Showing posts with label joints. Show all posts
Showing posts with label joints. Show all posts

Monday, July 31, 2017

Obesity and Joint Replacement, Part 2: Does Losing Weight First Improve Outcomes?


We have been discussing obesity and joint replacement operations, specifically knee replacements and hip replacements, and the common practice of denying these to people of size.

In Part One, we discussed the highly questionable ethics behind denying "obese" people joint replacement operations or requiring that they undergo weight loss counseling or bariatric surgery first. These practices keep many people of size from accessing joint replacements and improving their functional abilities and pain levels, sentencing many larger people to the difficulties of dealing with mobility challenges and a poorer quality of life.

Today, we discuss the data on whether losing weight before joint replacement actually improves long-term outcome, as so many doctors insist it will. Up till now it has been assumed that it will, but a closer look at longer-term research calls this assumption into question. Indeed, several recent studies that suggest that losing weight before knee replacement surgery does NOT improve outcome and might even result in worse outcomes.

Does Weight Loss Before Knee Replacement Help?

Of course, some readers will be asking, why not consider weight loss? If it will reduce the physical load on the joint and lessen pain and wear, why not pursue weight loss?

The answer is complicated.

It certainly seems logical that it would be advantageous to lose weight before an operation to replace a weight-bearing joint. There would be less weight and therefore less force on the joint, right?

And to be fair, there's definitely research that shows modest improvements in functionality, joint force load, and pain levels with weight loss in patients with knee pain.

However, like most weight-loss research, these studies usually follow patients only short-term so the usual weight rebound effect is conveniently overlooked or minimized.

Even studies that promote weight loss for knee osteoarthritis admit (my emphasis):
Whether substantial weight loss can delay or even reverse the symptoms associated with osteoarthritis remains to be seen.
In other words, they do NOT have long-term proof that weight loss improves outcomes; they just assume it does because short-term studies (often just a few months) suggest some improvement.

This is the problem with nearly all weight-loss research; it only follows the patients long enough to show some benefits of a quick loss, but rarely follow patients long-term because many of the benefits are lost and most of the weight is regained (and often more), and doctors don't want to acknowledge that.

Even the usual recommendation to "lose just 5-10%" of a person's weight is problematic. While some research indicates modest benefits, research is actually quite limited on the long-term effects of such a loss. And most dieters do not manage or just barely manage that 5-10% weight loss over time.

Reviews of long-term research shows that for most people, few maintain the weight loss over time, most of the weight loss is regained with time, and many people rebound to higher weights or greater abdominal fat than they began with. There are biological reasons for this weight regain; it's not just about willpower.

Furthermore, weight loss can present risks as well as benefits, frequent weight fluctuation can be detrimental to health, and intentional weight loss/"dietary restraint" is one of the strongest predictors of long-term weight gain.

As a result, some care providers are now recommending that obese patients strive for weight stability rather than weight loss, and that the emphasis be placed on improving health habits and health measures instead of reducing a number on a scale.

Unfortunately, because short-term research shows modest improvements in joint function with weight loss, doctors have extrapolated this to assume that significant weight loss will improve long-term outcomes for joint replacement surgeries. As a result, some deny joint replacement to people above a certain BMI, practically mandate attendance at weight loss programs first, browbeat their patients about weight loss, or strongly push for bariatric surgery instead.

But does weight loss before joint replacement improve outcomes?

Weight Loss Before Joint Replacement 

In two recent new studies, the common assumption that having patients lose weight before having knee replacement surgery will automatically improve outcomes is questioned.

In a California study, only 12.4% of more than 10,000 knee replacement patients studied and 18% of more than 4000 hip replacement patients  managed to lose at least 5% of their starting weight in the year before their surgery. Around 75% of both groups stayed stable. Those who did manage to lose weight before knee replacement surgery did no better than those who did not lose weight before surgery. They had similar rates of surgical site infections and re-admissions for complications.

This certainly calls into question how helpful weight loss supposedly is before knee replacement.

