Author Topic: Questions Part 46 (part b)  (Read 2189 times)

admin

  • Full Member
  • ***
  • Posts: 127
Questions Part 46 (part b)
« on: August 30, 2009, 12:42:30 PM »
patientwife



Joined: 18 Jul 2003
Posts: 47

   
PostPosted: 27 Jul 2003 21:40    Post subject: IV Iron    

Thank you for your helpful responses.<
><
>Clarification: The nephrologist did not put my husband on oral iron; he agreed to the trial that my husband requested.<
><
>One last question: How would the unit have known (between monthly labs) that oral iron was not working?

******************************************************       
Founding RN



Joined: 10 Jan 2003
Posts: 172

   
PostPosted: 27 Jul 2003 22:36    Post subject: Patientwife    

The labs would have shown an increase if it was working. When IV Iron is given, and the series is done, there is a significant increase in the lab value, oral Iron, if not working, would not show much if any increase. <
><
>If there is not enough Iron in the blood stream, EPO would be increased and the hct, or hgb, would show little increase. You can increase the EPO significantly and if there is not enough Iron, it just can't do the job needed. EPO depends on adequate iron stores in the blood to work at it's maximum efficiency.

******************************************************        
patientwife



Joined: 18 Jul 2003
Posts: 47

   
PostPosted: 31 Jul 2003 13:45    Post subject: Bicarbonate    

<
> How are low bicarbonate levels corrected?<
>What should be asked of physician/dialysis nurse?<
><
>My husband began tx at current unit in Nov 2002 with bicarbonate level in normal range, i.e., 23. (Ref range = 22-29). Each month thereafter, level has decreased. Average for past 6 months = 13.

******************************************************        
Founding RN



Joined: 10 Jan 2003
Posts: 172

   
PostPosted: 31 Jul 2003 14:03    Post subject: Patientwife    

Bicarbonate regulation is done by the kidneys and respitratory systems. What you are seeing is the result of his renal failure. Dialysis can only do so much and this is dependent on the techs or person responsible to mix up the bicarbonate portion of the dialysis solution correctly so that the pH and conductivity balance is correct for the machine. The pH of the mixture should be checked after the bicarbonate solution is mixed up and should be close to 7.0 this is usually done with a "Phoenix" meter. The machines are pre set so that if the conductivity of the mixture falls below a certain point, the machines should alarm. This is known as the conductivity and that should range between 13.5- 14.5. This can go higher if sodium modeling is used but the base sodium should be set at 140 and the sodium modeling should be shut off the last 15-30 min of the run.<
><
>The other thing he can do is exercise. Doing mild to moderate exercises that increase your
eathing so that you fill your lungs up completely, will help some. Please consult your Dr. if you feel you need specifics that pertain to your individual case. I can only give you the general mix of things.

******************************************************    
my angel got her wings



Joined: 07 Jul 2003
Posts: 12

   
PostPosted: 31 Jul 2003 15:10    Post subject: dds (dialysis disequalibrium syndrome)    

if u have a patient who is constantly experiencing headaches mainly when on hemo an ahour after starting,,,and u also notice wieght loss (major) and the fact that the patient is always very sick for the entire day after as well as total loss of appetite,,,,do u just for go it and say it is in their head or do u try to find a way to help them...y is it doctors seem to think they know so much just because they have a degree,,,and ur just the patient or the patients mother?????

******************************************************
my angel got her wings



Joined: 07 Jul 2003
Posts: 12

   
PostPosted: 31 Jul 2003 15:13    Post subject: high pulse    

my question to u is r u felling really sick during and or after ur sessions. do get headaches loss of appetite,,

