For every outbreak of E. coli O157:H7 there is a corresponding number of cases (usually 5 to 15 percent of the total) that develop into a life-threatening complication known as hemolytic uremic syndrome (HUS). What follows is an E. coli HUS FAQ (Frequently Asked Questions). It was created by the HUS lawyers at Pritzker Olsen Attorneys, a national food safety law firm representing children and their families in cases involving hemolytic uremic syndrome. If you have questions or comments or wish to talk to one of the highly experienced foodborne illness attorneys at our firm, contact us toll-free at 1-888-377-8900 or by email at fhp@pritzkerlaw.com.
Frequently Asked Questions about Hemolytic Uremic Syndrome (HUS)
What is hemolytic uremic syndrome (HUS)?
HUS is a disease that destroys red blood cells. Healthy red blood cells (left) are smooth and round. In hemolytic uremic syndrome, toxins destroy red blood cells (right). These misshapen cells may clog the tiny blood vessels in the kidneys. A healthy kidney is a filtration device that removes waste products from the blood. It contains hundreds of thousands of tiny filters (glomeruli), tiny tubes through which blood passes.
When kidneys are healthy, the artery brings blood and wastes from the bloodstream into the kidneys. The glomeruli clean the blood. Then wastes and extra fluid go out into the urine through the ureter. Clean blood leaves the kidneys and goes back into the bloodstream through the vein.
The red blood cells damaged and misshaped by HUS cannot pass through the glomeruli and cause blockage. This blockage results in destruction of the glomeruli. If enough glomeruli are damaged, function of the kidney is compromised. In severe cases, the person suffers end-stage renal disease or even death.
What causes HUS?
HUS develops when Escherichia coli (E. coli) bacteria lodged in the digestive tract make toxins that enter the bloodstream and start to destroy red blood cells. Most cases of HUS occur after an infection of the digestive tract by the E. coli bacterium, which is found in foods like meat, dairy products, leafy greens and juice when they are contaminated. Some people have contracted HUS after swimming in pools or lakes contaminated with feces. Most people who suffer E. coli O157:H7 poisoning do not suffer HUS.
What are the signs and symptoms of HUS and kidney failure?
With HUS, the child remains pale, tired, and irritable. Other signs include small, unexplained bruises or bleeding from the nose or mouth that may occur because the toxins also destroy the platelets, cells that normally help the blood to clot. Signs and symptoms of HUS may not become apparent until a week after the digestive problems have occurred.
More than half of children with HUS develop acute kidney failure. With kidney failure, the child’s urine output decreases. The urine may also appear red. Urine formation slows because the damaged red blood cells clog the tiny blood vessels in the kidneys, making them work harder to remove wastes and extra fluid from the blood. The body’s inability to rid itself of excess fluid and wastes may in turn cause high blood pressure or swelling of the face, hands, feet, or entire body.
Parents or guardians should call the child’s doctor immediately if the child has unexplained bruises, unusual bleeding, swollen limbs or generalized swelling, extreme fatigue, or decreased urine output. A child who goes 12 hours without urinating should be taken to a doctor or an emergency room.
How is HUS diagnosed?
A doctor may suspect that a child has HUS after examining the child and learning the history of symptoms. The diagnosis is confirmed by microscopic examination of a blood sample to see if the red blood cells are misshapen.
How is HUS treated?
Treatments, which consist of maintaining normal salt and water levels in the body, are aimed at easing the immediate symptoms and preventing further problems. A child may need a transfusion of red blood cells delivered through an intravenous, or IV, tube. In severe cases, several sessions of dialysis, a blood-cleansing treatment, may be required to temporarily take over the kidneys’ job of filtering wastes and extra fluid from the blood.
Some children may sustain significant kidney damage that slowly develops into permanent kidney failure and will then require long-term dialysis or a kidney transplant. Some studies suggest that limiting protein in the child’s diet and treating high blood pressure with a medicine from a class of drugs called angiotensin-converting enzyme (ACE) inhibitors helps delay or prevent the onset of permanent kidney failure.
How can HUS be prevented?
Washing and cooking foods adequately, especially meats, and avoiding unclean swimming areas are the best ways to protect a child from this disease.
What are the most serious outcomes resulting from HUS?
Death and end-stage renal disease (ESRD).
End-stage kidney disease is the complete, or almost complete failure of the kidneys to function. The kidneys can no longer remove wastes, concentrate urine, and regulate many other important body functions.
End-stage kidney disease occurs when the kidneys are no longer able to function at a level needed for day-to-day life. It usually occurs when chronic kidney disease has worsened to the point at which kidney function is less than 10% of normal.
Patients who have reached this stage need dialysis or a kidney transplant. Most people who die or develop ESRD do so during the acute phase of HUS. According to a leading medical journal article, the incidence of death or permanent ESRD from HUS is 12%.
If my child survives HUS, does that mean there will be no future problems?
Unfortunately not.
A 2003 study appearing in the prestigious Journal of the American Medical Association (JAMA) entitled “Long-term Renal Prognosis of Diarrhea-Associated Hemolytic Uremic Syndrome” analyzed almost 50 other journal articles on the subject and found that 25% of people who developed HUS had long-term kidney problems resulting from the disease.
Some of the same authors published a follow-up article in 2009 analyzing data from a Canadian water-borne E. coli O157:H7 outbreak. The data from that study were more encouraging: although some abnormalities persisted, no child with HUS had serious kidney problems five years after the outbreak. The authors cautioned, however, that this more favorable data may be a function of factors unique to that particular outbreak and not prognostic for outcomes from other outbreaks.
What are those kidney complications?
