Common complications during HD - Copy.pptx

Common complications during Hemodialysis in children

1. Common Complications in Pediatric HD and Their Managements

2. agenda Introduction. Epidemiology of common complications of HD. Acute complications of HD and their managements. Chronic complications of HD and their managements.

3. Overview Of Pediatric HD Pediatric HD is a renal replacement therapy (RRT) used to remove waste products and excess fluids from the blood in children with ESRD. HD is typically indicated for children with ESRD or AKI who require immediate management of fluid overload, electrolyte imbalances, or toxins. Pediatric patients are at a higher risk for several acute and chronic complications due to their smaller body size and developing immune systems. 3

4. acute complications of Pediatric HD Intradialytic hypotension and hypertension Muscle cramps Dialysis disequilibrium syndrome (DDS) Dialyzer reactions. Acute haemolysis Air embolism Electrolytes imbalances Vascular access Complications: CRBSIs, Bleeding, Clotting, Blockage. Other nonspecific complications 4

5. Chronic Complications of Pediatric HD Anemia Growth retardation. Cardiovascular diseases. Psychosocial disorders Vascular access complications Dialysis-related infections Dialysis-related malnutrition 5

6. Epidemiology of common Pediatric HD Complications Hypotension: Affects up to 20-30% of pediatric HD session. Hypertension (HTN): ~ 50-75% of pediatric patients on HD experience HTN. Electrolyte imbalance: Particularly hyperkalemia and hyperphosphatemia, are common in over 30% of pediatric patients. DDS prevalence: Less common, occurring in~1-5% of new pediatric dialysis cases, particularly in those with high urea levels. Infection: infection rates are high, with catheter-related bloodstream infections occurring in 10-25% of pediatric patients annually Bleeding events: reported in about 5-10% of pediatric HD patients, particularly related to vascular access. Anemia: Nearly all pediatric patients on HD experience anemia , with varying degrees of severity. Psychosocial complications: Anxiety and depression are common, affecting up to 30-50% of pediatric patients. Growth Retardation (GR): GR occurs in up to 50 to 60% of children on long-term HD. Cardiovascular Complications : Cardiovascular disease is a leading cause of morbidity and mortality, with a high incidence in pediatric HD patients. 6

7. acute complications 7

8. 1- Dialysis disequilibrium syndrome (DDS) 8 DDS occurs due to a substantial gradient between the urea concentrations in the CSF and blood that causes water movement into the central nervous system (CNS), resulting in raised intracranial pressure. It manifests during or immediately after HD as a self-limiting entity, but recovery can take several days. It os more common in patients during or soon after their first treatment. It DDS is a clinical syndrome characterized by neurologic deterioration, restlessness, mental confusion, headache, occasional muscle twitching, and coma. Patients undergoing fast dialysis develop seizures and cerebral edema more often.

9. 1- Dialysis disequilibrium syndrome (DDS) 9 The diagnosis is often one of exclusion. The dialysis prescription can be adjusted to reduce the rate of plasma urea clearance by using a smaller dialyser, decreasing the blood or dialysate flow rate, or switching to more frequent, shorter, treatments. A reasonable goal of urea concentration reduction is 40% over two hours, URR of 0.4. Intradialytic osmotic shifts can be minimized with the use of sodium profiles or higher dialysate sodium concentrations, or if the patient is grossly fluid overloaded use sequential HD in which an initial period of UF alone is followed by conventional dialysis. Adding an osmotic agent to the blood could prevent the gradient from forming. IV mannitol, infusion of 3–5 % sodium chloride or the use of higher dialysate sodium baths. Are usually used. Concurrent antiepileptic therapy is required with this therapy if the patient is seizing.

