Hemodialysis hypotension

Flynn JJ III, Mitchell MC, Caruso FS, McElligott MA. Midodrine treatment for patients with hemodialysis hypotension. Clin Nephrol 1996 45 261-267. 

Yalcin AU, Sahin G, Frol M, Bal C. Sertraline hydrochloride treatment for patients with hemodialysis hypotension. Blood Purif 2002 20 150-153. 

With either type of dialysis, studies suggest that recovery of renal function is decreased in ARF patients who undergo dialysis compared with those not requiring dialysis. Decreased recovery of renal function may be due to hemodialysis-induced hypotension causing additional ischemic injury to the kidney. Also, exposure of a patient s blood to bioincompatible dialysis membranes (cuprophane or cellulose acetate) results in complement and leukocyte activation which can lead to neutrophil infiltration into the kidney and release of vasoconstrictive substances that can prolong renal dysfunction.26 Synthetic membranes composed of substances such as polysulfone, polyacrylonitrile, and polymethylmethacrylate are considered to be more biocompatible and would be less likely to activate complement. Synthetic membranes are generally more expensive than cellulose-based membranes. Several recent meta-analyses found no difference in mortality between biocompatible and bioincompatible membranes. Whether biocompatible membranes lead to better patient outcomes continues to be debated. 

Dysequilibrium, dialysis, hypotension, and muscle cramps are common. May require months before patient adjusts to hemodialysis. 

Hypotension is the most common complication seen during hemodialysis. It has been reported to occur with approximately 10% to 30% of dialysis sessions, but maybe as frequent as 50% of sessions in some patients.46... 

Pathophysiology Hypotension associated with hemodialysis manifests as a symptomatic sudden drop of more than 30 mm Hg in mean arterial or systolic pressure or a systolic pressure drop to less than 90 mm Hg during the dialysis session. The primary cause is fluid removal from the bloodstream. Ultrafiltration removes fluid from the plasma, which... 

Pathophysiology Muscle cramps can occur with up to 20% of dialysis sessions.48 The cause is often related to excessive ultrafiltration, which causes hypoperfusion of the muscles. Other contributing factors to the development of muscle cramps include hypotension and electrolyte and acid-base imbalances that occur during hemodialysis sessions. 

Evaluate the patient for complications associated with dialysis. Does the patient develop hypotension or cramps during hemodialysis Does the patient have symptoms consistent with peritonitis or a catheter infection ... 

Intermittent RRT (e.g., hemodialysis) has the advantage of widespread availability and the convenience of lasting only 3 to 4 hours. Disadvantages include difficult venous dialysis access in hypotensive patients and hypotension due to rapid removal of large amounts of fluid. 

Infusion Iron sucrose may be also administered by infusion (into the dialysis line for hemodialysis patients). This may reduce the risk of hypotensive episodes. The content of each vial must be diluted exclusively in a maximum of 100 ml of 0.9% NaCI, immediately prior to infusion. Infuse the solution at a rate of 100 mg of iron over a period of 15 minutes or more. Discard unused diluted solution. 

General supportive care should be provided. Aggressive gut decontamination should be carried out using repeated doses of activated charcoal and whole bowel irrigation. Propranolol or other blockers (eg, esmolol) are useful antidotes for B-mediated hypotension and tachycardia. Phenobarbital is preferred over phenytoin for convulsions most anticonvulsants are ineffective. Hemodialysis is indicated for serum concentrations greater than 100 mg/L and for intractable seizures in patients with lower levels. 

A 42-year-old man developed nausea and vomiting and felt suicidal. He had type 2 diabetes and was taking metformin (56). His blood lactate concentration was 8.9 mmol/1, bicarbonate 16 mmol/1, and pH 7.2. Severe hypotension required intensive care. The lactate concentration rose to 22 mmol/1 and the bicarbonate fell to 6.7 mmol/1 and the pH to 6.89. The metformin concentration was high at 191 mg/1. He survived, having been treated with intermittent hemodialysis. 

Five patients with metformin-associated severe lactic acidosis, seen between 1 September 1998 and 31 May 2001, have been reported (58). Two had attempted suicide. All had severe metabolic acidosis with a high anion gap and raised blood lactate concentrations. Four developed profound hypotension and three had acute respiratory failure. Three had normal preceding renal function. Three required conventional hemodialysis and two continuous renal replacement therapy. 

For example, DFO treatment has been used to facilitate the removal of aluminum from bone and its entry into the blood where it can be removed by hemodialysis (Haddad and Winchester 1990). DFO is also used in dialyzed uremic patients for the treatment of neurological, hematopoietic, and skeletal toxicity. It should be noted that the clinical usefulness of DFO is limited by a variety of toxic effects including hypotension, skin rashes, stimulation of fungal growth, and possibly cataract formation. 

