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Presentation on theme: "به نام خداوند جان و خرد کزین برتر اندیشه بر نگذرد."— Presentation transcript:

1 به نام خداوند جان و خرد کزین برتر اندیشه بر نگذرد

2 Complications During Hemodialysis A. A. Nassiri, M.D., D.I.U. SBUMS

3 Complications Common Complications Intra-Dialytic Hypotension Cramps Nausea & Vomiting Headache Chest Pain Back Pain Itching Fever & Chills Un-common Complications Disequilibrum Syndrome Dialyser reactions Arrhythmia Cardiac tamponade Intra-cranial Bleeding Seizure Hemolysis Air Embolism Visual & Hearing Loss Dx-associated Hypoxemia

4 Complications Common Complications Intra-Dialytic Hypotension Cramps Nausea & Vomiting Headache Chest Pain Back Pain Itching Fever & Chills Un-common Complications Disequilibrum Syndrome Dialyser reactions Arrhythmias Cardiac tamponade Intra-cranial Bleeding Seizure Hemolysis Air Embolism Visual & Hearing Loss Dx-associated Hypoxemia

5 Intra-Dialytic Hypotension Intradialytic hypotension (IDH) is defined as a decrease in systolic blood pressure by ≥20 mm Hg or a decrease in MAP by 10 mm Hg associated with symptoms that include: abdominal discomfort; yawning; sighing; nausea; vomiting; muscle cramps; restlessness; dizziness or fainting; and anxiety. It impairs the patient’s well-being, can induce cardiac arrhythmias, predisposes to coronary and/or cerebral ischemic events. In addition, IDH precludes the delivery of an adequate dose of dialysis, as hypotension episodes lead to the compartment effect and result in suboptimal Kt/V urea.

6 Intra-Dyalytic Hypotension Cardiovascular ”Intolerance” to Hemodialysis a state of Hemodynamic instability or Cardiovascular ”Intolerance” to Hemodialysis an abrupt decline in BP:  SBP by ≥ 20 mm Hg or  MAP by 10 mm Hg + symptoms  The pattern of IDH may be: early (<1 hour), late (after 1 hour), or unremitting (sustained) posttreatment.

7 Intra-Dialytic Hypotension Intra-dialytic hypotension (IDH) is defined as a decrease in SBP by ≥20 mm Hg or a decrease in MAP by 10 mm Hg associated with symptoms that include: abdominal discomfort; yawning; sighing; nausea; vomiting; muscle cramps; restlessness; dizziness or fainting; and anxiety.

8 Intra-Dialytic Hypotension Consequences : 1- Syncope, Seizure, TIA, Cerebral infarction 2- Cardiac ischemia, Arrhythmias (QTc dispersion) 3- Mesenteric venous ischemia (non-occlusive) 4- Vascular access thrombosis 5- Nausea/ Vomiting/ Cramps/ Extreme fatigue 6- Inadequate dialysis ( suboptimal Kt/V urea ) due to frequent interruption  suboptimal UF (fluid boluses, volume overload & inter-dialytic HTN, LVH) 7- Death

9 Intra-Dialytic Hypotension It impairs the patient’s well-being, can induce cardiac arrhythmias, predisposes to coronary and/or cerebral ischemic events. In addition, IDH precludes the delivery of an adequate dose of dialysis, as hypotension episodes lead to the compartment effect and result in suboptimal Kt/V urea.

10 Cardiovascular complications of IDH include: ischemic (cardiac or neurological) events; vascular access thrombosis; dysrhythmias; and mesenteric venous infarction. Long-term effects of IDH include: volume overload due to suboptimal ultrafiltration and use of fluid boluses for resuscitation; LVH, with its associated morbidity and mortality; and interdialytic hypertension.

11 During the past 10 years, despite improvements in dialysis technology, the frequency of IDH has remained unchanged at about 25% of all HD sessions. In addition, the incidence of IDH will continue to increase as an increasing number of elderly patients will develop CKD, and also due to the progressive increase in the number of diabetic patients with CKD. Patient subgroups most likely to have IDH include those with diabetic CKD, CVD, poor nutritional status and hypoalbuminemia, uremic neuropathy or autonomic dysfunction, severe anemia, age ≥65, and predialysis systolic blood pressure <100 mm Hg.

12 There are no large-scale, epidemiological studies to define the risk factors that are associated with the risk of developing IDH, although IDH appears to be more common in patients with diabetes and predialysis hypotension. Both normotensive or hypertensive dialysis patients can develop IDH. The degree of IDH in the same patient may vary from time to time or may have seasonal variations.