10. 2- Muscle Cramps During HD Occur in majority of dialysis treatments, mainly towards the end of dialysis. They are a significant cause for early termination and underdialysis. The exact pathogenesis is unknown. Causes of Muscle Cramps in HD: Fluid and electrolyte imbalance: Rapid fluid removal (high UF rate). Electrolyte shifts (Na, K, Ca). Low-sodium dialysis solution. Intradialytic hypotension: Catheter with poor blood flow. Carnitine deficiency. 10 These factors trigger vasoconstriction and muscle hypo-perfusion, with secondary impairment of muscle relaxation

11. Muscle Cramps During HD Management of muscle cramps: Minimize interdialytic weight gain and minimize need for excessive UF. Prevent intradialytic hypotension. Higher sodium dialysate, or sodium profiling. For severe cases: IV saline (normal or hypertonic) and IV 50% glucose are very effective. Some patients respond to diazepam, carbamazepine, amitriptyline, or phenytoin. Preventive measurements: Gentle stretching exercises may offers some relief. Quinine sulfate may help some patients, it is best used 2h before dialysis. Vitamin E (200–400IU) was as effective as quinine in an RCT. Carnitine replacement therapy helps some patients (20 mg/kg IV after each session. 11

12. 3-Reactions to dialyzer membranes These reactions are not always due to the membrane itself, but can be due to the sterilant, associated drugs, complement activation, or unknown mechanisms. Mainly there are two types: type A and type B. Anaphylactic type A reactions: These occur within minutes of starting dialysis. Present with dyspnea, increased body and local temperature at the fistula site, a feeling of impending doom, itching, urticaria, coryza, watery eyes, abdominal cramping, and diarrhea. It is due to hypersensitivity to ethylene oxide used to sterilize dialyzers. Also occur in patients taking ACEIs and dialyzed with AN69®. Management includes: IV antihistamines, steroids, and epinephrine. Prevention: proper rinsing of dialyzers before use eliminates residual allergens and helps prevent them.

13. Reactions to dialyzer membranes Nonspecific type B dialyzer reactions: These are more common but much milder. Present with chest or back pain 20 to 40 minutes after commencing dialysis. It is attributable to complement activation. Trying a different dialyzer membrane may help prevent it.

14. 4-Hemolysis Acute hemolysis during HD is a medical emergency. Severe hemolysis is rare, but can cause chest pain, abdominal or back pain, chest tightness, headache, nausea, and malaise. May indicated by the port-wine appearance in the venous blood line, a marked fall in the hematocrit , and a pink- colored plasma centrifuged blood sample. Life-threatening hyperkalaemia can occur if unrecognized. The patient should be evaluated by hematologic investigations and kept under observation for delayed hemolysis . A dialysate sample must be investigated to find the cause . 14

15. Hemolysis Management Stop blood pump immediately and clamp lines. Check Hb and potassium (risk of severe hyperkalaemia). Haemolysis may continue for several hours after removal of precipitant. Seek cause urgently, as multiple patients may be affected if it is due to water or a central dialysate problem. Causes: Overheating of dialysate. Contamination with bleach, formaldehyde, or peroxide from water purification or reprocessing. Contamination with chloramine, nitrates, or copper from water supply. Hypotonic dialysate. Kinks in blood tubing. Malfunctioning blood pump. 15

16. 5- Air embolism It is rare, as air detectors will clamp venous blood lines if air is detected in the return circuit. May occur while manipulating CVCs. Introduction of 1 mL/kg air may be fatal. This is a fatal complication. Presentations: In sitting patients, air tends to move upwards into cerebral venous circulation and cause fitting and coma. In recumbent patients, it causes chest pain, dyspnoea, chest tightness, and cough. Foam is usually seen in the venous blood line. A churning sound may be heard during chest auscultation. Managements: Clamp venous line and stop blood pump. Place the patient in a left lateral recumbent position. Administer 100% oxygen by mask. Rarely, percutaneous aspiration of air from the ventricle is necessary. 16

17. 6- Electrolyte imbalance 17 Hyperkalemia and Hypokalemia Hypernatremia and Hyponatremia Hypocalcemia and Hypercalcemia Hyperphosphatemia and Hypophosphatemia Hypermagnesemia and Hypomagnesemia