In a companion study, those who lost weight before joint replacement surgery and managed to keep it off afterwards actually did worse than those whose weight stayed stable. The weight loss knee replacement group had more hospital re-admissions than those who did not lose weight. Furthermore, the hip replacement group who lost weight had more deep-site surgical infections. The authors noted:
These findings raise questions about the safety of weight management before total replacement of the hip and knee joints.
Why this increase in infections occurred is not clear. One theory is that when people are placed on a significantly low-calorie diet, nutrition can be impaired. It is difficult to get the proper amounts of all the nutrients when caloric intake is too low, and diets for these mobility-impaired people are often quite low-calorie because increasing exercise is difficult. As a result, some people with significant weight loss or chronic dieting histories develop nutrient deficiencies, and these may impair immune function. Research confirms that people with nutrient deficiencies have a greater risk for infections and other complications after joint surgery.

So while weight loss may reduce stress on the joint, nutrient deficiencies from this weight loss may affect immune function and ability to "bounce back" after surgery, negating any potential benefits of weight loss.

Furthermore, many people who lose substantial weight before joint replacements gain back that weight and more after the surgery. The end result of weight loss before joint replacement may be that the patient ends up weighing MORE later on, as one study found:
A patient with [hip replacement] had increased risk of important post-surgical weight gain of 12% (OR = 1.12, 95% CI, 1.08, 1.16) for every kilogram of pre-operative weight loss...Patients less than 60 years and who have lost a substantial amount of weight prior to surgery appear to be at particularly high risk of important post-surgical weight gain.
Ironically, requiring or strongly encouraging patients to lose a substantial amount of weight prior to joint replacement may backfire and ultimately add to the patient's weight, not lessen it. Yet most doctors continue to demand weight loss before joint replacement. Only now the emphasis is on weight loss via bariatric surgery instead.

Quote from Ragen Chastain, found here.

What About Bariatric Surgery First?

Because bariatric surgery is one of the only ways to lose weight in the long term (though it comes with many other complications and ususally involves some weight regain), many orthopedic surgeons are forming de-facto partnerships with bariatric surgeons.

As a result, many people of size are effectively blackmailed into weight loss surgery by BMI restrictions on joint replacements. 

One study from the Mayo Clinic states, "Morbidly obese individuals with severe degenerative joint disease who are considered unsuitable for arthroplasty because of excess weight should be considered for bariatric surgery."

Another surgeon reports that he accepts patients for knee replacements up to a BMI of 50, but after that he refers them for bariatric surgery first. (Because it makes SO much sense for someone too "at-risk" for one type of surgery to undergo a different type of surgery instead.)

Yet the common assumption that bariatric surgery should be promoted because it would surely improve outcomes in "morbidly obese" patients with significant osteoarthritis should also be questioned.

Some research does indicate improved outcomes in those who had bariatric surgery before joint replacement. And one recent study that looked only at short-term (90 days!) complications found lower rates of complications in those who had had bariatric surgery. Of course, the media was all over this study and it has been widely cited to justify requiring weight loss surgery.

However, other research does not support better outcomes with bariatric surgery, yet the press conveniently ignores that. In one study, complications were actually higher in the group with recent bariatric surgery (less than 2 years). The authors concluded:
Bariatric surgery prior to TJA [Total Joint Arthroplasty] may not provide dramatic improvements in post-operative TJA surgical outcomes. 
In another study from a major research hospital, researchers found an increased rate of joint replacements in bariatric patients who had experienced large or very rapid weight loss. They noted, "These results contradict the tenant that weight loss is universally protective against arthritis and merit larger prospective investigations."

Another recent study did not find improved outcomes in those who had had bariatric surgery before joint replacement. Indeed, many had worse outcomes instead, needing more revision surgeries afterwards.

This was echoed in a recent large retrospective cohort study that found worse outcomes in the group that had bariatric surgery first, compared to high-BMI people who did not. The WLS group had more infection, pneumonia, blood clots, heart issues, revisions, and manipulations of the prosthetetic.

A recent meta-analysis found no significant benefit from bariatric surgery before joint replacement. The authors concluded:
For most peri-operative outcomes, bariatric surgery prior to THA or TKA does not significantly reduce the complication rates or improve the clinical outcome. This study questions the previous belief that bariatric surgery prior to arthroplasty may improve the clinical outcomes for patients who are obese or morbidly obese.
It may be that the potential benefits of reducing the load on the joint via weight loss from bariatric surgery may be outweighed by the nutrient deficits that are so common after weight loss surgery, even non-restrictive procedures. It may also be that the stresses on the body from rapid weight loss cause long-term damage to the body's ability to repair itself.