13 Intra-Dialytic Hypotension Physiology: 2-5 L (  1.5 L/d) removed over 3-5 hours Plasma volume approx.: 40cc/Kg   2.8 to 3 L Plasma water: 2.5 to 2.8 L 1-2  plasma volume must be removed  The reason the pt survive  Compensatory Mechanisms: Cardiac mechanisms Plasma Refilling 3Vascular changes Passive Venoconstriction 1- Cardiac mechanisms 2- Plasma Refilling 3- Vascular changes 4- Passive Venoconstriction

14 Intra-Dialytic Hypotension Systemic Blood Pressure   Peripheral Vascular Cardiac Output Peripheral Vascular Resistance   Resistance Heart Rate Heart Rate Stroke Volume   Plasma VolumeMyocardial Contractility Plasma Volume Myocardial Contractility ”Cardiac Compensatory Mechanisms”

15 Intra-Dialytic Hypotension Systemic Blood Pressure   Peripheral Vascular Cardiac Output Peripheral Vascular Resistance   Resistance Heart Rate Heart Rate Stroke Volume   Plasma VolumeMyocardial Contractility Plasma Volume Myocardial Contractility ”Cardiac Compensatory Mechanisms” 1- Cardiac rate change appear to be less important in maintaining COP under conditions of decreased filling 2- Contractility affected by a number of electrolyte changes (K+, HCO3, Ca) 3- Diastolic dysfunction: difficult to fill a stiff heart with blood during diastole when the filling pressure is reduced.

16 2 Intra- cellular Space Extra- cellular Space Intra- Vascular Space Circulating Blood Volume Toxins Fluid Toxins Fluid Toxins Fluid Dialyzer 23 Liters 17 Liters 5 Liters

17 2 Intra- cellular Space Extra- cellular Space Intra- Vascular Space Circulating Blood Volume Toxins Fluid Toxins Fluid Toxins Fluid Dialyzer Three Compartment Model Fluid Shifts 23 Liters 17 Liters 5 Liters

18 Plasma Refilling 2 Intra- cellular Space Extra- cellular Space Intra- Vascular Space Circulating Blood Volume Toxins Fluid Toxins Fluid Toxins Fluid Dialyzer

19 Intra-Dialytic Hypotension Plasma Refilling Rate The ultimate cause of hypotension is:. reduced cardiac filling The initial compensatory mechanism is: refilling of the plasma water space from surrounding tissue space (ECF). As a result of refilling, even though “1” entire plasma volume is removed during dialysis, the blood volume typically decrease only by 5% to 20%.

20 Intra-Dialytic Hypotension Plasma Refilling Rate Factors that impair PRR: 1-  size of the interstitial fluid compartment. (  Dry Weight) 2-  plasma protein level (  oncotic forces) 3-  dialysate Na+ level (  osmotic forces) 4-  UF rate (to treat large interdialytic weight gain & shorter dialysis time) 5-Vasodilators (  hydrostatic pressure to the capillary bed; ex: acetate)

21 A small group of patients (5%-10%) may have low systolic blood pressure (<100 mm Hg) at the initiation of dialysis. This group includes anephric patients, those who are on dialysis for a longer period, and diabetic patients with persistent orthostatic hypotension due to autonomic dysfunction. Patients on dialysis with autonomic dysfunction show an exaggerated drop in systolic and diastolic blood pressures and MAP, compared to those without underlying autonomic dysfunction. Other risk factors include older age (>60 years), female sex, diabetes mellitus, presence of CAD, and the use of nitrates before a dialysis session.

22 The following subgroups of chronic HD patients should be evaluated carefully for the risk of developing IDH: 1- Patients with diabetic CKD Stage 5 2- Patients with CVD: LVH and diastolic dysfunction with or without CHF LV systolic dysfunction and CHF Patients with valvular heart disease Patients with pericardial disease (constrictive pericarditis or PE) 3- Patients with poor nutritional status and hypoalbuminemia 4- Patients with uremic neuropathy or autonomic dysfunction due to other causes 5- Patients with severe anemia 6- Patients requiring high volume ultrafiltration; more than expected interdialytic weight gain 7- Patients with predialysis SBP of <100 mm Hg 8- Patients 65 years or older age

23 Hypotension Plasma Refilling Rate The extent to which plasma volume falls during dialysis (associated with UF), depends on: 1-The relative UF rate 2-Plasma refilling rate (PRR)  PRR can be defined as the rate at which plasma volume is restored from intracellular & interstitial fluid compartments, when fluid is removed from the vascular space.

