Complications of haemoperfusion
The table presented here is modelled on the table representing the complications of renal replacement therapy in general. It was felt that haemoperfusion is sufficiently unique to merit its own table of complications; however many complications are shared by all RRT types. The better resource for this is a chapter by James Winchester from the textbook "Complications of Dialysis" which is available for free on Google Books.
Generic complications, common to all RRT
All RRT requires access of some sort. Be it fistula or vas cath, there are risks:
All RRT filters tend to eat red cells, but with the haemoperfusion filters this issue is exaggerated. Haemolysis of some degree is to be expected.
The consumption of cellular blood components in the cartridge is significant, but the platelets are the most affected.
The haemoperfusion membrane is a proinflammatory surface. Modern membranes are a massive improvement, but some inflammatory reaction (particularly complement activation) is to be expected. In addition to the proinflammatory effect of broken red blood cells, there is a risk of widespread inflammation due to cartridge embolism.
Blood loss due to circuit loss
If a perfusion cartridge clots, the whole thing is discarded, just like any other dialysis circuit. The perfusion cartridge may be slightly larger, and so the blood loss may be slightly greater.
The drop in the core body temperature due to heat exchange via the circuit occurs via similar mechanisms. Just as in CVVHDF, one can be cooled by the haemoperfusion circuit.
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.
Charcoal does not tend to cause any sort of electrolyte changes, but the macroporous resins can remove calcium phosphate and potassium from the blood stream.
Malnutrition due to adsoprtion of useful molecules
Adsorption of all lipophilic molecules occurs, and thus one ends up missing out on the fatty acids from TPN, fat-soluble vitamins A, D, E and K, or dietary cholesterol.
Over the initial hour or so, glucose and calcium levels can drop (even with charcoal hemoperfusion).
Unique complications, specific to haemoperfusion
The hemodynamic instability due to haemoperfusion is wholely due to the generation of an inflammatory response due to an incompatible blood/adsorbent interface. The chances of this have been greatly reduced by the use of modern immunoneutral coatings. In comparison, much of the early interest in this technique was lost due to major haemodynamic complications.
Again, this is mainly a complication of older, less "evolved" cartridges, where bits of the adsorbent would break off and embolise downstream. In modern cartridges this is almost unheard of.
Carbon in the cartridge, though a highly purified form, is still an organic product, and therefore prone to the usual peculiarities of natural materials. Weird hydrocarbons and potentially even toxic heavy metals may elute out of the cartridge and into the patient. Repeated treatments will therefore result in accumulation toxicity. This is largely a theoretical complication; as far as I am aware, such heavy metal elution has only ever been observed in vitro.
- The sorbent is a foreign material, and you expose your bloodstream to it.
- The first few sorbent filters activated the complement cascade in a very impressive way.
- Subsequently, new coatings have reduced this effect
Thrombocytopenia and hemolysis
- The sorbent is abrasive, and you grind your blood cells against it.
- One solution is to separate the blood cells and the plasma, and then to only expose the plasma to the sorbent
- The sorbent is microscopic particles, which can break off and sail downstream
- These days, there are filters for that.