therapy
Case Report Use of Early Inhaled Nitric Oxide Therapy in Fat Embolism Syndrome to Prevent Right Heart Failure
Fat embolism syndrome (FES) is a life-threatening condition in which multiorgan dysfunction manifests 48-72 hours after long bone or pelvis fractures. Right ventricular (RV) failure, especially in the setting of pulmonary hypertension, is a frequent feature of FES. We report our experience treating 2 young, previously healthy trauma patients who developed severe hypoxemia in the setting of FES. Neither patient had evidence of RV dysfunction on echocardiogram. The patients were treated with inhaled nitric oxide (NO), and their oxygenation significantly improved over the subsequent few days. Neither patient developed any cardiovascular compromise. Patients with FES that have severe hypoxemia and evidence of adult respiratory distress syndrome (ARDS) are likely at risk for developing RV failure. We recommend that these patients with FES and severe refractory hypoxemia should be treated with inhaled NO therapy prior to the onset of RV dysfunction
Impact of Bariatric Surgical Intervention on Peripheral Blood Neutrophil (PBN) Function in Obesity
Healthcare Personnel Safety During Percutaneous Tracheostomy in Patients With COVID-19: Proof-of-Concept Study
Comparison of high-flow nasal oxygen cannula therapy versus a standard oxygen face mask in patients with hypostatic pneumonia
Iodine-Induced Hyperthyroidism—An Old Clinical Entity That Is Still Relevant to Daily ICU Practice: A Case Report
Objective. Hyperthyroidism has been described as elevated serum free T3 and/or
free T4 levels with decreased thyrotropin (TSH) concentrations. The main causes are related to
autoimmune and neoplastic pathology. However, it might be caused due to a long-term topical
exposure (iodine solution dressing) or by intravenous administration of
iodine-containing substances.
Both clinical and laboratory features might be presented. The
main management is based on interruption of all exposures with
iodine solutions and also antithyroid medicine in case of severe
laboratory and clinical disturbances.
Data Sources.
We present a case of iodine-induced hyperthyroidism
in a critically ill ICU patient caused by excessive iodine
containing antiseptic solution washes and contrast agent administration.
The patient was successfully treated by discontinuing iodine exposure and
beta-blocker administration.
Conclusions.
In patients with underlying thyroid gland pathology, thyroid-function
tests and clinical observation in the ICU are of critical importance
Extracorporeal methods of blood glutamate scavenging: a novel therapeutic modality
Pathologically elevated glutamate concentrations in the brain's extracellular fluid are associated with several acute and chronic brain insults. Studies have demonstrated that by decreasing the concentration of glutamate in the blood, thereby increasing the concentration gradient between the brain and the blood, the rate of brain-to-blood glutamate efflux can be increased. Blood glutamate scavengers, pyruvate and oxaloacetate have shown great promise in providing neuroprotection in many animal models of acute brain insults. However, glutamate scavengers' potential systemic toxicity, side effects and pharmacokinetic properties may limit their use in clinical practice. In contrast, extracorporeal methods of blood glutamate reduction, in which glutamate is filtered from the blood and eliminated, may be an advantageous adjunct in treating acute brain insults. Here, we review the current evidence for the glutamate-lowering effects of hemodialysis, peritoneal dialysis and hemofiltration. The evidence reviewed here highlights the need for clinical trials