24 Intra-Dialytic Hypotension Common causes A- Related to excessive decrease in blood volume 1- High UF rate (to treat a large interdialytic. weight gain). 2- Fluctuations in the UF rate. 3- Target “dry weight” set too low. 4- Dialysis solution Na+,(K+, Ca++) level too low B- Related to lack of vasoconstriction 1- Acetate-containing solutions 2- Dialysis solution too warm. 3- Food ingestion (splanchnic vasodilatation) 4- Tissue ischemia (adenosine release,  NE) 5- Autonomic neuropathy (e.g., diabetic) 6- Anti-hypertensive medications

25 Intra-Dialytic Hypotension C- Related to cardiac factors 1- COP unusually dependent on cardiac filling.. a- Diastolic dysfunction (  filling pressure). due to LVH, IHD, Pericarditis, PE, AF. 2- Failure to increase cardiac rate.... a- ingestion of β-blockers.. b- uremic autonomic neuropathy.. c- aging. 3- Inability to increase COP for other reasons. a- poor myocardial contractility due to age,.... HTN, atherosclerosis, myocardial calcification,.. valvular disease, amyloidosis

26 Intra-Dialytic Hypotension Uncommon causes 1- Pericardial disease 2- Myocardial infarction 3- Occult hemorrhage 4- Septicemia 5- Arrhythmia 6- Dialyzer reaction (IL hypothesis) 7- Hemolysis 8- Air embolism 9- ANEMIA (Hct < 20% to 25%)

27 Intra-Dialytic Hypotension Management (a dilemmas !) The numerous therapies offered to treat IDH suggest the incomplete effectiveness of any individual treatment. Indeed, ”Dialysis-Related Hypotension” is a complex phenomenon, and it is best thought of as analogous to. ”Essential HTN ” in wich multiple factors contribute (+ individual factors)  Response to interventions is variable.

28 Intra-Dialytic Hypotension Acute Management of IDH 1- Trendelenburg position. 2- UF rate  reduced or stopped. 3- Blood Flow Rate (Qb),  reduced. 4- A bolus of 0.9% saline (  100 cc) alternative to saline: Hypertonic saline (10cc/23% or 30cc/7.5%), Glucose, Mannitol (12.5grams IV), Albumin, hypertonic saline plus Dextran 6% (dextran to prolong the duration of BP response). 5- Nasal O 2

29 Intra-Dialytic Hypotension Prevention: Dialysate temperature modeling Dialysate calcium modeling Dialysate sodium modeling Midodrine Carnitine Sertraline

30 Dialysate temperature modeling During standard dialysis, an increase in core body temperature is usual and increases the risk for IDH. The increase in body temperature is either related to heat load from the extracorporeal system, or secondary to volume removal. Volume removal is associated with increased metabolic rate with decreased thermal losses either directly, or secondary to peripheral vasoconstriction 370 and impaired convective mechanisms of heat loss. 370 Temperature monitoring is difficult in dialysis patients due to variability in room, core body, and dialysate temperatures, as well as the lack of sensitive equipment to monitor the dialysate-blood temperature gradient. The use of low-temperature dialysate (i.e., lower than the patient’s core temperature) compared with standard dialysate-temperature (37–38°C) 371,372 decreases the frequency and intensity of symptomatic hypotension. Low-temperature dialysis improves the reactivity of capacitance and resistance vessels, and is associated with improvement in cardiac contractility

31 37°5 36°5 35°8 36°2 37°5 37°1 BTM ET Dialysate Temperature Modeling

32 IMPACT DE LA TEMPERATURE DU DIALYSAT SUR LA TOLERANCE HEMODYNAMIQUE DE L'HEMODIALYSE INTERMITTENTE CHEZ LES PATIENTS EN CHOC SEPTIQUE S. Siami SRLF 2003 H0 15 mn 30 mn 60 mn 120mn 180 mn Après le début de la séance d'hémodialyse + 20% + 10% +0% -10% - 20% Dialysat à 35°, n=55 Dialysat à 37°, n=49

33 Dialysate calcium modeling The long-term hemodynamic and osseous consequences associated with the use of different levels of dialysate calcium need careful evaluation. The use of low-calcium dialysate has been associated with decreased LV contractility and a corresponding decrease in blood pressure. 378,379 It was further associated with a significant intradialytic decrease in blood pressure in both healthy and cardiac- compromised HD patients and patients with decreased LV ejection fraction. 378,380 Significant changes in blood pressure, 380 myocardial contractility 378,380,381 and changes in intradialytic blood pressure in cardiac compromised patients 382 have been associated with the changes when dialysate calcium concentration is ≤2.5 mEq/L. A dialysate Ca of 3.5 mEq/L may lead to hypercalcemia and decreased bone turnover. 78 Furthermore, limited studies have shown only marginal benefit on the frequency of IDH episodes with the use of dialysate Ca >3.0 mEq/L