In patients undergoing chronic hemodialysis, the safety profile did not differ from that reported in other populations, except for some rare cases of hypotension during hemodialysis. Hemodialysis does not affect the kinetics of candesartan. Because of the variability of oral clearance and the pronounced influence of hemodialysis-induced volume contraction on the hemodynamic effects of candesartan, careful monitoring is recommended (2). 

Losartan was evaluated in 406 patients with end-stage renal insufficiency undergoing hemodialysis (24). Only 15 patients discontinued losartan because of adverse effects. In seven the adverse reaction was hypotension. Two patients reported a possible anaphylactoid reaction on treatment with AN69 dialysis membranes. However, nine patients with a history of previous anaphylactoid reactions on treatment with AN69 have not shown this complication with losartan and AN69. 

Midodrine has been extensively tested in several of the orthostatic hypotension sjmdromes, including neurogenic hjrpertension due to autonomic neuropathies (2,3) neu-rocardiogenic syncope (4-8) the controversial syndrome of orthostatic hypotension and tachycardia that may be associated with chronic fatigue (9,10) the hypotension seen during hemodialysis (11) and hypotension due to neuroleptic drugs (12). 

A 67-year-old woman took about 7 g of procainamide and developed nausea, vomiting, lethargy, a junctional tachycardia, hypotension, and oliguria (61). She was treated with hemodialysis. 

The utility of continuous renal replacement therapies (CRRT) such as continuous venous-venous hemodialysis (CWHD) in the treatment of poisoning is uncertain. As CRRT provides slower clearance than conventional hemodialysis it may not be appropriate for drug removal in acute intoxications [25]. However, the lower blood flow rates and longer treatment times of continuous modalities may be desirable for vulnerable, hemodynamically unstable, patients who are not candidates for conventional hemodialysis [7]. Unlike hemodialysis, CRRT can give effective clearances in hypotensive patients. If the clinical condition of the patient requires a low intensity treatment that will necessarily decrease diffusive clearance, slow extended dialysis (SLED) or continuous treatment times with additional convective clearance (CVVHF and CVVHDF) can likely provide adequate total drug clearance [24]. 

In their series of 32 patients Neto et al [13] showed that seven patients died after intoxication episodes. The main characteristics of the patients who died were convulsive activities in 6 and severe mental confusion in all 7 patients, while 2 of them presented hemodynamic instability (hypotension and shock). Most of the patients who died were treated by peritoneal dialysis or did not receive any other kind of treatment. The other 25 patients improved without sequelae and they were treated either by conventional hemodialysis, daily hemodialysis (6 to 8 hours duration) or even by continuous methods of dialysis. A few patients were treated by peritoneal dialysis. Complete recovery time in these 25 patients ranged from 1 to 12 days (mean 4.4 days and median 4.0 days). 

Individuals overexposed to isopropanol should be removed from exposure, affected areas of the skin should be washed with soap and water, and the eyes should be irrigated with water. Isopropanol is rapidly absorbed from the gastrointestinal tract. Efforts to decrease absorption are unlikely to be beneficial. Severe isopropanol overdoses have been managed successfully with either peritoneal dialysis or hemodialysis. Since the vast majority of patients respond completely with only supportive therapy, dialysis (hemodialysis much more effective than peritoneal) should be instituted in those patients with a history and physical exam consistent with a very large ingestion (blood isopropyl alcohol >400 mg dl ), those patients with hemodynamic instability (hypotension) and coma. 

The basis of clinical management is supportive care. The airway should be secured and protected as needed. Symptomatic patients should have intravenous access and cardiac monitoring. Accidental ingestions exceeding 500-800 mg, and all intentional overdoses, should be treated with oral activated charcoal if patients present within 60 min of exposure. Seizures should be treated with benzodiazepines, or phenobarbital if refractory. Hypotension should be treated with intravenous fluids and vasopressors (dopamine or norepinephrine) if needed. Hemodialysis or hemoper-fusion may enhance elimination of both the parent compound and metabolites, but the clinical value of... 

Hypotension not responsive to intravenous fluids should be managed with vasopressors, such as dopamine, norepinephrine, epinephrine, and/or phenylephrine. If seizures occur, benzodiazepines should be administered. Due to their pharmacokinetic characteristics, moderate volume of distribution, and low protein binding, procainamide and NAPA may be removed via hemodialysis and hemoperfu-sion. Both procainamide and NAPA serum concentrations should be obtained. Normal therapeutic ranges are procainamide, 3-14pgml NAPA, 12-35 pg ml Measurement of electrolytes, renal function tests, and arterial blood gases should be considered. 

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