Being in D.C. this week allowed me both to do my day job of being a lawyer and my other day job of trying to put myself out of business (I do blogging at night). Thanks to the lack of function in politics here, retirement is not yet in the cards for me. I did, however, do a series of confidential E. coli settlements. Here are some of the details:
A) 15-year-old girl, hospitalized for several days with ongoing Irritable Bowel Syndrome. She has incurred $34,000 in medical bills. As she says:
I feel like I live in a nightmare of pain day to day. Sometimes I feel like I’m waiting to be well but it will never come true. This is the most stressful thing I have ever been through. I never thought that eating food would change my whole life. The hardest thing to know is that there will never be a day where I’m not in pain. My favorite sport is basketball and I can’t even go to a practice without being in pain or crying.
B) Another, a 21-year-old woman hospitalized for days with $14,000 in medical expenses and the risk of ongoing Irritable Bowel Syndrome. As one medical provider said:
As you know she had acute colitis (documented by colon wall thickening on abdominal CT scan) due to E coli O157:H7 (culture proven), and was hospitalized from 5/8/10 to 5/11/09. Acute symptoms were lower abdominal pain and bloody diarrhea. Following discharge from hospital, she continued to have intermittent symptoms, described as crampy abdominal pain, sometimes with diarrhea, usually occurring an hour after eating, and lasting about half an hour. These symptoms occur about twice a week, with diarrhea about three times per month. On June 30, 2010, her symptoms were more severe and with bloody diarrhea she presented to an emergency room, where no cultures were done and she was given symptomatic therapy and gradually improved over the next several days. A follow up evaluation on 8/9/2010 at the MUSC resulted in further workup, with normal upper endoscopy and colonoscopy, although biopsies from the right colon showed mild focal inflammation. Since that time she has continued to have intermittent symptoms as described above that are clearly different from before her E coli infection. In my opinion, it is more likely than not that she has post infectious irritable bowel syndrome related to her acute E coli O157:H7 infection.
C. And, yes another 21-year-old woman, who was hospitalized for weeks, incurring $110,000 in medical expenses and as one expert opined:
She unfortunately, has been left with significant chronic and progressive renal damage. Her proteinuria and reduced GFR, more than a year post-HUS, indicates that she is experiencing hyperfiltration injury and has already lost substantial renal function. It is therefore my opinion that, more likely than not, she will develop end-stage renal disease (ESRD), also known as stage 5 kidney disease, within the next 20 years. As her renal failure worsens, and she develops ESRD, the two options will be dialysis and/or transplant.
The long, slow decline in renal function will have multiple impacts:
1. She will experience a progressive reduction in her ability to excrete waste products and maintain fluid and electrolyte balance: Kidneys play a critical role not only in excreting waste products, but also in maintaining electrolyte (e.g., sodium, potassium, bicarbonate) and water balance.
• As kidney function declines, nitrogenous waste products will accumulate, and eventually she will experience uremic toxicity characterized by weakness, loss of appetite, nausea and vomiting, and if not treated with dialysis, seizures, coma and death.
• Normal kidney function allows wide latitude in the amount of salt, potassium and fluid ingested because the kidneys make the proper adjustments, that is, they retain what the body needs and excrete what it does not need. A her kidney failure progresses and her kidneys lose their ability to maintain homeostasis (balance), salt, potassium and fluid intake will have to be restricted accordingly. Working with her Renal Dietitian will be essential.
2. Accumulation of body acid: Normal metabolism produces large quantities of acid, mainly sulfuric acid, resulting from protein metabolism. Healthy kidneys excrete this acid.
• Once her renal excretion of acid is insufficient to offset its production, reducing its source by restricting dietary protein is helpful, but alone will be insufficient to maintain acid base balance.
• Thus, she will also need to take base (alkali) such as sodium bicarbonate to neutralize remaining body (not stomach) acid. Failure to do so will result in poor appetite and weakened bones.
3. Anemia: Bone marrow is dependent on a hormone called erythropoietin that is produced by normal kidneys, and that directs the bone marrow to make red blood cells (RBC). Damaged kidneys have a limited ability to produce erythropoietin.
• Prior to the availability of human recombinant erythropoietin, blood transfusions were the only choice.
• Today, the injection of erythropoietin generally makes that unnecessary. It can be anticipated that she will depend on injections of this hormone that will begin no later than the start of dialysis, and probably sooner.
4. Loss of bone density: Healthy bones require renal modification of regular vitamin D before it is biologically active and able to control the intestinal absorption of calcium, the renal excretion of phosphorous, and bone deposition of calcium and phosphorous. Achieving and maintaining this delicate balance will require a complex plan consisting of medications, frequent blood tests, phosphorous binders and close adherence to a low phosphorous diet.
• In health, parathyroid home (PTH) keeps blood calcium and phosphorous levels normal and bones healthy. But as her kidneys progressively fail, the hormone’s attempt to maintain a normal blood calcium level will occur at the expense of her bones. That is, the elevated PTH level will draw calcium out of her bones placing her at high risk for bone pain and fractures.
• She will therefore need to adhere to a very difficult regimen consisting of:
o Oral administration of a special form of vitamin D that has been modified in the laboratory to its biologically active form (1-25-vitame D);
o Calcium supplementation;
o Phosphorous restriction combined with binders to reduce absorption of phosphorous from the intestine.
5. Blood pressure control: BP is, to a large extent, controlled by the kidneys via the production of the proper balance of vasoconstrictive and vasodilatory chemicals and by maintaining normal salt and water balance.
• High blood pressure afflicts the majority of renal failure patients, and it can be anticipated that her BP will worsen as renal function declines.
• Failure to maintain normal blood pressure will increase her risk of heart failure, heart attack and stroke.
6. Bearing children will inadvisable: This is for a variety of reasons, not the least of which will be:
• A very increased risk of experiencing Toxemia of Pregnancy (pre-eclampsia and eclampsia),
• Worsening hypertension and acceleration of her progressive renal failure (even in the absence of Toxemia).
The average waiting time for patients age 18-44 years is approximately 700 days (United States Renal Data Systems, Table 7.8, 2005). Even after transplantation though, new challenges arise, including those presented by immunosuppressive medications. Medications used to prevent rejection have considerable side effects. Corticosteroids are commonly used following transplantation. The side effects of corticosteroids are Cushingnoid features (fat deposition around the cheeks and abdomen and back), weight gain, emotional liability, cataracts, osteomalacia and osteonecrosis (softening of the bones and bone pain), hypertension, acne and difficulty in controlling glucose levels.
Cyclosporine and/or tacrolimus are also commonly used as immunosuppressive medications following transplantation. Side effects of these drugs include hirsutism (increased hair growth), gum hypertrophy, interstitial fibrosis in the kidney (damage to the kidney), as well as other complications. Meclophenalate is also commonly used after transplantation (sometimes imuran is used); each of these drugs can cause a low white blood cell count and increased susceptibility to infection. Many other immunosuppressive medications and other medications (anti-hypertensive agents, anti-acids, etc) are prescribed in the post operative period.
Lifelong immunosuppression as used in patients with kidney transplants is associated with several complications including an increased susceptibility to infection, accelerated atherosclerosis (hardening of the arteries), increased incidence of malignancy (cancer) and chronic rejection of the kidney.
Right, ignoring food safety make a lot of sense.