34 Dialysate Sodium Modeling

35 Dialysate sodium modeling Sodium profiling is based on the principle that there is a linear relationship between the changes in plasma sodium concentration and blood volume (BV). The intradialytic decrease in plasma volume can be as much as three-fold greater with dialysate sodium of 134 mEq/L than with a dialysate sodium of 144 mEq/L. 383–386 In this technique, the dialysate sodium concentration at the beginning of treatment is hypertonic, and during the final hours of dialysis is progressively reduced, reaching almost normal levels before the end of dialysis Sodium modeling prevents the development of IDH by: a) an increased ECF sodium level at the time of peak UF rate improves shift of water from ICF to the ECF compartment with improved venous refill and prevention of the Bezold-Jarisch reflex; 387,388 and b) hypertonic dialysate—to a greater extent—accelerates urea equilibration between ICF and ECF while urea removal is at its peak during the first hour of dialysis

36 Dialysate Sodium Modeling Limitations : a) poor temporal correlation between the time of onset of IDH and an antecedent decrease in blood volume; b) interdialysis and interindividual variation c) postdialysis hypernatremia : with thirst, dysphoria, hypertension, and increased interdialytic weight gain.  In some instances, a reverse sodium profile prescribed, dialysate sodium concentration increases toward the end of the session when plasma volume is lowest.

37 Limitations of dialysate sodium modeling include the following: a) there is poor temporal correlation between the time of onset of IDH and an antecedent decrease in blood volume; b) there is a significant interdialysis and interindividual variation in serum sodium, and for any given level of serum sodium, the amount of diffusible plasma water varies based on total body water, serum proteins and other nondiffusible elements in the plasma; c) the development of postdialysis hypernatremia can be associated with thirst, dysphoria, hypertension, and increased interdialytic weight gain. In some instances, a reverse sodium profile is prescribed, in which the dialysate sodium concentration increases toward the end of the session when plasma volume is lowest. Various profiles of ultrafiltration modeling can also be used to decrease the incidence of hypernatremia.

38 Convection : Réduction de la surcharge hydrosodée Diffusion : Réduction du volume plasmatique avec hypotension Œdème cellulaire (cérébral) Eau Solutés Eau Dialysâ t Rapid Solute Removal “Disequilibrum”

39 Midodrine Midodrine prevents IDH by a- maintaining the central blood volume (CBV) and COP, and ↑ PVR A single dose of midodrine (5 mg), 30 minutes before the HDx: improv. in intradialytic and postdialytic systolic and diastolic BP and MAP Midodrine is effectively cleared by HD and its half-life is reduced to 1.4 hours by HD Midodrine has minimal cardiac and CNS effects, due to its specificity for α1 receptors The most frequent side effects of midodrine are piloerection, scalp itching or tingling, nausea and heartburn, headache, nervousness, and sleep disturbance. Long-term use : supine systolic hypertension in less than 10% of patients Midodrine: used cautiously in pts with CHF and in those using other negative chronotropic agents such as beta-blockers, digoxin and CCBs.

40 Midodrine Midodrine prevents IDH by maintaining the central blood volume (CBV) and cardiac output, and a marginal increase in peripheral vascular resistance (PVR). A single dose of midodrine (5 mg) administered 30 minutes before the dialysis session was associated with an improvement in intradialytic and postdialytic systolic and diastolic blood pressures and MAP, compared to dialysis sessions without the use of Midodrine. 392 Others have reported the continued efficacy of midodrine use for more than 8 months without development of adverse events. 392

41 Midodrine is effectively cleared by HD and its half-life is reduced to 1.4 hours by HD. 394 Such pharmacokinetic data are not available in PD patients at the time of writing these guidelines. Midodrine has minimal cardiac and central nervous system effects, due to its specificity for α1 receptors, and it does not cross the blood-brain barrier. The most frequent side effects of midodrine are piloerection, scalp itching or tingling, nausea and heartburn, urinary urgency, headache, nervousness, and sleep disturbance. Long-term use has been associated with supine systolic hypertension in less than 10% of patients; this side effect warrants cessation of therapy. 395 Patients should also be monitored for bradycardia, as midodrine is associated with reflex parasympathetic stimulation. 396 Since midodrine is administered on the days of dialysis, both prodrug and active metabolite are removed effectively by HD; therefore, the risk of developing supine hypertension is possible, but very rare

42 Midodrine should be used cautiously in patients with CHF and in those using other negative chronotropic agents such as beta-blockers, digoxin and nondihdropyridine CCBs. Concomitant use with other α- adrenergic agents—such as ephedrine, pseudoephedrine and phenylpropanolamine—should be avoided, as this may aggravate supine hypertension. Midodrine can also antagonize the actions of α-adrenergic blockers (such as terazosin, prazosin and doxazosine) and could result in urinary retention. The combination of cool dialysate and predialysis doses of midodrine may lead to decreased frequency and intensity of symptoms of IDH without side effects.

