**4. Miscellaneous pearls**

Most of the content discussed in previous sections refers to general considerations for understanding and prescribing competently RRT in ICU. However, some challenging situations encountered in clinical practice and pragmatic concerns will be briefly reviewed.

## **4.1 Severe dysnatremias**

Mild to moderate dysnatremias are frequent in critically ill patients, especially at initial presentation. Maximum correction rate and approach to treatment differ between guidelines [58]. Though, consensus exists that inadequate correction of chronic severe hyponatremias (<125 mmol/L for >48 hours) should be avoided due to risk of developing osmotic demyelination syndrome (ODS) [59]. Concurrent urgent need for RRT and this condition can be particularly challenging. Since most IHD machines have a minimum sodium of 130 mmol/L, even by prescribing short duration, low blood and dialysate flow rates, overcorrection is a possibility. In the opposite, CRRT has been used effectively at correcting hyponatremias in a predictable manner either by adding a 5% dextrose pre-filter infusion or via customized hypoosmolar dialysate fluids [60].

Limited evidence exists about hypernatremia. Most IHD machines have maximum sodium of 160 mmol/L and CRRT correction protocol has also been published. Published protocols for **hyponatremias**:


Published protocols for **hypernatremias**:

• Paquette, Goupil [63] – PMID: 27478592, DOI: 10.1093/ckj/sfw036

## **4.2 Acute hepatic failure or acute severe neurologic injury**

Patients suffering from acute liver failure (ALF) and acute severe neurologic injury are associated with cerebral edema and increased intracranial pressure. Rapid clearance of plasma solutes/toxins, as in intermittent therapy, can also lead to intracranial pressure (probably by water shift from sudden plasma hypoosmolality) [64].

In ALF, both the KDIGO-AKI and European Associated for Study of Liver (EASL) guidelines recommend CRRT instead of IHD in patients with ALF [19, 65]. Furthermore, RRT may be initiated before usual thresholds since it has been associated with increased transplantation-free survival, probably by clearance of ammonia as hyperammonemia is associated with increased intracranial pressure [66, 67]. Some published protocols used very high doses of CVVHDF (effluent 90 mL/kg/h) [68]. Also, targeting mild hypernatremias (145–150 mmol/L) is recommended in high-risk patients (acute renal failure, ammonia >150 μmol/L, grade IV encephalopathy and use of vasopressor) [65]. Options are customized reinjection and dialysis fluids as discussed above or by adding hypertonic saline perfusion.

## **4.3 Vascular access**

Vascular access should deliver stable and sufficient blood flow. In acute care setting, temporary dual-lumen central venous access is used for most patients. Ultrasound-guided catheter insertion is associated with higher successful placement, reduced attempts and time of procedure with less complications [69]. Choosing the site might have short-, mid- and long-term consequences.

Higher rates of catheter dysfunction are observed with femoral and left jugular site compared to right jugular, but no significant difference of urea reduction ratio or RRT downtime was observed [70]. More pneumothoraxes are observed with subclavian access [71].

Risks of catheter-related bloodstream infections and symptomatic deep-vein thrombosis are higher in femoral than subclavian and similar between jugular and femoral [71].

In patient with considerable risk of RRT dependence (mainly with pre-existing advanced CKD), large-bore venous subclavian catheter should be avoided since it can compromise future ipsilateral vascular access due to stenosis.

## **4.4 Disequilibrium syndrome**

Dialysis disequilibrium syndrome is a rare, potentially fatal but usually preventable complication of RRT. The pathophysiology is still debated but commonly reports an

intracranial osmotic gradient due the rapid removal of urea and osmotic solute by RRT, leading to cerebral edema [72]. The large variation of symptoms and severity, from mild nausea to fatal cerebral herniation makes the diagnosis challenging. The syndrome is mostly reported in ESRD patients with advanced uremia who are initially started on high efficiency/ standard IHD prescription. Patients with ESRD (or with unknown kidney failure duration) should be treated with an adapted low-efficiency IHD prescription, for the first treatments, in order to minimize osmotic shift and risk of disequilibrium syndrome. A progressive increase in dialysate and blood flows and duration can therefore be implemented for the following treatments. Occurrence of this syndrome has also been reported in frail patients with septic shock and AKI even after repeated IHD sessions [73]. In patients who develop symptoms compatible to a disequilibrium syndrome during or quickly after an IHD session, management should include rapid treatment cessation and the administration of osmotic agents (mannitol, hypertonic saline) to quickly raise osmolality, despite the paucity of evidence. However, prevention should still be privileged. The overall risk of dialysis disequilibrium syndrome is lower with PIRRT, and notably reduced in patients treated with CRRT with standard dosing.
