Chief Complaint Norma is a 54 ye

Chief Complaint
Norma is a 54 year-old, former ICU nurse, referred from the Clinic for admission due to symptoms of increasing dyspnea, peripheral edema and hypotension.

History of Present Illness

She is well known to the cardiologists from previous evaluations. Norma has a history of hospitalizations that average an admission every 5 months, the latest being at the beginning of June 2003. This hospitalization lasted approximately 5 days with very little fluid removed using IV Lasix®, Natrecor®, and a Primacor® drip.

Previous Medical History
On August 6, 2003, she presented at the Clinic in a similar manner to her admission in June. Prior to this admission, Norma has been taking Lasix® 80 mg b.i.d., Aldactone® 25 mg q.d., K-Dur® 10 mEq b.i.d., Digitek® 0.125 mg q.d., Darvocet®, Zaroxolyn®, Restoril® 30 mg q hs, Altace® 5 mg q.d., Coreg® 6.2 mg b.i.d., in addition to attending the Infusion Clinic twice a week for Primacor® and the recently added, Natrecor® infusions.

Norma has a history of hypertension, diabetes mellitus, coronary artery disease, status-post coronary artery bypass grafting in April 1994 with repeat bypass grafting due to graft occlusion in March 2002. She has a history of ventricular arrhythmia and is status-post automatic implantable cardioverter defibrillator (AICD) implant. She was upgraded to a biventricular pacer with AICD in June 2003.

Case Details
Her worsening condition required her admission to Hospital and her treatment plan was unknown at the time of her admission. She was showing signs of becoming refractory to most medications. In April of 2003, the hospital began evaluating the use of our system for fluid removal. When Norma was admitted, it was clear that she would be a strong candidate for use of the device. A venous catheter was placed for blood withdrawal and an existing peripheral IV catheter was used for infusion.

After spending 2 nights in the hospital and going through two (2) treatments, Norma was discharged from the hospital. With no clinically significant effects to her hemodynamics or blood chemistry, a total of 9.75 liters of fluid was removed. Although this amount only represented a portion of her excess fluid, Norma’s cardiologist believed that by removing this initial bulk of fluid through this system, the kidneys would become more responsive to the medications and diurese the remaining fluid. This theory was confirmed when Norma called the hospital 3 days after the final treatment to report that she did in fact void the remainder of the fluid. Norma is scheduled to resume her visits to the Clinic where she will be evaluated for continued maintenance therapy or for additional system treatments with our unit.

After her our unit treatments, Norma has been responding well to her oral diuretics. In fact, her doses have been cut in half to what they were prior to treatment. She is currently prescribed Lasix® 40 mg b.i.d., Aldactone® 12.5 mg q.d., K-Dur® 10 mEq b.i.d., Digitek® 0.125 mg q.d., Darvocet®, Zaroxolyn®, Restoril® 30 mg q hs, Altace® 5 mg q.d., Coreg® 6.2 mg b.i.d.

Discussion
The nurses reported that our system is quite simple to use. After seeing how effectively the device operates, they are eager to use it to help more patients. More than this, they are impressed by how stable the patient remains on the device, the levels of monitoring it really requires, and the immediate improvements to the patient’s fluid overloaded condition with a reduction of symptoms. Norma would have to agree. As the treatments began, she soon stated that her breathing had improved and she could now lean over, bend her legs, and put her socks and slippers on. Upon admission, she was unable to lift or bend her legs to get into the car without assistance. Norma summed up her feelings in the following quote:

“As a former ICU nurse, I have taken care of patients in the same condition that I am now. I never dreamed I would be the patient. After one treatment, my abdomen went way down, I was able to bend my legs to sit in a chair, and my breathing became so much better. The difference in how I feel, in such a short period of time, is remarkable.”