43 Carnitine Hemodialysis therapy for more than 6 months is associated with reduction of plasma and tissue levels. Carnitine deficiency is associated with several metabolic defects, defined as dialysis-related carnitine disorders, including IDH. The reasons for this beneficial effect are not clear, but could be due to improvement in vascular smooth muscle and cardiac muscle function.

44 Carnitine Hemodialysis therapy for more than 6 months is associated with reduction of plasma and tissue levels of carnitine and carnitine esters. Carnitine deficiency is associated with several metabolic defects, defined as dialysis-related carnitine disorders, including IDH. 397 A multicenter trial of intravenous L-carnitine therapy at 20 mg/kg into the dialysis venous port with each session of dialysis was associated with reduced frequency of IDH and muscle cramps (44% versus 18% and 36% versus 13%, respectively), as compared with the placebo group. 397–399 The reasons for this beneficial effect are not clear, but could be due to improvement in vascular smooth muscle and cardiac muscle function

45 Sertraline Sertraline is a selective serotonin reuptake inhibitor and has been shown to improve symptoms in patients with neurocardiogenic syncope, idiopathic orthostatic hypotension & IDH. These disorders share a common pathogenic mechanism with IDH: a paradoxical withdrawal of central sympathetic outflow, resulting in sudden decrease in blood pressure with bradycardia. Side effects of sertraline include dizziness, insomnia, fatigue, somnolence, and headache.

46 Sertraline Sertraline is a selective serotonin reuptake inhibitor and has been shown to improve symptoms in patients with neurocardiogenic syncope, idiopathic orthostatic hypotension & IDH. These disorders share a common pathogenic mechanism with IDH: a paradoxical withdrawal of central sympathetic outflow, resulting in sudden decrease in blood pressure with bradycardia. Both retrospective and prospective studies in small number of patients demonstrated that treatment with sertraline hydrochloride was associated with an improvement in the hemodynamic parameters in patients with IDH. 402– 404 Side effects of sertraline include dizziness, insomnia, fatigue, somnolence, and headache

47 Resistant IDH Resistant cases of IDH should be treated with a combination of modalities, such as: a- combination of midodrine and dialysate temperature profiling b- combination of dialysate temperature profiling and 3 mEq/L dialysate calcium c- combination of dialysate temperature modeling and sodium modeling d- isolated ultrafiltration and other techniques providing a high convective solute transport e- extended daily dialysis or nocturnal HD

48 Volume plasmatique Contractilité myocardique VES FC QcRVP PAM + Na Bicarbonate UF seule T°C Bicarbonate Calcium UF adaptée à la volémie Potassium

49 Limitations It is unclear if episodes of IDH, per se, are associated with increased morbidity and mortality. The data supporting the effectiveness of various therapeutic options for the treatment of IDH are available in the form of case series and case reports. Very few multicenter randomized studies have been published. Objective assessment of dry weight using such methods as IVC sonography, or bioimpedance or tissue impedance techniques, have not been rigorously tested in relation to IDH and long-term clinical outcomes.

50 Conclusion Patients with CKD who are at risk for IDH may require evaluation for the presence of underlying cardiovascular and autonomic function. The patients’ medications list should be verified very carefully to avoid the use of short-acting anti-hypertensive medications and peripheral vasodilators immediately before the dialysis session. Hemodialysis patients at risk for, or predisposed to, IDH may benefit from lowering dialysate temperature, dialysate sodium modeling, and maintaining dialysate calcium at 3 mEq/L. Further benefits may be derived from treatment with pharmacological agents that prevent the development of IDH. If modifications in dialysis prescription and adjustments in antihypertensive medications do not improve IDH, these patients should be considered for extended daily dialysis or nocturnal HD. If no improvement is seen after these measures, patients may be counseled for living-donor kidney transplantation.

51 Muscle Cramps Common complication  33-85% Prolonged & involuntary contraction in a muscle, when it is already in its most shortened and vulnerable position Often in the early termination of HDx session EMG: begins with fasciculations in various muscle parts and subsequent progression to high frequency potentials (the origin is neural and not muscular).

