Case Based Pediatrics For Medical Students and Residents
Department of Pediatrics, University of Hawaii John A. Burns School of Medicine
Chapter XIII.4. Dialysis
James H.E. Ireland, MD
Julie Won Ireland, MD
July 2002

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A 16 year old girl with a past medical history of systemic lupus erythematosus (SLE) presents with intractable nausea and vomiting, increasing edema and no urine output for two days. She had been diagnosed with SLE at age 14. A biopsy of her kidney at that time revealed a diffuse proliferative glomerulonephritis with prominent crescents and minimal fibrosis. Her creatinine at that time was 1.5, and she was started on cyclophosphamide, prednisone and furosemide.

Exam: VS T 36.5, P 110, RR 18, BP 180/110, weight 75 kilograms. She is very nauseated and actively vomiting. She responds to verbal commands and is slightly somnolent, but oriented. She has pale conjunctiva and no oral lesions or thrush. Her lungs are clear. She is tachycardic and has a rub. Her abdomen is soft and nontender and her upper and lower extremities have 1-2+ edema.

Her CBC is significant for a low hemoglobin of 7.5 g/dl with an MCV of 92. Her chemistries show an elevated potassium at 5.7; a low bicarbonate at 13 and a markedly elevated BUN at 119 and a creatinine of 14. Her ANA is elevated at 160 and her TSH is normal. A renal ultrasound shows small echogenic kidneys with no hydronephrosis, masses or stones. A chest x-ray shows engorged pulmonary vessels (fluid overload) and an enlarged heart. An echocardiogram reveals a moderate pericardial effusion, but is otherwise normal. Emergent vascular access is obtained, and she is taken to hemodialysis. She receives dialysis daily and within a week, her symptoms resolve. A follow-up echocardiogram demonstrates a reduction in the pericardial effusion.

The above case illustrates the use of acute hemodialysis for a patient with uremia secondary to chronic renal failure in the setting of SLE. There are a number of indications for acute hemodialysis (HD). One is renal failure (creatinine clearance less than 10) as manifested by a urea nitrogen over 150 mg/dL or a serum creatinine elevated 10-fold over normal, or signs and symptoms of uremia. This may include nausea and vomiting, altered mental status, seizures, pericarditis or bleeding diathesis (platelets become progressively dysfunctional in the setting of uremia). Other indications for HD include uncontrolled hyperkalemia, refractory fluid overload, severe metabolic acidosis, tumor lysis syndrome, certain inborn errors of metabolism, and certain acute poisonings/overdoses.

When a teenager needs HD, vascular access must be obtained prior to initiating therapy. In the acute or emergent setting, a double-lumen catheter (such as a Vas-Cath) can be placed in a large vein. The internal jugular or femoral vein is preferred, but sometimes the subclavian vein is used. This vascular access device has large lumens to permit optimal blood flow. As with any central venous line, there is a risk of pneumothorax if the internal jugular or subclavian sites are used; a risk of bleeding (especially in the uremic patient) and a risk of infection. Although placed with sterile technique, the risk of infection increases the longer the line is kept in place. If kept in for an extended period, infection is one of the drawbacks to having this type of vascular access; however, it can be used immediately and is ideal when dialysis needs to be done quickly.

If chronic, "maintenance" dialysis is planned for some future time (as with chronic renal failure), more permanent vascular access should be established. One method involves connecting a vein to an artery to create an AV fistula. It is usually done in the non-dominant arm, in case ischemia or other complications occur. Once it is decided that permanent vascular access is needed, the patient and nurses should be instructed to make that limb "off-limits" for blood draws, intravenous lines or arterial punctures. This is done to minimize any potential trauma to the blood vessels prior to fistula surgery. As a reminder, a large sign is usually placed above the patient's hospital bed stating "No Draws: Left Arm." A number of artery-vein anastomoses are possible, but the two most common are the wrist radiocephalic and the elbow brachiocephalic. After surgery, the fistula needs about 6 weeks to mature and cannot be used during this time. Maturation is the histologic process of venous thickening and dilating, essentially taking on some of the characteristics of the attached artery. These changes enable the venous portion of the graft to accept the repeated insertion of the dialysis needle. If the patient is already requiring dialysis, a temporary percutaneous double lumen catheter can be used until the fistula is mature and usable. After surgery, the fistula should have a palpable thrill and audible bruit. This should be checked at least daily as an assessment of patency.