- Norma, August 8, 2003

Marion, OH

in a Patient That Suffered a Perioperative Myocardial Infarction with Depressed Ejection Fraction and Pulmonary Edema

Introduction
In the postoperative period, fluid shifts in patients on cardiopulmonary bypass are common. These can often be treated with vigorous diuresis, but when patients have depressed myocardial function or acute injury, diuretic refracturiness may occur as the response to loop diuretics and is related to cardiac output and renal perfusion. This report describes the use of our system in a patient that suffered a perioperative myocardial infarction with depressed ejection fraction and pulmonary edema.

Case Report
A 71-year-old diabetic male presented with unstable angina pectoris and after cardiac catheterization, was found to have left main coronary disease and an associated high-grade anterior descending coronary lesion. The patient underwent three-vessel bypass surgery the day following angiography with saphenous vein graft to the LAD diagonal branch and the obtuse marginal branch, as well as an internal mammary artery bypass to the LAD. At the time of surgery, when the anterior descending artery was opened, thrombus was noted in the artery. The patient was readily weaned from cardiopulmonary bypass; but required significant inotropic support on the first postoperative night. Electrocardiography the morning following surgery showed a new Q wave in V-2, 3 and 4 and troponins were as high as 400. He was extubated the day following surgery. On the evening of the second postoperative day, the patient developed marked tachypnea, decreasing oxygen saturations, and respiratory fatigue. His pulmonary artery diastolic pressure went from 20 to 33 mmHg and required re-intubation. On the fourth postoperative day, the patient was hemodynamically stable and had decreasing oxygen needs on the ventilator. He was awake and alert and responding well to diuresis. On the fifth postoperative day, however, the patient had decreasing urinary responses to diuretics. The PAD was 21 mmHg. The CVP was 16 torr. The BUN had risen to 36 mg% and the creatinine to 1.7 mg% from a baseline 22 mg% and 1.4 mg%. He also had hypochloremic, hypokalemic, metabolic alkalosis related to loop diuretic utilization. Alif -1 Eboo Safe was prescribed at a fluid removal rate of 300 to 500 cc per hour for a period of up to eight (8) hours. A total of 2 liters of free water was removed over 4.4 hours. The patient’s oxygenation improved and he was extubated on the following day.

Comment
Over diuresis occurs commonly, manifested by arteriolar intravascular volume contraction, increased systemic vascular resistance, and decreased renal perfusion particularly in the case of myocardial damage in which the cardiac output may be diminished or fixed. Intravascular volume as measured by the central venous pressure will remain increased. Pulmonary edema will then be refractory. Patients develop problems with electrolyte imbalance, induced arrythmias, particularly atrial fibrillation and enhanced activity of the neurohormonal axis. The use of our system, a form of veno-venous filtration, reduces this fixed preload without impacting hemodynamics or electrolyte concentrations. Pulmonary edema can readily resolve and patients can be more easily removed from mechanical ventilatory support.

Case history courtesy of:

Co-Director of Cardiac Surgery

Minnesota

In A High-Risk, Peri-Operative Setting Following Complex Cardiac Surgery

Chief Complaint
The patient was an 80 year old male who presented with shortness of breath, signs of right heart failure, and ascites.

History of Illness
He had a right heart catheterization and right ventricular biopsy to rule out restrictive cardiomyopathy and infiltrative diseases of the heart. He had equalization of pressures suggestive of pericardial constriction. The patient had been on high dose diuretics and had multiple abdominal paracenteses for drainage of ascitic fluid.

Peri-operative Details
He underwent a limited incision exploration of the pericardium because of the presence of a loculated pericardial effusion on echocardiography. This was then converted to a complete median sternotomy. There were dense pericardial adhesions and a radical stripping of the pericardial was performed from phrenic nerve to phrenic nerve. The posterior aspects of the myocardium were freed up to the inferior pulmonary veins. He did well immediately post-operatively, but had a low urine output despite a good cardiac output. Despite adequate blood pressure and cardiac output, he developed oliguria and his creatinine started to rise. He was extubated and was oxygenating well.