52 Muscle Cramps Prolonged involuntary muscle contractions (cramps), are the most common neuro-muscular complications observed during dialysis ( 5-20%). Cramps tend to occur during the 2 nd half of the HD treatment & usually involve the lower extremities. Although intra-dialytic cramp is not considered life- threatening, its impact on the overall quality & quantity of dialysis is immense  Premature ”sign-offs”

53 Muscle Cramps Etiology (the pathogenesis is unknown) 1- EMG studies  progressive rise in tonic activity & Alterartion in muscle function (BDZ & Quinine). 2- Volume Depletion  IDH & Rapid fluid shift. ”Aggressive UF   Intravascular Volume  Vasoconstriction &  Muscle Blood Flow  Impaired Mucsular Relaxation (ATP- dependent).”

54 Muscle Cramps Etiology 3- Hypo-Osmolality  Acute lowering of the plasma Na+ level  ”skeletal muscle vasoconstriction”. (Hypertonic saline, Mannitol, 50%D/w) 4- Overactivity of the sympathetic nervous system: Vasoconstriction (partial effect). 5- Carnitine deficiency 6- Tissue Hypoxia 7-  Mg2+ 8- Hypo-calcemia 9- Hypo-kalemia

55 Muscle Cramps Acute Management  Directed at increasing the plasma osmolality, more effective in dilating muscle-bed vessels. 1- Hypertonic glucose (in non-DM) (50%D/w): 25-50cc 2- Hypertonic saline (23.5%): 10-20cc/ 3-5min 3- Mannitol (25%): cc (may accumulate in Dx pts.)  If concomitant with IDH 1- Normal saline: cc  If necessary :  UF Rate &/or  Qb  Nifedipine SL: 10mg (  intracellular Ca2+) in hemodynamically stable pts.  Forced stretching (massage ?)

56 Muscle Cramps Prevention 1- Minimizing inter-dialytic weight gain  avoid plasma volume contraction & hypo-Osm. that occurs with high UF, required to achieve the pts.´s dry weight during a brief HD session. (Dietary counseling &/or Enalapril 5mg bid). 2- Prevention of IDH  IDH may precede or accompany cramps. 3- Higher dialysate Na+ 4- Use HCO3-buffered dialysate.

57 Muscle Cramps Prevention 5- The use of Na+gradient dialysis  start with 145 to 155 mEq/L and program a linear decrease (  ) to 135 to 140 mEq/L. 6- Carnitine supplementation  20 mg/kg/IV/HD session or 330 mg bid-tid/PO 7- Vit E: 400 IU qhs 8- Quinine sulfate, effective in preventing cramps (  motor end-plate excitability)  250 to 325 mg x 1 or 2/ prior the HDx session (  by FDA: thrombocytopenia).

58 Muscle Cramps Prevention 9- Stretching exercises performed during HD 10- Medications of variable efficacy: a- BDZ  Oxazepam: 10 mg proir to HDx session b- Phenytoin c- Carbamazepine d- Amitryptiline e- Prazosin f- Gabapentin

59 Muscle Cramp Etiology: one or more of the following 1- Plasma volume contraction 2- Hyponatremia 3- Tissue hypoxemia 4- Hypomagnesemia 5- Carnitine deficiency

60 Nausea & Vomiting Up to 10% of routine HDx Multifactorial Most related to hypotension Can be an early manifestation of DDS Related to dialyzer reactions ( type A & B ) Gastroparesis in DM & non-DM ( exacerbated by HDx ) Contaminated or incorrectly formulated Dx solution ( high Na & Ca ) Dx pts develop nausea & vomiting more readily than other pts ( with URTI, narcotics, hypercalcemia )

61 Nausea & Vomiting Management 1- Treat any associated hypotension...a- Reduce UF rate...b- Reduce Qb (only if acetate solution) 2- Anti-emetic (if nausea persist) Prevention 1- Avoidance of IDH is of prime importance 2- Reduction of the Qb by 30% during the initial hour (the time must then be lenghtened) 3- Metoclopramide 5-10 mg pre-Dx

62 Headache Headache is a common symptom during dialysis & occur in  60% of HD pts. The etiology is largely unknown: 1-May be a sublte manifestation of DDS 2-May be related to the use of acetate dialysate. 3-May be a manifestation of caffein withdrawal 4-Due to metabolic disturbances:....a-Hypoglycemia b- Dysnatremia 5-Uremia 6-Sub-dural hematoma

63 Headache Management Analgesic can be given during dialysis: Acetaminophen (650 mg PO) Prevention 1- Reduction in the Qb during eraly part of the dialysis treatment 2- Use of HCO3 dialysate 3- Caffein ingestion during dialysis 4- Mg supplementation (risk of giving Mg !).