******************************************************
   
my angel got her wings



Joined: 07 Jul 2003
Posts: 12

   
PostPosted: 31 Jul 2003 15:21    Post subject: dds    

First described in 1962, the dialysis disequili
ium syndrome (DDS) is a central nervous system disorder that remains an important clinical problem in dialysis patients. It is characterized by neurologic symptoms of varying severity that are thought to be due primarily to cere
al edema. New patients just being started on hemodialysis are at greatest risk, particularly if the BUN is markedly elevated (above 175 mg/dL or 60 mmol/L). Other predisposing factors include severe metabolic acidosis, older age, pediatric patients, and the presence of other central nervous system disease such as a preexisting seizure disorder.<
><
> CLINICAL MANIFESTATIONS  The classic DDS refers to acute symptoms developing during or immediately after hemodialysis. Early findings include headache, nausea, disorientation, restlessness, blurred vision, and asterixis. More severely affected patients progress to confusion, seizures, coma, and even death. It is now recognized, however, that many milder signs and symptoms associated with dialysis  such as muscle cramps, anorexia, and dizziness developing near the end of a dialysis treatment  are also part of this syndrome. The incidence of DDS varies according to the patient population and the attention paid to the preventive measures described below. Severe DDS is now rare in adults because of the standard use of the preventive recommendations made below. However, children may remain at increased risk. A retrospective analysis of 180 children and adolescents on maintenance dialysis foundthat 13 (7 percent) had dialysis-associated seizures. All but one of these patients were treated with hemodialysis. The development of the above symptoms during dialysis is strongly suggestive of DDS. Nevertheless, there are a number of other disorders that must be excluded including uremia itself, subdural hematoma, metabolic disturbances (hyponatremia, hypoglycemia), and drug-induced encephalopathy. Drug accumulation is a particular problem in renal failure with drugs that are normally excreted by the kidney.<
>PATHOGENESIS  The symptoms of DDS are caused by water movement into the
ain, leading to cere
al edema. Two theories have been proposed to explain why this occurs: a reverse osmotic shift induced by urea ; and a fall in cere
al intracellular pH. Hemodialysis rapidly removes small solutes such as urea, particularly in patients who have marked azotemia. The reduction in BUN lowers the plasma osmolality, thereby creating a transient osmotic gradient that promotes water movement into the cells. In the
ain, this water shift produces cere
al edema and a variable degree of acute neurologic dysfunction. The loss of extracellular water can also cause extracellular volume depletion which can contribute to the development of hypotension. The pathogenetic importance of urea in the DDS has been demonstrated by experiments in uremic rats. In one report, for example, rapid dialysis lowered the BUN from 200 to 95 mg/dL (72 to 34 mmol/L) in 90 minutes . This change was associated with a six percent increase in
ain water. Neither undialyzed rats nor those rats dialyzed against a bath to which urea was added to prevent a fall in BUN developed cere
al edema. Furthermore, the retention of
ain urea appears to be account for most of the increase in
ain water. Urea is generally considered an "ineffective" osmole, because of its ability to permeate cell mem
anes. However, this effect may take several hours to reach completion. Thus, there is insufficient time for urea equili
ation when hemodialysis rapidly reduces the BUN; as a result, urea transiently acts as an effective osmole, promoting water movement into the
ain. In the above experiments, for example, the 53 percent acute reduction in BUN was only associated with a 13 percent reduction in
ain urea nitrogen. Intracere
al acidosis  Some investigators have suggested that the reverse urea effect cannot account for the development of cere
al edema in the DDS, since urea movement out of the
ain is sufficiently rapid to prevent a large osmotic gradient between the
ain and extracellular fluid . They have proposed that a decrease in cere
al intracellular pH, occurring via an uncertain mechanism, is of primary importance. Both displacement of bound sodium and potassium by the excess hydrogen ions and enhanced production of organic acids can increase intracellular osmolality and promote water movement into the
ain. However, an increase in
ain organic osmolytes has not been confirmed in all studies. In most reports, the reverse urea effect appears sufficient to explain most of dialysis disequili
ium.<
>TREATMENT  Prevention is the mainstay of therapy in the DDS, particularly in new dialysis patients who are at highest risk. The initial dialyses should be gentle, but repeated frequently. The aim is a gradual reduction in BUN, which will be protective but may not prevent
 mild
 symptoms such as headache and malaise. Slow urea removal can be achieved by one of the following methods: With hemodialysis, therapy can be initiated with two hours of dialysis at a relatively low blood flow rate of 150 to 250 mL/min with a small surface area dialyzer. This regimen, which is repeated daily for three or four days, is different from the standard every other day four-hour regimen at high flow rates. If the patient shows no signs of DDS, the blood flow rate can be increased by 50 mL/min per treatment (up to 300 to 400 mL/min) and the duration of dialysis can be increased in 30 minute increments (up to four or more hours, as necessary for adequate solute removal). Patients who also have marked fluid overload can be treated with ultrafiltration (which removes less urea per unit time) followed by a short period of hemodialysis. The patient can be started on peritoneal dialysis in which the low rate of peritoneal blood flow results in a urea clearance per unit time that is much lower than that with hemodialysis. The DDS has not been reported with continuous peritoneal dialysis. Some physicians recommend prophylactic phenytoin (1000 mg loading dose followed by 300 mg/day until uremia is controlled) and/or the administration of 12.5 g of hypertonic mannitol intravenously every hour of dialysis in high-risk patients with marked azotemia (BUN above 150 to 200 mg/dL [54 to 71 mmol/L]) or an underlying alteration in mental status. Symptoms of DDS are self-limited and usually dissipate within several hours. Severe DDS with seizures can be reversed more rapidly by raising the plasma osmolality with either 5 mL of 23 percent saline or 12.5 g of hypertonic mannitol. <
>hope this helps some<
>

******************************************************    
Founding RN



Joined: 10 Jan 2003
Posts: 172

   
PostPosted: 31 Jul 2003 15:57    Post subject: My Angel got her Wings    Reply with quote Edit/Delete this post Delete this post View IP address of poster
This does happen and the key is to start a new patient out on dialysis slowly using a slower blood flow rate and maybe shorter runs. <
><
>My expereince has been that we start with a 2 hour run and a blood flow rate of 150-200 run the patient for 3 days in a row. This gets them used to dialysis, starts them getting used to having the waste products and excess fluid removed from their bodies. Usually no fluid is removed the first day, then each succeding day, fluid is removed slowly, as needed per individual.<
><
>Headaches at this time are fairly normal and most Dr's will order a medication called Mannitol to be given during the 1st and 3rd hours on to help with the fluid shift from the
ain into the vascular system. Mannitol is usually only needed during these first 3 runs. Some patients do expereince severe headaches and a through work up should be done to uncover the underlying reasons for this. Education in diet, fluid restrictions and taking their medication will all help in making this process much easier on the patient. It does take time for some patients to adjust to dialysis.<
><
>The whole picture needs to be looked at when dializing a patient. If a patient is not eating, continues to drink fluids and not watch their diet, then yes, fluid must still be removed otherwise the patient could end up with Congestive Heart Failure. This could lead to permenet damage to the heart. If a pateint is having headaches, has lots of fluid on, yes, you have to weigh the immediate needs and getting that fluid off and cleaning the waste products out are major needs. The Dr's need to be told of the headaches and medication and a work up for them should be done.<
><
>Remember, your kidneys worked 24 hours a day, 7 days a week. If you are dializing only 4 hours, 3 times a week, that doesn't come close to what your kidneys did for you and waste products and fluid do build up fast in the body. <
><
>The above is based on my experience only, it can and does vary for other people. <
><
>
"Like me, you could.....be unfortunate enough to stumble upon a silent war. The trouble is that once you see it, you can't unsee it. And once you've seen it, keeping quiet, saying nothing,becomes as political an act as speaking out. Either way, you're accountable."

Arundhati Roy