If an AV fistula is not anatomically possible, another type of permanent access is an arterial-venous (AV) graft. This involves the use of a synthetic tube to connect the artery and the vein. Common sites for AV grafts include the radial artery to the basilic vein, the brachial artery to the basilic vein and the brachial artery to the axillary vein. Maturity is faster than the fistula, usually occurring in 2-3 weeks. The major drawback of the AV graft is it is much more likely to clot and occlude than the native fistula, due to intimal hyperplasia in the native vein to which the graft is attached. If this should occur, medical therapy (thrombolysis) or a surgical procedure can be done to salvage the graft (interventional procedures or thrombectomy). Both AV fistulas and AV grafts have a number of long-term complications. This includes edema or ischemia of the hand, pseudoaneurysm at the graft or fistula site, infection, thrombosis and congestive heart failure. If a hemodialysis patient has a fever or positive blood cultures and fistula or graft infection is suspected, a nuclear WBC scan can be done to help confirm the diagnosis. Staphylococcus is a frequent infecting organism, but gram negative rods and enterococcus infections can also occur. Empiric therapy should be directed at these organisms, and may require vancomycin coverage for methicillin-resistant Staphylococcus aureus (MRSA). Species of Candida can also infect these sites.

Vascular access in infants and small children is more complicated than in older children and teenagers. In neonates, an umbilical vein may be used. Some hemodialysis machines permit a single lumen or needle to be used. For permanent access, AV grafts may be necessary if native blood vessels are too small to create a fistula.

Once vascular access is established, blood leaves the body via tubing into the dialysis unit. It passes along a semipermeable membrane with a dialysis solution (dialysate) flowing along the other side of the membrane. Solute particles from the blood then pass down their concentration gradient into the dialysate for removal. The mechanism of dialysis can be simplified based on standard diffusion: where particles (solutes) of high concentration (in the blood) move down their concentration gradient to an area of low concentration (the dialysate). The movement is across a semipermeable membrane, so larger particles will cross more slowly or not at all. Thus the smallest particles will be removed the fastest. Also, the steeper the concentration gradient, the quicker the removal. Blood and dialysate run through a filter in opposite directions, with the membrane separating them. This countercurrent flow maximizes the concentration gradients for solute removal. The blood is then returned to the body. Other aspects of the dialysis prescription include the type of membrane, flow rate of blood and dialysate, temperature, length of time on dialysis, and composition of the dialysate. Modern machines can monitor these functions and monitor for potential air emboli and blood leaks in the dialyzer as well.

The dialysate is purified water with precise amounts of various ions and glucose. For example, a typical solution would contain: Na+ 145 mEq/L; K+ 3.5 mEq/L; Ca++ 3.5 mEq/L; Mg++ 0.75 mEq/L; and dextrose 200 mg/L. Different ionic concentrations can be used for different clinical situations. For example, if a stable patient needs routine dialysis, and her pre-dialysis potassium is usually 5.0, a dialysate with 3.0 mEq/L of potassium would be used. If the same patient had a viral gastroenteritis and her pre-dialysis potassium was 3.0 then a dialysate with 4.0 mEq/L of potassium would be used. If that same person was feeling fine and ate some high potassium foods such as fruit the day before dialysis and her pre-HD potassium was 7.0, a dialysate with zero potassium would be used.

Besides normalizing ionic concentrations and removing waste, another function of dialysis is to remove accumulated water. Water moves across the membrane under hydrostatic forces and this is known as ultrafiltration. The degree of that force determines the amount of net water movement. Small particles within the water are also removed during this process, which is called convection. Particles larger than the dialysis membrane pore size will be left behind in the blood.

Major complications of hemodialysis are unusual. These can include: seizures, hypotension and hypothermia. The seizures are a severe manifestation of the dysequilibrium syndrome. The syndrome has a characteristic EEG tracing and in mild cases can be associated with headaches, nausea and vomiting. More severe manifestations include seizures and coma. The cause of the syndrome is unknown, but it may have to do with osmotic shifts in the brain. It can occur during or after hemodialysis. Preventative measures include limiting the flow and the total time on hemodialysis for the first few sessions to prevent large fluxes.

Hypotension is another common complication during hemodialysis. If significant, it can be treated with volume replacement. If fluid removal is necessary, however, more frequent dialysis sessions with smaller volumes removed per session may be required. Additionally, some patients tolerate fluid removal better if dialysate sodium concentrations are increased, something known as sodium modeling. If large changes in fluid status are avoided, hypotension during the session is minimized. Finally, hypothermia can be a problem, as removed blood can be cooled in the tubing and machinery. This is prevented by heating units in the dialysis machine to keep the temperature constant.

As mentioned, hemodialysis can be associated with large fluid shifts that can result in hypotension. When patients are unable to tolerate such a drop in blood pressure or are already on vasopressor support (for example, in septic shock) another form of dialysis may be required. This typically is known as continuous renal replacement therapy (CRRT) or slow continuous therapies. When done via a Vas-Cath, it may also be called continuous veno-venous hemofiltration (CVV-H). This form of dialysis is done continuously (compared to three times a week for 4-5 hours in standard hemodialysis). It is used almost exclusively in the intensive care unit for critically ill patients. This type of therapy is also better than standard hemodialysis for clearing elevated phosphorus seen in tumor lysis syndrome in leukemia or lymphoma, in part because a different and more porous membrane is used.