While some bariatric surgery patients have good outcomes and health improvement from the WLS, others have terrible outcomes, with significant nutritional deficits (sometimes despite supplements) and physical health problems. Some even die from the surgery or its after-effects. The problem is that you don't know which outcome group you are going to be in until after you've had the surgery. To strongly pressure joint replacement patients into bariatric surgery first means doctors are engaging in a high-stakes gamble with their patients' lives and quality of life.

And if joint replacement surgery at larger sizes is "too dangerous," why isn't weight loss surgery at larger sizes also too risky? Funny how patients are too fat for one surgery but surgeons can't wait to usher them into the Operating Room for WLS.

There are good reasons to question the common recommendation to have bariatric surgery before joint replacement. WLS is dangerous in and of itself, it often results in significant long-term nutrient deficits and other health problems, and it may not improve long-term outcomes for joint replacement.

However, as always, every person gets to make their own health decisions. Some people choose to have bariatric surgery before joint replacement and they have the right to do that. Others choose not to, and they also should have the right to do that. It's a choice with many pros and cons but one that should not be forced upon someone, which many doctors are essentially doing by denying joint replacement without bariatric surgery first.

In the past, care providers rarely studied whether or not bariatric surgery actually improved outcomes; they just assumed it will because it seems logical. But recent research shows there is good reason to question whether bariatric surgery really improves long-term outcome after all.

Mitigating Risk Through Better Management

Critics will no doubt point out that the risk for blood clots and post-operative infection are higher in obese patients and this is why they are concerned about operating on this group. This is true, and obese patients should be counseled about this fact. For example, one study found 6.7x the risk for infection in obese knee replacement patients, and 4.2x the risk for infection in obese hip replacement patients. The risk for infection is particularly strong among diabetics with a BMI over 40.

However, remember the dangers of using relative risk to discuss risk/benefit ratios; it can distort one's perception of risk. It is more helpful to use absolute numerical values so the magnitude of risks patients are assuming is more clear. One very large British study found that for knee replacements, risk for blood clots was increased from 2.0% to 3.3% and risk for infection from 3.0% to 4.1%, in obese patients with total knee replacements. For hip replacements, the risk for blood clots was increased from 2.2% to 3.3% and the risk for infection from 1.6% to 3.5% in obese patients. The authors noted (my emphasis):
Whilst an increased risk of wound infection and DVT/PE was observed amongst obese patients, absolute risks remain low and no such association was observed for MI, stroke and mortality.
However, the most important thing to point out is that an increased infection and clotting risk may be at least partly due to mismanagement of obese patients. Re-examining and changing the management protocols of these patients may improve outcomes independent of weight loss. 

For example, research shows that obese patients are chronically under-dosed with many medications. This is particularly relevant in antibiotics for preventing and treating infections, and in thromboprophylaxis medications for preventing blood clots after surgery. In other words, the two biggest risks of surgery in high-BMI patients may actually be largely preventable.

Obese patients, especially "morbidly-obese" (BMI 40+) and "super-obese" (BMI 50+) patients, are at particular risk for infections and may require larger initial antibiotic doses, extended or more frequent dosing regimens, use of more than one type of antibiotic, and perhaps topical infusions of antibiotics during surgery. This may help reduce their increased risk for infection after joint replacement surgery.

One recent study on infection in obese joint replacement patients strongly raised this issue of antibiotic underdosing. The authors found that above 100 kg (~220 lbs.), the rate of infections rose strongly. They noted that most patients in the study, regardless of BMI, were treated with a uniform dose (1.5g) of pre-op antibiotics and speculated that an increased antibiotic dose would help lower the rate of infections in this group. They stated:
The link between obesity and infection may be explained by several factors, but under-dosing of antibiotics is probably the most important to consider.
They also noted that noted that research examining the question of proper antibiotic dosage for obese patients undergoing joint replacement surgery was lacking. The problem of underdosing antibiotics in obese patients has been acknowledged in obstetric and bariatric surgery for several years. Why is it only NOW being brought up in orthopedic surgery?