18. 18 Immediate therapy Definitive therapy Symptomatic Symptoms Causes ECG changes The most effective method of K+ removal is through dialysis. Dietary potassium intake should also be controlled, and K+ binders may be used in chronic management. IV insulin with glucose to shift K+ intracellularly. Sodium bicarbonate can be given if the child is acidotic. Albuterol can be used to drive K+ into cells. The first step is to stabilize the cardiac membrane using IV calcium gluconate. Inadequate dialysis (insufficient K removal), high dietary potassium intake, or tissue breakdown (e.g., hemolysis or rhabdomyolysis). ECG characteristic changes such as peaked T waves, prolonged PR interval, and widened QRS complex may be observed. M uscle weakness, fatigue, and paresthesias (tingling sensations). In severe cases, arrhythmias (palpitations, chest pain, or even sudden cardiac arrest) may occur. Hyperkalemia

19. Muscle weakness, cramps, and fatigue. Severe hypokalemia can cause respiratory muscle weakness, paralysis, and cardiac arrhythmias on the ECG. It can result from excessive removal of K+ during dialysis, dietary K+ restriction, gastrointestinal losses (e.g., vomiting or diarrhea), or use of diuretics. Oral potassium supplements are usually effective in treating mild to moderate hypokalemia . IV potassium replacement is necessary for severe hypokalemia , particularly when associated with symptoms or ECG changes. Symptoms Causes Managements of severe case Managements of mild to moderate case Hypokalemia Preventive: Adjusting the dialysate potassium concentration can help maintain stable potassium levels, and regular monitoring of serum potassium is essential.

20. Hypocalcemia Presentation Hypocalcemia may present with muscle cramps, tetany, perioral tingling, and paresthesias. Severe hypocalcemia can lead to seizures, laryngospasm, and cardiac arrhythmias like prolonged QT interval on ECG. Acute Management Preventive IV calcium gluconate is administered to treat severe hypocalcemia or symptomatic cases. Oral calcium supplements and active vitamin D analogs (e.g., calcitriol) are used for maintenance therapy. Regular monitoring of calcium levels and adjusting the dialysate calcium concentration are essential to prevent recurrence. Causes It can be due to: Low calcium in the dialysate, Inadequate dietary calcium intake, Vitamin D deficiency, Excessive use of phosphate binders that do not contain calcium.

21. Hypercalcemia Presentation It can present with nonspecific symptoms such as nausea, vomiting, constipation, polyuria, and polydipsia. Neurological symptoms include confusion, lethargy, and in severe cases, stupor or coma. ECG changes may include a shortened QT interval. Immediate Management Preventive Discontinuing calcium supplements and Reducing calcium intake from all sources. Bisphosphonates or calcitonin can be used in severe cases to inhibit bone resorption. Optimizing calcium-phosphate balance, Using non-calcium-based phosphate binders, and Possibly adjusting the dialysate calcium concentration. Causes It often results from: Excessive calcium intake (e.g., calcium-based phosphate binders or vitamin D analogs ), High calcium dialysate, or Hyperparathyroidism.

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23. Hypophosphatemia Presentation Hypophosphatemia can cause muscle weakness, respiratory failure, impaired cardiac function, and, in severe cases, rhabdomyolysis, hemolysis , or osteomalacia . Causes It can result from overzealous use of phosphate binders, malnutrition, or excessive phosphate removal during dialysis. Management of Mild Cases Oral phosphate supplements are generally effective for mild to moderate hypophosphatemia. Management of Severe Cases IV phosphate may be required in severe cases, but it should be administered cautiously due to the risk of hypocalcemia and soft tissue calcification . Preventive Adjusting the use of phosphate binders and ensuring adequate dietary intake are essential preventive measures

24. Hyperphosphatemia Presentation Chronic hyperphosphatemia is often asymptomatic but can lead to complications like pruritus (itching), bone pain, and soft tissue calcification, including vascular calcification. Causes It is typically due to inadequate phosphate removal during dialysis or excessive dietary phosphate intake. Management of Mild Cases Dietary phosphate restriction is the first line of management. Management of Severe Cases Phosphate binders (e.g., calcium acetate, sevelamer, lanthanum carbonate) are prescribed to reduce phosphate absorption from the gut. . Preventive Increasing the frequency or duration of HD sessions may be necessary to enhance phosphate removal.