64 Dialysis Disequilibrum Dialysis disequilibrum syndrome (DDS) consists of a variety of neurologic symptoms, all of which appear to be secondary to cerebral edema. DDS usually occurs toward the end of dialysis and may be delayed up to 24 hours. DDS is usually self-limited, but full recovery may take several days. DDS remains a clinical diagnosis since lab.tests, including EEG, are nonspecific.

65 Dialysis Disequilibrum Symptoms of DDS Mild Symptoms Severe Symptoms Headache Delirium Blurred vision Drowsiness Naus./Vomit./Anorexia Confusion Hypertension Arrhythmias Muscle cramps Seizure Agitation / Restlessness Coma Tremor Dizziness

66 Dialysis Disequilibrum Etiology  The precise mechanism of DDS is undefined, but it may arise because of.. ”Acute Increase in Brain Water Content” (Brain edema confirmed by CT scan &  CSF pressure) 1- Reverse urea effect  Transient osmotic disequilibrum due to more rapid removal of urea from blood than from CSF.

67 Water movement during standard hemodialysis Water movement Intracellular fluidExtracellular fluid Dialyzer Osmolality 320 mosm/kg Osmolality 320 mosm/kg Loss of urea and water step1 step2 step3 280 Osmolality Falling as diffusion occurs

68 Convection : Réduction de la surcharge hydrosodée Diffusion : Réduction du volume plasmatique avec hypotension Œdème cellulaire (cérébral) Eau Solutés Eau Dialysâ t Rapid Solute Removal “Disequilibrum”

69 Dialysis Disequilibrum Etiology  The precise mechanism of DDS is undefined, but it may arise because of.. ”Acute Increase in Brain Water Content” (Brain edema confirmed by CT scan &  CSF pressure) 1- Reverse urea effect  Transient osmotic disequilibrum due to more rapid removal of urea from blood than from CSF. 2- Paradoxic CSF acidosis.   brain H+ ion   brain cell osmolytes

70 Dialysis Disequilibrum Risk Factors for Development of DDS 1- Extremes of age ( pediatric > elderly ) 2- Initial hemodialysis ( new pts !) (AKI & pts.with ESRD initiating HDx) 3- Pre-existing neurologic conditions ( Hx of seizure ) 4- Conditions with cerebral edema (Malignant HTN,  Na+, Hepatic encephalopathy, severe metabolic acidosis) 5- Severe azotemia: BUN >175 ( esp.with short HDx time ) 6- High-efficiency dialysis (large surface area & high-flux dialyzers)

71 Dialysis Disequilibrum Management A-Mild Disequilibrum 1- Treatment is symptomatic 2- If mild symptoms of DDS develop in an acutely uremic patient   Qb & termination of HDx 3- Hypertonic saline or Glucose solution (as for cramps) B-Severe Disequilibrum 1- Dialysis should be stopped +  in dialysate osmolality (5cc of 23.5%saline) or mannitol (12.5 gr.) 2- Specific treatment of seizure, coma 3- Consider the DDx. of severe disequilibrum syndrome.

72 Dialysis Disequilibrum Prevention 1- Identify high-risk patient. 2- Perform ”slow ” HDx. Ex: Daily dialysis for 3 to 4 days with gradual increase in dialysis time (2h.to 4h.) & blood flow (BFR  cc/min up to cc/min). 3- Increase dialysate Na+ concentration 4- Extremely high risk pts.for seizure.  Continuous infusion of mannitol during HD or prophylactic use of anti-convulsants (?) Ex: 1000 mg. Phenytoin before HDx & 300 mg./day for 2 to 3 days.or Mannitol 12.5 gr./hr. IV during HD session. Festina Lente

73 Water movement during standard hemodialysis Water movement Intracellular fluidExtracellular fluid Dialyzer Osmolality 320 mosm/kg Osmolality 320 mosm/kg Loss of urea and water step1 step2 step3 280 Osmolality Falling as diffusion occurs Compensatory refilling

74 Arrhythmias Ventricular arrhythmias: 5 to 75 % Risk factors for arrhythmias and sudden death in dialysis pts. include: a- coronary artery disease b- advanced age c- myocardial dysfunction d- LVH e- pts receiving digitalis f- changes in plasma K+

75

76 Background Fluid removal during hemodialysis ▫Goal 1: Achieving dry weight  With fluid overload, can develop:  Hypertension, cardiovascular disease, pulmonary edema ▫LVH common in pediatric dialysis patients ▫HTN and volume overload contribute to LVH ▫Goal 2: Preventing intradialytic morbidity  Hypotension, N/V, cramping, headache

77 Fluid removal in hemodialysis A large volume is removed in a short period of time Intracellular space Interstitia l space Plasma space