After the first 20 hours post-op, we ultrafiltered him with the system. We were able to take between 50 and 120 mL of fluid off every hour for 36 hours in the cardiac surgery ICU with a dramatic improvement in urinary output. His creatinine fell to baseline and he was discharged to the ward on the 4th post-operative day. He was then discharged home within a week after surgery.

Discussion
Peri-operative fluid overload is common in cardiac surgery patients. Many of them have been on diuretics for months if not years prior to seeking medical attention and surgical intervention. Post-operative renal failure carries a high mortality in cardiac surgery patients.

This patient illustrates the efficacy of ultrafiltration in actually promoting urine output and allowing incipient renal failure to actually regress. The mechanism of this might be debatable, but the presence of tissue edema and higher right sided filling pressures predispose to end-organ dysfunction in our experience. Our aggressive stance with our system in this setting has helped rescue many a patient and their kidneys!

Case history courtesy of:

Associate Professor of Surgery, Director of Research

Illinois

Managing Late Post-Operative Fluid Retention Following Cardiac Surgery Using our system

Introduction
Following open heart surgery, particularly in patients with valvular heart disease and those with pre-operative congestive heart failure, late volume shifts may occur. Whether related to inadequate diuretic administration, dietary indiscretion, or medication interaction; following discharge, patients may present emergently with peripheral and/or pulmonary edema. The removal of free water is required and diuretic therapy alone may not suffice.

Case History
A 62-year-old female with mitral and tricuspid insufficiency, who had an enlarging left ventricular chamber and decreasing ejection fraction, was referred for surgery. Post-cath, she developed contrast induced nephropathy (Creatinine reaching 2.7 mg%). She was admitted with pulmonary hypertension and fulminant congestive heart failure. Surgical repair was accomplished with a P-2 quadrangular mitral leaflet resection, placement of a #28 Taylor ring, a DeVega tricuspid annuloplasty and closure of a patent foramen ovale.

In the immediate postoperative period, the patient was treated with diuretics and had mild bilateral pleural effusions. Her postoperative course was otherwise uncomplicated, and she was discharged on diuretics (Bumex® 2mg PO bid) with her weight declining. Seventy-two (72) hours following discharge, the patient re-presented with an eight (8) pound weight gain, shortness of breath, decreased urine output, hyponatremia (Na = 129), pleural effusions and peripheral edema.

A PICC line was placed in the right antecubital fossa and the patient underwent our systems form of filtration. Using our system, she underwent two eight (8) hour runs removing over 7 kg of fluid bringing her to preoperative weight. The medical regimen was adjusted and she was discharged without peripheral edema or shortness of breath. She has required no further hospitalizations.

Comment
This situation represents an example of using the peripheral UF unit to manage late postoperative fluid retention. The patient had congestive heart failure and edema preoperatively, and in the early postoperative period, and acute renal insufficiency, which limited effective diuresis. In spite of being discharged on an adequate medical regimen, there were significant fluid shifts following discharge that resulted in pulmonary and peripheral edema. The response to diuretics was inadequate on readmission, and fluid removal with our system resolved the hyponatremia and edema, did not impact potassium levels, and limited the aggressive use of diuretics resulting in a shortened hospital stay.

Case history courtesy of:

Director of Cardiovascular Surgery

Minnesota

in the Early Post-Operative Period in a Patient Receiving an LVAD as a Bridge to Transplantation

Introduction
Patients with end-stage heart failure secondary to either ischemic or idiopathic cardiomyopathy frequently demonstrate worsening renal function prior to initiating mechanical circulatory support. Extended cardiopulmonary bypass times and large post-operative transfusion requirements contribute to the development of third space fluid retention often seen in this population. Additionally, diuretic response can be extremely variable in the early post-operative period in these patients. This report describes the use of our system in the early post-operative period in a patient receiving an LVAD as a bridge to transplantation.

