Excellent chapters in Critical Care Nephrology (2009, 2nd ed) exist, but are perhaps too long for the time-poor exam candidate. Some effort has been spent to summarise these into the tables presented below. Additionally, excellent free-to-read articles are available on the intrawebs, containing vast lists of complications.
All RRT requires access of some sort.
Be it fistula or vas cath, there are risks:
- Vessel damage
- Bloodstream or localised infection
- Air embolism
All RRT filters tend to eat red cells. This is a complication of forcing blood to rub against a cheesegrater-like porous membrane.
The dialyser membrane is a proinflammatory surface. Modern membranes are a massive improvement, but some inflammatory reaction (particularly complement activation) is to be expected. Additionally, one's bloodstream becomes showered with the shredded remains of red blood cells, which exerts its own proinflammatory effect.
Blood loss due to circuit loss
If a filter clots, the whole thing is discarded, together with whatever blood is in the circuit. This could be a little or a lot, depending on the filter and circuit. Usually, the amount of blood lost is no greater than 200-300ml, equivalent to a drop of 10g/L of haemoglobin.
Because a large volume of blood (roughly 5-10% of the blood volume) spends every minute outside the body, it is exposed to the ambient temeperature, which in the ICU is typically rather chilly. The returning blood is usually cool. The patient may become hypothermic as a result. This phenomenon may obscure the presence of a fever, or it may result in a clinically significant drop in the core body temperature.
Unintelligently prescribed dialysis can lead to electrolyte disturbance. If you have prescribed a dialysate or replacement fluid which is completely free of potassium, you should not be surprised that the patient becomes dramatically hypokalemic.
The dialyser membrane is no obstacle for the highly water-soluble CO2; some CO2 will diffuse through the membrane and into the dialysate.
Activation of complement and the inflammatory mechanisms leads to an increase in the activity of nitric oxide synthase, which countracts the normal mechanisms of hypoxic pulmonary vasoconstriction. Increased shunt develops; therefore hypoxia ensues.
Malnutrition due to dialytic nutrient loss
The bloodstream is a necessary destination for all the absorbed nutrients, as well as for TPN. Dialysis removes many of the useful nutrient molecules. Specific easily cleared nutrients are amino acids (all highly water soluble small molecules) and water-soluble vitamins. Depending on one's ultrafiltration volume, the total amino acid loss may be around 10-20g/day. If on TPN, up to 10% of infused protein content may end up in the effluent bags.
Delayed renal recovery
This point is in bold because it is important. Renal recovery may be delayed by the very use fo dialysis, or it may never occur at all. This may be counterproductive if you suspect the patient will not be offered long-term dialysis. The following mechanisms have been implicated as causes of this "dialysis-induced dialysis dependence":
- Haemodynamic instability
- Haemofilter membrane-induced complement and cytokine activation, with subsequent "cytotoxic" tubular injury (analogous to septic nephropathy).
- Trophic hormone depletion (missing paracrine triggers for nephron regeneration)
Complications specific to intermittent haemodialysis
Consider that with an IHD or SLEDD session, one is removing 2-4 litres of fluid from the patient over 3-8 hours, whereas with CRRT one is removing the same amount over the cours eof 24 hours. Naturally, patients who are preload-sensitive will not enjoy such rapid fluid movements.
Haemodynamic instability may also occur in situations where the patient is dependent on high levels of vasopressor/inotrope support. In such circumstsances, one can assume that the infused catecholamines are being cleared by the circuit.
Dialysis disequilibrium syndrome
Only with IHD is the movement of small solutes so rapid and in such massive volume, that the concentration of chronically accumulated uraemic wastes in the brain becomes substantially greater than the extracellular fluid. The resulting osmotic movement of water can give rise to cerebral oedema, which manifests at first as confusion, progressing into unconsciosness.
Complications specific to CRRT
Complications related to anticoagulation
Unlike IHD circuits, CRRT circuits run over long periods, and are disadvantaged by a rather sluggish blood flow. Consequently, they must be anticoagulated. This is usually achieved by using heparin; although other forms of anticoagulation are available, they are not in routine use. Anyway; circuit anticoagulation usually results in at least some degree of systemic anticoagulation, which in turn results in bleeding complications.
There is a risk of HITTS eahc time heparin is used. Complications related to citrate anticoagulation are even more interesting, and are discussed in greater detail elsewhere.