78 Fluid removal in hemodialysis Fluid from the interstitial space refills the plasma space as fluid is removed during HD Intracellular space Interstitia l space Plasma space

79 Fluid removal in hemodialysis Problems: ▫Achieving the 2 goals of ultrafiltration are counterproductive to each other  Removing a large amount of fluid to achieve dry weight leads to symptoms  Reducing fluid removal to prevent signs and symptoms can lead to fluid overload ▫Dry weight can be difficult to determine clinically

80 Fluid removal in hemodialysis The ideal HD treatment will: ▫Remove enough fluid to achieve the true dry weight ▫Avoid adverse intradialytic events Options to achieve this ideal ▫Daily HD ▫Prolonged treatments ▫Continuous blood volume monitoring?

81 Principles of CRIT-LINE Continuously monitors the hematocrit (Hct) during the HD treatment Change in Hct during HD reflects the change in blood volume as the treatment proceeds

82 Principles of CRIT-LINE Hct= RBC volume Blood Blood volume Hct = RBC volume Blood volume BV Plasma volume RBC volume

83 Principles of CRIT-LINE With hemodialysis: ▫RBC volume stays constant ▫Plasma volume decreases ▫BV decreases ▫Hct increases Change in Hct directly reflects change in BV Hemodialysis

84 Importance of dialysis frequency higher than thrice weekly Sudden and cardiac death highest on Monday and Tuesday in HD but not in CAPD ▫Bleyer AJ; Russell GB; Satko SG. Kidney Int 1999; 55:1553 QOD, 4, 5, 6, and 7 times weekly HD decrease fluctuations in pre and post dialysis fluid volumes and solute concentrations ▫Decrease interdialytic and intradialytic symptoms  IDH, cramps, and postdialysis hangover ▫Improve mental health, energy, social functioning, physical activity, vitality, blood pressure control with decreased use of antihypertensive drugs, and hematocrit with decreased use of erythropoietin

85 Reasons that patients do better on quotidian HD with the same overall weekly dialysis duration Alleviation of hemodialysis “unphysiology” ▫Kjellstrand CM, et al. The "unphysiology" of dialysis: A major cause of dialysis side effects? Kidney Int 1975; 7: S30 ‑ S34. Less swings in concentrations of all solutes (lower time average deviation)  Urea, creatinine, uric acid, etc. Maintenance of concentrations within normal limits  Potassium, phosphorus, calcium, pH, bicarbonate Less swings in hydration/ECV  Lower interdialytic weight gains  Elimination of hypervolemia/hypovolemia

86 NO NORMAL RANGE OF ECV, K, Bicarb, P, Ca, pH Weekly fluctuations in routine hemodialysis

87 NORMAL RANGE OF ECV, K, Bicarb, P, Ca, pH Weekly fluctuations in daily hemodialysis

88 Call for change of paradigm Kt/V should be abandoned as the most important measure of dialysis quality Clinical symptoms and signs should be accepted instead Blood flow should range from 200 to 300 ml/min High performance dialyzers should continue to be used

89 Call for change of paradigm Time and frequency of dialysis must be adjusted to residual urine output and tolerance of ultrafiltration. Ultrafiltration rate should range from 0.5%-1.5% of body weight/hr Dialysis frequency and duration should permit the achievement of blood pressure control without antihypertensive medications in 90%-95% of patients Anuric patients should not have dialysis shorter than five hours in thrice weekly schedule. More frequent dialysis is preferred in anuric patients, but weekly dialysis time should not drop below 15 hrs

90 Festina lente [hasten slowly (deliberately)] Motto of Gaius Julius Caesar Octavian Augustus (63BC - 14AD) The first and greatest Emperor (27BC - 14AD) This Latin motto should be written on a wall of every hemodialysis room

91 EXCESS FLUID WEIGHT Body weight at which composition of body fluid compartments is normal. At higher weights there is expansion of compartments At lower weights there is depletion of compartments. Both these states have adverse clincal consequences. CONCEPT of DRY WEIGHT DRY WEIGHT

92 “The lowest [post-dialysis] weight a patient can tolerate without intradialytic symptoms and/or hypotension and in the absence of overt fluid overload” Henderson KI 17: ; 1980 Dry weight “ The post-dialysis weight at which the patient is and remains normotensive until the next dialysis in spite of interdialytic fluid retention and without antihypertensive medication” Charra 1996

93 2 Intra- cellular Space Extra- cellular Space Intra- Vascular Space Circulating Blood Volume Toxins Fluid Toxins Fluid Toxins Fluid Dialyzer Three Compartment Model Fluid Shifts 23 Liters 17 Liters 5 Liters


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