There are three primary kidney complications: decreased glomerular filtration rate (GFR), hypertension and/or proteinuria.
Regarding decreased GFR, GFR is a test used to check how well the kidneys are working. Specifically, it estimates how much blood passes through the tiny filters in the kidneys, called glomeruli, each minute.
The GFR test measures how well your kidneys are filtering a waste called creatinine, which is produced by the muscles. When the kidneys aren’t working as well as they should, creatinine builds up in the blood.
According to the National Kidney Foundation, normal GFR results range from 90 – 120 mL/min. Older people will have lower normal GFR levels, because GFR decreases with age. Levels below 60 mL/min for 3 or more months are a sign of chronic kidney disease. Those with GFR results below 15 mL/min are a sign of kidney failure.
Regarding hypertension, or high blood pressure, in this context, it is usually defined as requiring antihypertensive medication or blood pressure measurement higher than the 90th percentile. Uncontrolled high blood pressure can lead to a number of problems including artery damage, aneurysm, heart failure, stroke and other serious problems. At a minimum, it requires medical monitoring and medication. Hypertension also increases the risk of further kidney disease.
Regarding Proteinuria, it is the presence of excessive amounts of protein in the urine. It occurs in the context of HUS as a result of decreased kidney function. It is a sign of chronic kidney disease.
If my child suffered a milder form of HUS, does that mean there will be no future problems?
Some HUS cases are milder than others. For example, cases in which urine output is preserved and no dialysis is required are considered less severe than cases in which there is no urine output and/or longer term dialysis.
However, some studies have shown that even some mild cases of HUS develop renal problems at longer-term follow-up. Those problems include chronic renal failure. There does not appear to be any reliable data about the frequency of long-term kidney problems following mild HUS cases.
If my child survives HUS, does that mean there will never be future kidney problems?
The usual measure of full recovery following HUS is a normal GFR.
According to some studies, the presence of a normal GFR following acute HUS does not guarantee long-term kidney health, although the data is far from conclusive. For example, in four studies of patients who apparently completely recovered after acute illness, anywhere from 8% to 61% went on to develop a lower-than-normal GFR, hypertension or proteinuria during long-term follow-up. Other studies, however, seem to indicate that full recovery following acute HUS means there will be no future complications. These studies are limited by follow-up times of five years or less which means that the full extent of future problems requires further study.
Are there problems other than kidney damage that my child may experience?
Sadly, kidney damage is not the only problem that can result from HUS. Other complications include neurological deficits (acute and chronic), diabetes and gastrointestinal problems.
Studies about the long-term problems associated with these complications are inconsistent. For example, in one study of patients with HUS who had major neurological symptoms during their acute illness, on long-term follow-up they continued to show subtle neurological deficits including posturing, clumsiness, poor fine-motor coordination, hyperactivity and distractibility.
A recent study involving adults with complications similar to HUS (thrombotic thrombocytopenic purpura (TTP)) noted that “After recovery, patients have significantly abnormal health-related quality of life; neurocognitive studies have documented deficits of attention, processing speed and memory, and also fatigue.”
A recent report about the long-term outcomes of selected foodborne pathogens, including E. coli O157:H7, may be found at the Center for Foodborne Illness.
If my child develops HUS, should I make a legal claim?
The decision to undertake legal action should not be taken lightly.
Few people who suffer serious injury are “sue happy.” Any sane person would gladly give up the right to collect money damages in return for his/her health. But when that is not possible, especially in catastrophic loss cases such as HUS, it is important to think about issues like “Who will pay for the medical bills (or even the co-pays if insurance is involved) now and in the future?” “Who will care for my child while I’m away at work or, worse, after I’m gone?” “What if my child has permanent injuries and life-long complications?”
It’s also important to understand that in order to successfully make a claim, one has to identify the source of the E. coli O157:H7 that resulted in HUS, determine how and when the food product became contaminated and prove by the greater weight of the evidence that the resulting harms and losses were the direct result of the illness. This is often a very complicated process. In fact, in the majority of HUS cases, the source of the contamination is never identified (and therefore a claim is not possible).
Whether you ultimately decide to make a claim or not, you should speak with an attorney to better understand your rights and the issues involved and then decide whether it’s right for you and your family to make a claim (or whether it’s even possible to do so).
What kind of lawyer should I consult with?
Very, very few lawyers in the United States have experience with foodborne illness cases in general and E. coli HUS in particular.
These cases are extremely complicated and require extensive knowledge and experience in fields such as epidemiology, microbiology, medicine, food safety, sanitation and, of course, trial law. Only a tiny percentage of lawyers have this training and experience and fewer still have ever successfully handled an HUS case to conclusion.
The attorneys at Pritzker Olsen have handled E. coli O157:H7/HUS cases resulting from virtually every major foodborne illness outbreak in the United States. The firm has collected millions of dollars for HUS survivors and their families and its lawyers have been interviewed by and quoted in the New York Times, Wall Street Journal, USA Today and a host of national and local television news programs. Firm attorneys meet with HUS survivors and their families at the hospital or in their homes and are available virtually any time. We believe in the importance of frequent, direct and personal contact with our clients.
If I decide to hire your firm, how much will it cost and how will I pay you?
Our firm is paid a percentage of the recovery, usually one-third. If there is no recovery, you owe us nothing. There are no up-front fees or retainers. We are not paid until we obtain a recovery for you.
Costs involved in prosecuting the case are advanced by our firm. If a recovery is obtained, we are reimbursed for our costs. This is in addition to our fee.
If you would like to discuss your case or learn more about our firm, visit us on the web , call for a free consultation at 1-888-377-8900 or email us at fhp@pritzkerlaw.com
