Cardiac perforation due to delayed migration of a chronic dialysis catheter: A case report

BACKGROUND Tunnelled haemodialysis catheters are commonly used to perform haemodialysis. Rare complications of these catheters include perforations of major blood vessels or the heart. Albeit rare, these complications can lead to significant morbidity and mortality. CASE SUMMARY We present a case of late migration of a tunnelled haemodialysis catheter causing a right atrial perforation with subsequent pericardial tamponade, haemodynamic shock, and cardiac arrest. A 51-year-old female patient with end-stage renal disease presented with hypotension and lactate acidosis, indicating circulatory shock, during ambulatory intermittent haemodialysis. Dialysis was performed through a tunnelled haemodialysis catheter that had been implanted more than 1 year ago. Upon admission to the hospital, initial diagnostics, including transthoracic echocardiography and computed tomography scan, showed a circumferential pericardial effusion which was not haemodynamically significant and no other pathological findings. After being transferred to the intensive care unit, the patient again showed signs of haemodynamic shock at the start of another dialysis session which deteriorated to cardiac arrest. Ultimately, using multi-modality imaging, migration of the catheter tip through the right atrial wall into the pericardial space was diagnosed. Emergency sternotomy and surgical extraction of the tunnelled haemodialysis catheter were performed and the patient recovered completely. DISCUSSION Migration and perforation of a tunnelled haemodialysis catheter can occur late after implantation and lead to circulatory shock, thus requiring immediate diagnostic workup and surgical therapy. Routine diagnostic procedures may be insufficient for making a correct diagnosis. More specific approaches, such as multi-modality imaging including contrast echocardiography, should be implemented upon clinical suspicion.

Hyperkalemic circulatory shock and cardiac arrest altered by therapeutic management: A case report

Hyperkalemia is one of the few potentially lethal electrolyte disturbances. Severe hyperkalemia (Serum potassium concentration > 6.5 mmol/L) occurs most commonly from renal failure or the release of potassium from cells and can cause circulatory shock, cardiac arrhythmias or cardiac arrest. Current BLS (Basic Life Support) and ACLS (Advanced Cardiovascular Life Support) protocol should be used to manage cardiac arrest associated with hyperkalemia. But early consideration should be given to using the selective method of therapeutic management in addition to standard ACLS protocols that can be provided rapidly, effectively in patients with cardiovascular instability. We describe here a case of chronic kidney disease and congestive heart failure who developed circulatory shock and eventually cardiac arrest due to hyperkalemia managed with Calcium Gluconate, Sodium Bicarbonate and Insulin along with standard advanced cardiovascular life support protocol. Keywords: Potassium, hyperkalemia, acidosis, calcium, insulin, cardiac arrest.

Target arterial PO2 according to the underlying pathology: a mini-review of the available data in mechanically ventilated patients

There is an ongoing discussion whether hyperoxia, i.e. ventilation with high inspiratory O2 concentrations (FIO2), and the consecutive hyperoxaemia, i.e. supraphysiological arterial O2 tensions (PaO2), have a place during the acute management of circulatory shock. This concept is based on experimental evidence that hyperoxaemia may contribute to the compensation of the imbalance between O2 supply and requirements. However, despite still being common practice, its use is limited due to possible oxygen toxicity resulting from the increased formation of reactive oxygen species (ROS) limits, especially under conditions of ischaemia/reperfusion. Several studies have reported that there is a U-shaped relation between PaO2 and mortality/morbidity in ICU patients. Interestingly, these mostly retrospective studies found that the lowest mortality coincided with PaO2 ~ 150 mmHg during the first 24 h of ICU stay, i.e. supraphysiological PaO2 levels. Most of the recent large-scale retrospective analyses studied general ICU populations, but there are major differences according to the underlying pathology studied as well as whether medical or surgical patients are concerned. Therefore, as far as possible from the data reported, we focus on the need of mechanical ventilation as well as the distinction between the absence or presence of circulatory shock. There seems to be no ideal target PaO2 except for avoiding prolonged exposure (> 24 h) to either hypoxaemia (PaO2 < 55–60 mmHg) or supraphysiological (PaO2 > 100 mmHg). Moreover, the need for mechanical ventilation, absence or presence of circulatory shock and/or the aetiology of tissue dysoxia, i.e. whether it is mainly due to impaired macro- and/or microcirculatory O2 transport and/or disturbed cellular O2 utilization, may determine whether any degree of hyperoxaemia causes deleterious side effects.

A New Physiologic Based Integrated Algorithm in the Management of Neonatal Hemodynamic Instability

Physiologic based management of hemodynamic instability is proven to guide to logical selection of cardiovascular approach, and shorten time to clinical recovery, compared to empiric approach which is ignoring the heterogeneity of the hemodynamic instability related mechanisms. In this report we classified neonatal hemodynamic instability, circulatory shock, and degree of compensation to 5 physiologic categories, based on blood pressure (BP) different phenotypes, other clinical parameters, echocardiography markers, and oxygen indices. This approach is focused on hemodynamic instability in infants with normal heart structure.