Patient History
A 61 year old male with ischemic cardiomyopathy listed as status lb on our transplant waiting list presented with decompensated congestive heart failure despite chronic Milrinone infusion. The patient had insertion of a Swan-Ganz catheter and augmentation of his inotropic support with the addition of Dobutamine. Attempts to diurese the patient with loop diuretics initially were effective with some decrease in the patient’s pulmonary artery wedge pressure. However, after 72 hours he became refractory to diuretics and demonstrated continued decompensation with reduced cardiac output and serum sodium levels as well as a rising serum creatinine level.

At this point, the decision was made to implant an LVAD as a bridge to transplantation. The patient had a cardiopulmonary bypass time of 225 minutes. Multiple rounds of platelets and fresh frozen plasma were transfused in the early post-operative period to control bleeding and correct his coagulopathy. On post-operative day number one, the patient was found to be 9 Kg over his preoperative weight. Additionally, he was demonstrating moderate to severe right ventricular dysfunction with central venous pressures running in the range of 20 to 24 mmHg. Diuresis was attempted for 24 hour using a continuous infusion of loop diuretics without significant response.

On postoperative day number two , our system was begun through a subclavian vein central line. Initial volume removal goals were an average of 150 to 200 cc of fluid removal every hour. Treatment lasted approximately 24 hours with nearly 6 liters of fluid removed. The patients’ central venous pressures decreased to 12 to 15 mmHg and inotropic support was able to be weaned. The patient tolerated our system well with stable hemodynamics and LVAD flow rates in the range of 5 to 5.5 liters per minute.

This patient was ultimately successfully transplanted and currently maintains normal renal function.

Discussion
Decompensated congestive heart failure is typically characterized by a constellation of findings including reduced cardiac output, volume overload, decreased systemic perfusion, and worsening renal function. Reduced renal perfusion leads to activation of the Renin-Angiotensin-Aldosterone System (RAAS), which in turn causes salt and water retention, expansion of intravascular volume and exacerbation of CHF.

While, diuretic therapy has been a mainstay in the treatment of end stage congestive heart failure, many patients become resistant to diuretic therapy with prolonged exposure. Additionally, loop diuretics have been shown to decrease glomerular filtration rate in patients with heart failure making adequate fluid removal in the face of decompensation difficult [1].

Patients requiring LVAD placement for bridge to transplantation are characterized by continued hemodynamic deterioration and organ function despite maximal medical therapy [2]. Given time, ventricular support can reverse the end organ ischemic insult seen in these patients. However, in the early post-operative period these patients still have profound RAAS activation in addition to elevated levels of neurohormones that in combination can make diuretic responsiveness unpredictable [3].

We have found that our system to be a safe and effective technique for volume reduction in the early post-operative period in these patients. This technique is well tolerated hemodynamically, and does not appear to affect the performance of the LVAD in regards to cardiac output or stroke volume.

Case history courtesy of:

Cardiothoracic and Transplant surgeon

Texas

for Fluid Volume Overload in Congestive Heart Failure with Renal Insufficiency

Chief Complaint
The patient was a 73 year old male with atrial fibrillation, coronary artery disease with previous inferior MI, preserved left ventricular systolic function, mild pulmonary hypertension, and renal insufficiency who presented to the hospital with complaints of shortness of breath and fatigue while performing activities of daily living.

History of Present Illness
The patient was volume overloaded and had failed outpatient attempts to adequately diurese using oral and IV diuretics, and a short course of nesiritide. At the time of admission, his serum creatinine was 3.1 mg/dl and his BNP level was 1200. His hospitalization was complicated by a new diagnosis of multiple myeloma, and as part of an evaluation for renal dysfunction, a renal ultrasound demonstrated severe right sided and mild left sided hydronephrosis. The patient underwent bilateral ureteral stenting with subsequent significant bleeding from his urinary tract resulting in a hematocrit of 23. Because of increasing resistance to diuretics and worsening heart failure symptoms, a cardiology consult was obtained on hospital day 13.

