List the complications associated with renal replacement therapy. Consider in your answer continuous renal replacement therapy, peritoneal dialysis and chronic intermittent dialysis.
Access related complications:
CVL risks: insertion complications/infection/disconnection/blood loss/air embolism
Fistula complications: stenosis, varices, shunt, infection, steal syndrome
Peritoneal dialysis: peritonitis
Insertion complications: bowel perforation
Pleural effusions and respiratory compromise
Haemodynamic changes –vasodilation, hypercirculation, pericardial effusion, cardiomyopathy Anaemia
Osmolality shifts- dialysis disequilibrium
Cellular activation; Thromocytopaenia, leukocytosis Nutrient losses
Peptides and protein loss: albumin, cytokines, hormones
Electrolyte changes: hypo/hyperkalaemia, hypo/hypernatraemia, hypomagnesaemia, hypophosphataemia., hypocalcaemia
Increased risk of infections/impaired immunity
Side effects of anticoagulation: Heparin-bleeding, hypocalcaemia
Citrate-citrate lock, hypocalcaemia
Adjustment of drug doses
This answer would benefit from a tabulated format, or indeed from any attempt at structure whatsoever. Without a model, one may try to compile a list of complications for all haemodialysis modalities, separate from a list of complications which are unique to each modality, and all of them separate from the complications of peritoneal dialysis which is a completely different animal. Then, within each modality, one might organise the complications by system. This cumbersome attempt is offered below.
|Generic complications for all types of RRT|
All RRT requires access of some sort.
Hypoxia: Activation of complement and the inflammatory mechanisms leads to an increase in the activity of nitric oxide synthase, which counteracts the normal mechanisms of hypoxic pulmonary vasoconstriction. Increased shunt develops; therefore hypoxia ensues.
Hypocapnea: The dialyser membrane is no obstacle for the highly water-soluble CO2; some CO2 will diffuse through the membrane and into the dialysate.
Haemodynamic instability: with all modalities of RRT, one can expect some fluid and electrolyte shifts, and therefore some effect on the haemodynamics of the patient. Of these effects, some patients will be quite tolerant, even in the face of wildly erratic dialysis prescriptions. In other circumstances, even the most careful CRRT regimen will produce severe cardiovascular bewilderment. In short, though this is mostly seen with IHD, haemodynamic instability can be regarded as a generic feature of RRT.
Hypothermia: 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 temperature, 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.
Dialysis disequilibrium syndrome: this 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. It is usually only seen with careless IHD, but one needs to acknowledge that an insane CRRT prescription can also produce this complication.
Electrolyte disturbance, which can be described as "hypo-everything-aemia". Unintelligently prescribed dialysis can lead to electrolyte depletion. 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.
Hyper-electrolytaemia is also a possibility, in the event that you have removed too much fluid and haemoconcentrated the patient (or, alternatively, if you have prescribed some sort of unusual dialysate with an excess of electrolytes in it).
Delayed renal recovery is possible.Renal recovery may be delayed by the very use of 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":
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.
Haemolytic complications: All RRT filters tend to eat red cells. This is a complication of forcing blood to rub against a cheesegrater-like porous membrane.
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.
Inflammatory response: 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.
|Specific to IHD|
Fistula complications are in some ways unlike complications from a vas cath, and include the following list of problems:
Haemodynamic instability: 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 course of 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 circumstances, one can assume that the infused catecholamines are being cleared by the circuit.
|Renal||Amyloidosis develops in chronic haemodialysis patients because of the formation of small extracellular tissue deposits, made up of low-molecular-weight subunits of a variety of proteins.|
|Specific to CRRT|
|Electrolyte||Hypocalcemia with citrate toxicity is a particularly interesting cause of metabolic acidosis (and then alkalosis) which is associated with 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 each time heparin is used. Complications related to citrate anticoagulation are even more interesting, and are discussed in greater detail elsewhere.
|Specific to PD|
Complications associated with establishing access: bowel perforation
Complications related to routine regular access: peritonitis
Complications related to chronic PD:
|Respiratory`||Pleural effusions and ascites: these impact on respiratory function much like a gravid uterus might, i.e. by displacing the diaphragm and bases of lungs cephalad the extra water ends up decreasing FRC and increasing the work of breathing.|
|Gastrointestinal||Ileus: chronic PD gives rise to adhesions and peritoneal thickening; bowel function suffers mechanically.|
Oh's Manual, Chapter (pp. 540) 48 Renal replacement therapy, by Rinaldo Bellomo
Bellomo, R., and C. Ronco. "Renal replacement therapy in the intensive care unit." Intensive Care Med (1999) 25: 781±789