25. Symptoms May cause thirst, irritability, lethargy, and confusion. Severe cases can lead to seizures, coma, or intracranial hemorrhage . Causes It may occur due to excessive Na+ gain (e.g., high Na+ dialysate or saline infusions) or significant water loss (e.g., diarrhea, or inadequate water intake). Immediate Mx The primary goal is to restore fluid balance by administering hypotonic fluids (e.g., D5W or 0.45% saline) to slowly reduce sodium levels . Chronic Mx Ongoing management involves careful control of Na+ intake, appropriate dialysate Na+ concentration, and ensuring adequate hydration.   Hypernatremia

26. Symptoms May cause headache, nausea, and vomiting. More severe manifestations include seizures, altered mental status, or coma. Causes Hyponatremia may result from overhydration (e.g., excessive fluid intake), inappropriate dialysate concentration, or underlying conditions like SIADH. Immediate Mx Acute symptomatic hyponatremia is a medical emergency. Hypertonic saline (3% NaCl) may be administered to rapidly raise sodium levels in severe cases, but this must be done cautiously to avoid demyelination syndrome. Chronic Mx Chronic hyponatremia is managed by fluid restriction and adjusting the dialysate Na+ concentration. The goal is to gradually correct the Na+ levels. Hyponatremia

27. Symptoms : Hypomagnesemia can lead to symptoms like muscle cramps, tremors, seizures, and arrhythmias such as torsades de pointes. Causes : It may result from dietary deficiency, gastrointestinal losses, or excessive removal during dialysis. Mx of mild cases: Oral magnesium supplements are usually sufficient for mild hypomagnesemia. Severe cases: IV mg sulfate is indicated for severe cases. Dialysate magnesium concentration may need to be adjusted to prevent recurrence. Immediate Mx : D/C any mg-containing drugs and initiating HD to remove excess magnesium. IV calcium gluconate can be used to counteract the effects of hypermagnesemia on the heart. Causes : It can occur due to excessive intake of magnesium-containing medications (e.g., antacids, laxatives) or inadequate removal during dialysis. Symptoms : Presents with nausea, vomiting, low BP, bradycardia, muscle weakness, and, in severe cases, respiratory depression or cardiac arrest. Hypermagnesemia Hypomagnesemia

28. Other nonspecific complications 28 These nonspecific complications include nausea and vomiting (10%), headache (70%), chest and back pain (1% to 4%), and itching. Cause: these are probably related to hypotension or could be an early manifestation of disequilibrium syndrome. Managements: Treating the associated hypotension resolves the symptoms. A single predialysis dose of 5 to 10 mg metoclopramide is sufficient for vomiting. Acetaminophen given during dialysis can help manage the headache. Switching to a different type of dialyzer membrane could reduce itching caused by low-grade hypersensitivity to blood circuit components. Reduction of blood flow rate (by 25–30%) during first hour of dialysis sometimes useful (but overall dialysis time must be lengthened to maintain dose of dialysis). Use bicarbonate rather than acetate dialysis.

29. CRBSIs are infections that occur when bacteria or other pathogens enter the bloodstream through a CVC. Definition R elevance in Pediatrics Pediatric patients on HD are particularly vulnerable due to the frequent use of CVCrs for vascular access. Incidence Higher incidence in pediatric patients due to immature immune systems and frequent catheter manipulations. Catheter-related bloodstream infections (CRBSIs)

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