Complications During Hemodialysis

Complications During Hemodialysis

Complications During Hemodialysis A. A. Nassiri, M.D., D.I.U. SBUMS 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 Intra-Dyalytic Hypotension 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. Intra-Dialytic Hypotension

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

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: 1- Cardiac mechanisms 2- Plasma Refilling 3- Vascular changes 4- Passive Venoconstriction Intra-Dialytic Hypotension Systemic Blood Pressure Cardiac Output

Peripheral Vascular Resistance Heart Rate Stroke Volume Plasma Volume Myocardial Contractility Cardiac Compensatory Mechanisms Plasma Refilling Intracellula r Space

Extracellular Space Circulating Blood Volume Toxins Toxins Flui d Flui d Di

aly zer Intra 2 Vascular Space Toxins Flui d 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) 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) 5Autonomic neuropathy (e.g., diabetic) 6- Anti-hypertensive medications 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 -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 . . . . . . .. .. 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%) 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. 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 O2 Intra-Dialytic Hypotension Prevention: Dialysate temperature modeling

Dialysate calcium modeling Dialysate sodium modeling Midodrine Carnitine Sertraline Dialysate Temperature Modeling 362 358 371 375


+ 10% +0% Dialysat 35, n=55 Dialysat 37, n=49 -10% - 20% H0 15 mn 30 mn mn

60 mn 120mn Aprs le dbut de la sance d'hmodialyse 180 Dialysate Sodium Modeling H2O Gradient osmotique Secteur intracellulaire

H2O Renouvellement du volume plasmatique (loi de Starling) Na+ Na+ Na+ Na+ Na+ Na+ [Na+]

Secteur interstitiel [Na+] Secteur plasmatique Na+ Dialysat haute Na+ Na+ Na+

Mouvements diffusifs dans la membrane concentration en sodium 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. 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 1 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 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. 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. 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 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).

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 (ATPdependent). 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 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%): 50-100cc (may accumulate in Dx pts.)

If concomitant with IDH 1- Normal saline: 100-500cc If necessary : UF Rate &/or Qb Nifedipine SL: 10mg (intracellular Ca2+) in hemodynamically stable pts. Forced stretching (massage ?) Muscle Cramps Prevention 1- Minimizing inter-dialytic weight gain avoid plasma volume contraction & hypoOsm. 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. 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 bidtid/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). 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 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) 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 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 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 !) . 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.

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

Confusion Seizure Coma 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.

Water movement during standard hemodialysis Intracellular fluid Extracellular fluid Water movement Dialyzer step1 280 step3 Osmolality Osmolality 320 320mosm/kg mosm/kg

Osmolality Falling as diffusion occurs step2 Loss of urea and water 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 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) 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. Dialysis Disequilibrum Prevention 1- Identify high-risk patient. 2- Perform slow HDx Festina Lente . Ex: Daily dialysis for 3 to 4 days with gradual increase in dialysis time ( 4h.) & blood flow

(BFR150-200cc/min up to 300400cc/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. 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+

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