Underdosing issues go beyond antibiotics. Research suggests that many obese patients are under-dosed with anti-clotting agents like heparin. One study found that weight-adjusted dosing cut the rate of blood clots in obese patients after surgery from 2.0% to 0.54% without increasing the risk for bleeding. Another study found that an extended prophylaxis period of anti-clotting agents lowered the risk for clots significantly, also without increasing bleeding.

Other surgical management protocols for obese patient need review as well. Some research suggests that surgical drains, often placed prophylactically in obese patients, have no benefit or may actually do more harm than good. Although further research is needed, one research review suggested omitting routine surgical drains in obese patients during joint replacement surgery.

As noted previously, another very interesting set of recent studies suggests that "morbid obesity" is less important that serum albumin levels on major complications like mortality and infections in joint replacement surgery. Serum albumin levels are an indicator of liver and kidney function but can also indicate nutrition status; obese people may be more at risk for malnutrition because of chronic dieting, highly restrictive intakes, or malabsorptive procedures like gastric bypass. Improving joint replacement outcomes might need to focus on measuring and fixing albumin levels and other nutrient deficits before surgery.

Bottom line, if the real concern is preventing poor outcomes, then perhaps the best approach is not to deny all high-BMI patients access to this surgery, but rather to lower morbidity by improving care for them instead via:
  • Utilizing weight-based dosing more uniformly in antibiotics and blood clot prevention drugs 
  • Using extended, adjunctive or more frequent antibiotic dosing regimens 
  • Avoiding routine prophylactic surgical drains 
  • Screening for and optimizing albumin and other nutrient levels before surgery
Ironically, a lot of the research on improving surgical outcomes in very obese patients is only done with bariatric surgery. It is past time to improve outcomes in high-BMI people in other types of surgery as well, including joint replacement surgery, instead of having to just extrapolate from bariatric surgery studies.

We need to know through evidence-based trials what the best protocols are for obese people undergoing joint replacement surgery. And in order to do that, we need for people of size to actually be given access to this surgery.

Summary

Sadly, even today, many orthopedic surgeons refuse to do knee replacements or hip replacements on anyone with a BMI over 35 or over 40 (or sometimes less).  In many places in the U.K., for example, people with a BMI over 35 have been routinely denied joint replacements and other surgeries. Some even deny joint replacements to those with a BMI over 30.

They do this because surgery is more technically challenging in very heavy people and because they view obesity as a voluntary condition brought on by poor lifestyle choices. They feel that losing weight is mostly a matter of willpower and choices, despite plenty of evidence to the contrary, and they feel they are doing their patients a favor by making them lose weight.

Surgeons also justify BMI restrictions by pointing out the short-term risks associated with orthopedic surgery in high-BMI people. They suggest that higher complication rates and somewhat lower functional outcomes justify denying surgery to this group and/or requiring weight loss or even bariatric surgery before joint replacement.

However, other surgeons are questioning the ethics of denying joint replacement surgery to high-BMI patients. They note that even very fat patients usually have good long-term outcomes from the surgery.

They recognize that the tremendous improvement in mobility, quality of life, knee function, and pain relief is worth the trade-off of a potentially increased risk for mild short-term morbidity. Many are willing to proceed with joint replacement surgery in high-BMI patients as long as they have been given informed consent about the benefits and risks.

It is reasonable to counsel obese patients about the potential risks of a higher weight before surgery, especially if they have co-morbidities like diabetes. However, the counseling should cover both risks and benefits. It should acknowledge that the magnitude of risk is relatively modest in most obese patients and that most have very good long-term results from both knee replacement surgery and hip replacement surgery.

Patients can also be counseled about the potential benefits of weight loss before joint replacement surgery, as long as the data used is realistic and the potential risks of weight loss are also covered. But weight loss should not be required in order to access such surgery because research is contradictory on whether this is helpful. Short-term research shows some benefits, but longer-term research shows little benefit and sometimes even harm. Furthermore, the risks of weight loss, yo-yo dieting, and bariatric surgery should not be overlooked. More research is needed, but requiring weight loss before surgery is certainly not evidence-based. The truth is that the evidence is mixed and the choice should be left to the patient.

