Facing acid-base disorders in the third millennium - the Stewart approach revisited.

Acid-base disorders are common in the critically ill. Most of these disorders do not cause harm and are self-limiting after appropriate resuscitation and management. Unfortunately, clinicians tend to think about an acid-base disturbance as a "disease" and spend long hours effectively treating numbers rather than the patient. Moreover, a sizable number of intensive-care physicians experience difficulties in interpreting the significance of or understanding the etiology of certain forms of acid-base disequilibria. Traditional tools for interpreting acid-base disorders may not be adequate for analyzing the complex nature of these metabolic abnormalities. Inappropriate interpretation may also lead to wrong clinical conclusions and incorrectly influence clinical management (eg, bicarbonate therapy for metabolic acidosis in different clinical situations). The Stewart approach, based on physicochemical principles, is a robust physiological concept that can facilitate the interpretation and analysis of simple, mixed, and complex acid-base disorders, thereby allowing better diagnosis of the cause of the disturbance and more timely treatment. However, as the concept does not attach importance to plasma bicarbonate, clinicians may find it complicated to use in their daily clinical practice. This article reviews various approaches to interpreting acid-base disorders and suggests the integration of base-excess and Stewart approach for a better interpretation of these metabolic disorders.

Phosphate induced crystal acute kidney injury - an under-recognized cause of acute kidney injury potentially leading to chronic kidney disease: case report and review of the literature.

Acute phosphate nephropathy or nephrocalcinosis is a tubulointerstitial nephropathy characterized by tubular calcium phosphate deposition - crystal nephropathy - and slowly progressive renal insufficiency during or following treatment with preparations containing sodium phosphate. We report a patient who developed nephrocalcinosis (crystal induced acute kidney injury) following the administration of a combination of oral and rectal sodium phosphate for treatment of postoperative constipation. A timely renal replacement therapy procedure may reverse the process of crystallization and the irreversible slope towards chronic dialysis.

New insights regarding rationale, therapeutic target and dose of hemofiltration and hybrid therapies in septic acute kidney injury.

Mediator removal from tissue (capillary blood compartment, CABC) and transport to the central circulation (central blood compartment, CEBC) must be effective. Effectiveness through a passive mechanism seems unlikely as the surface of CEBC (30 m(2)) is smaller than CABC (300 m(2)) whereby the former will be a limiting factor in passive transport. According to studies, a high exchange volume can induce an 80-fold increase in lymphatic flow. This results in displacement (active transport) of mediators to CEBC. Recent studies have shown that the delivered dose constitutes the mainstay of continuous renal replacement therapy. However, these results are not likely to change the recommendation: 35 ml/kg/h, adjusted for predilution, in septic acute kidney injury (AKI). Recently, studies were focusing on global intensive care unit AKI. In non-septic AKI, those studies show that 20-25 ml/kg/h was optimal. The DO-RE-MI trial underscored the importance of delivery which could be obtained by targeting doses between 5 and 10 ml/kg/h higher than prescribed. Until the IVOIRE trial becomes available, septic AKI should be treated by continuous veno-venous hemofiltration at 35 ml/kg/h. In non-septic AKI, 25 ml/kg/h remains optimal.

Monitoring the safety of antiepileptic medication in a child with Brugada syndrome.

We report the case of an 8 year old boy presenting with episodes of decreased consciousness. As the boy's father died of a sudden cardiac death (SCD) at the age of 31 years, among other causes a Brugada syndrome (BS) was suspected. The boy was further examined at the UZ Brussels Heart Rhythm Management Center. The intravenous administration of ajmaline confirmed a BS without ventricular arrhythmias. Syncope in children can be an imminent sign of BS. BS is a life threatening condition that can deteriorate into SCD. The boy presented with episodes of lowered consciousness, transpiration and paleness. Readmission for further investigation was required. Clinical observation and continuous registered EEG during sleep showed multiple epileptical incidents. Hence the child was diagnosed with new onset epilepsy. For initiation of antiepileptic therapy, the patient was admitted at the pediatric intensive care unit (PICU). Close clinical observation and cardiovascular monitoring with continuous 12-lead ECG registration were performed during orally administered sodium valproic acid. During this anticonvulsive treatment in a child with documented BS no significant alterations in ECG-findings were observed. In this particular patient sodium valproic acid treatment can be estimated as a safe anticonvulsive therapy.

Frey's syndrome after elective thyroidectomy: a case report.

This case report documents the case of a 41-year-old Caucasian woman who developed a Frey's syndrome after elective thyroidectomy. This patient developed a sudden redness on one side of the face in the recovery room after a total thyroidectomy under general anaesthesia. All other vital signs of the patient remained normal. There were no signs of infection. After a few hours the symptoms disappeared without any treatment. Frey's syndrome is a disorder characterised by unilateral flushing or sweating of the facial skin. This syndrome can occur after parotidectomy or after trauma, injury or inflammation of the parotid, the submandibular glands, or of cervical and thoracic parts of the sympathetic trunk. Frey's syndrome normally results from aberrant regeneration of auriculotemporal nerve fibers to sweat glands in the skin. This case describes a self-limiting Frey' s syndrome after irritation of the cervical portion of the truncus sympathicus following total thyroidectomy.