Case Details
At the time of consultation, his physical examination was remarkable for a chronically ill appearing man who looked older than his stated age. His blood pressure was 100/58, pulse 118 and irregular. Jugular venous pulsations were seen 3 cm above the clavicle with the patient at 90 degrees. Bilateral coarse crackles were heard throughout the lungs. The abdomen was firm and distended. Anasarca was present with 4+ edema from the feet to the lumbosacral area. Pertinent objective data at time of consult included a chest x-ray that showed cardiomegaly, pulmonary vascular congestion and bilateral pleural effusions.

Despite controlling the patient’s heart rate and several days of achieving net negative diuresis with high dose continuous intravenous infusion of lasix and nesiritide, there was little change in the patient’s edema and chest x-ray. Therefore, peripheral veno-venous our system filtration was performed. A 16 gauge, 35 cm peripheral catheter was placed in the basilic vein under fluoroscopic guidance for blood withdrawal and an 18 gauge standard peripheral IV catheter was placed in the opposite arm for blood return. The nursing staff from a telemetry unit, primed the blood circuit, administered a 1600 unit heparin bolus and followed-up with an infusion of heparin at 120 units/hour administered through the access port (pre-filter) of the system’s withdrawal line. filtration therapy removed 4 liters of plasma water over an 8 hour period. Identical treatments were administered on days 17 and 18, removing a total of 12 liters over 3 treatments. Additionally, this controlled and stable fluid removal allowed the patient to receive a blood transfusion without worsening congestion.

On day 18, the patient’s exam was much improved. His lungs were clearer, his edema was markedly improved and his jugular venous pulsations were not seen above the clavicle with the patient at 90 degrees. The serum creatinine was 2.4 mg/dl. His symptoms were much improved. The patient was transitioned to oral diuretics and discharged to home on hospital day 21.

Discussion
Fluid overload can be challenging to treat in patients showing resistance to conventional diuretics and/or a poor response to natriuretic peptides to stimulate urine output. In this case, filtration provided a rapid, predictable and safe removal of 12 liters of plasma water while maintaining hemodynamic stability and serum electrolytes. This therapy also allowed the patient to receive the benefits of blood transfusion. Because of concerns about the patient’s bleeding from his urinary tract, the usual systemic anticoagulation was successfully avoided by heparinizing the circuit pre-filter.

Case history courtesy of:

Assistant Professor of Medicine/Cardiology

Oregon

MEDICAL SPECIALIST CLINIC

MEDICAL SPECIALIST CENTRE

Dear reader,

First, I must express my gratitude to ------- and his fellow doctors at ------------- Specialist Centre, for giving me opportunities to participate in the management of their patients.

OUR treatment is a relatively new modality of therapy to me, although it has been used rather successfully in many parts of the world, for a good number of years. Since I started co-managed patients with ----, I started reviewing some literature about the role of extracorporeal blood oxygenation and ozonation, fondly called RHP Researchers have experimented with RHP ailments ranging from ischemic heart disease to peripheral vascular disease and even viral hepatitis. Clinicians have since applied this form of complimentary medicine to multifarious disorders.

-------- has referred patients of various diseases to me for opinion and assessment, particularly those with cardiac dysfunction. There were instances whereby patients were previously advised surgery, as in coronary by-pass by other doctors, subsequent referred to me by ------ for assessment of LV function, in preparations for RHP. I normally inform ------ to proceed with RHP if the LV ejection fraction > 45%.

Many of these cases have amazingly managed to avert surgery. Although their symptoms improved appreciably. The exact mechanism has yet to be elucidated, but it probably has something to do with plaque stability and endothelial function.

In conclusions, RHP is a new and up coming way to treat many vascular - based pathology. Although the evidence for it is not yet monumental, but many ongoing studies will substantiate its role in clinical medicine.

Thank You,

BSc MD, MRCP (UK)

Consultant Physician (Cardiology)