Another method of dialysis is peritoneal dialysis (PD). In this method, an indwelling catheter is placed in the abdomen, usually under general anesthesia in children, and the PD solution (another form of dialysate) is circulated through the peritoneal cavity. This is the most common method of chronic dialysis for pediatric patients. PD can also be used in the acute setting, but it is not efficient in correcting hyperkalemia, hyperphosphatemia or hyperammonemia and if these values are critical, another dialysis modality should be used. The advantages are that vascular access is not needed; no complicated machinery is required; it does not cause large volume shifts; and it can be performed at home after fairly brief training. In PD, the peritoneum acts as a biological dialysis membrane and solutes cross this from the blood to the dialysate. Fluid can be changed manually every six hours or changed through an automated cycling machine (such as during sleep.) The major complication of this method is peritonitis. Other drawbacks include the presence of an external catheter from the abdomen, which may make children self-conscious.

Long term complications of chronic renal failure in children include growth failure, anemia, hypertension, acidosis and renal osteodystrophy. The etiology of the growth failure is multifactorial. Children may respond to exogenous recombinant human growth hormone. Erythropoietin deficiency accompanies renal failure and results in anemia. Folic acid is usually added as a supplement and ferrous sulfate can be started if iron stores are low. If anemia persists, exogenous erythropoietin can be initiated. Hypertension may be due to dietary indiscretion, inadequate fluid removal during dialysis, or the renin-angiotensin axis. If these cannot be remedied, anti-hypertensive medications are used. Acidosis can interfere with growth hormone function and should be treated with exogenous alkali (calcium carbonate, sodium bicarbonate) to maintain a serum bicarbonate levels of 22 mEq/L or higher.

Renal osteodystrophy can be minimized with careful control of calcium and phosphate metabolism. As the kidney fails, phosphate excretion is impaired and the serum levels rise and a concurrent fall in serum calcium. The lower serum calcium levels stimulate parathyroid hormone production which acts on bone to release calcium. This can cause bone pain, deformities and growth retardation. Radiographically, osteopenia, epiphyseal slipping and subperiosteal resorption may be present. Laboratory findings can include elevated PTH and alkaline phosphatase with low levels of active vitamin D (1,25-dihydroxy-vitamin-D3). Vitamin D undergoes final hydroxylation and activation in the kidney, which is hampered in chronic renal failure. The reduction in active metabolites of vitamin D results in calcium malabsorption in the intestines and further exacerbates osteodystrophy, and in children with open epiphyses can lead to what is known as "renal rickets". Therapy should reduce excess phosphate by limiting dietary phosphorus to 1 gram per day, and if levels remain high, treatment with binders (calcium carbonate, calcium acetate, or sevelamer) should be initiated. These are given with meals to bind dietary phosphate and prevent absorption. Additionally, calcium and active vitamin D replacement should be optimized and PTH levels should be monitored for hyperparathyroidism.

In summary, dialysis can be a life-saving therapy for acute renal failure, certain poisonings and in severe electrolyte disturbances seen in the tumor lysis syndrome. It can also substitute for native kidneys in patients with end stage renal disease, although children do not thrive as well as they do with a functioning renal transplant. Ideally, dialysis can act as bridge until normal renal function returns or the patient is able to receive a kidney transplant.


1. What are the indications for dialysis in pediatric patients?

2. What situation is CVV-HD preferred over HD or PD?

3. What are the advantages of PD?

4. What are three complications that may occur in patients undergoing hemodialysis?

5. What are some long term complications of renal failure?


1. Daugirdas JT, Blake PG, Ing TS (eds). Handbook of Dialysis, 3rd edition. 2001, Philadelphia: Lippincott Williams and Wilkins, pp. 3-24, 67-97, 148-166, 562-579.

2. Chan JCM, Williams DM, Roth KS. Kidney Failure in Infants and Children. Pediatr Rev 2002;23(2):47-60.

Answers to questions

1. Renal failure with uremia; BUN over 150 mg/dl; creatinine over 10 mg/dL; severe hyperkalemia; severe acidosis; refractory fluid overload (CHF); certain inborn errors of metabolism; certain acute poisonings; tumor lysis syndrome.

2. In hemodynamically unstable patients.

3. Can be done at home; no complex machinery; no vascular access.

4. Hypotension, seizures, hypothermia.

5. Anemia; acidosis; hypertension; growth retardation, renal osteodystrophy, platelet dysfunction.

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