Joint replacement surgery in very obese patients is technically harder and does carry risks. However, the magnitude of this risk is modest and the potential for improvement in quality of life is very strong. Restricting high-BMI people from joint replacement surgery or requiring them to lose weight in order to access this surgery is NOT justified or ethical.

Rather, the risks are a call to surgeons to further examine the long-overlooked issue of how they manage obese patients. Risks can most likely be mitigated by proper medication dosing and more optimal surgical management of high-BMI patients.

Instead of restricting joint replacement or requiring weight loss in high BMI patients, orthopedic surgeons should be focusing on how they can improve outcomes in this group through modifications to surgical management protocols.


References

General Information about Joint Replacement

Weight Loss Before Joint Replacement

Bone Joint J. 2014 May;96-B(5):629-35. doi: 10.1302/0301-620X.96B5.33136. The risk of surgical site infection and re-admission in obese patients undergoing total joint replacement who lose weight before surgery and keep it off post-operatively. Inacio MC, Kritz-Silverstein D, Raman R, Macera CA, Nichols JF, Shaffer RA, Fithian DC. PMID: 24788497
This study evaluated whether obese patients who lost weight before their total joint replacement and kept it off post-operatively were at lower risk of surgical site infection (SSI) and re-admission compared with those who remained the same weight. We reviewed 444 patients who underwent a total hip replacement and 937 with a total knee replacement who lost weight pre-operatively and sustained their weight loss after surgery. After adjustments, patients who lost weight before a total hip replacement and kept it off post-operatively had a 3.77 (95% confidence interval (CI) 1.59 to 8.95) greater likelihood of deep SSIs and those who lost weight before a total knee replacement had a 1.63 (95% CI 1.16 to 2.28) greater likelihood of re-admission compared with the reference group. These findings raise questions about the safety of weight management before total replacement of the hip and knee joints.
J Arthroplasty. 2014 Mar;29(3):458-64.e1. doi: 10.1016/j.arth.2013.07.030. Epub 2013 Sep 7. The impact of pre-operative weight loss on incidence of surgical site infection and readmission rates after total joint arthroplasty. Inacio MC, Kritz-Silverstein D, Raman R, Macera CA, Nichols JF, Shaffer RA, Fithian DC. PMID: 24018161
This study characterized a cohort of obese total hip arthroplasty (THA) and total knee arthroplasty (TKA) patients (1/1/2008-12/31/2010) and evaluated whether a clinically significant amount of pre-operative weight loss (5% decrease in body weight) is associated with a decreased risk of surgical site infections (SSI) and readmissions post-surgery. 10,718 TKAs and 4066 THAs were identified. During the one year pre-TKA 7.6% of patients gained weight, 12.4% lost weight, and 79.9% remained the same. In the one year pre-THA, 6.3% of patients gained weight, 18.0% lost weight, and 75.7% remained the same. In TKAs and THAs, after adjusting for covariates, the risk of SSI and readmission was not significantly different in the patients who gained or lost weight pre-operatively compared to those who remained the same.
Osteoarthritis Cartilage. 2013 Jan;21(1):35-43. doi: 10.1016/j.joca.2012.09.010. Epub 2012 Oct 6.
Clinically important body weight gain following total hip arthroplasty: a cohort study with 5-year follow-up. Riddle DL, Singh JA, Harmsen WS, Schleck CD, Lewallen DG. PMID: 23047011
...DESIGN: We used multi-variable logistic regression to compare data from one of the largest US-based THA registries to a population-based control sample from the same geographic region. We also identified factors that increased risk of clinically important weight gain specifically among persons undergoing THA. The outcome measure of interest was weight gain of ≥5% of body weight up to 5 years following surgery. RESULTS: ...A patient with THA had increased risk of important post-surgical weight gain of 12% (OR = 1.12, 95% CI, 1.08, 1.16) for every kilogram of pre-operative weight loss. CONCLUSIONS: While findings should be interpreted with caution because of missing follow-up weight data, patients with THA appear to be at increased risk of clinically important weight gain following surgery as compared to peers. Patients less than 60 years and who have lost a substantial amount of weight prior to surgery appear to be at particularly high risk of important post-surgical weight gain. 
Arthritis Care Res (Hoboken). 2013 May;65(5):669-77. doi: 10.1002/acr.21880. Clinically important body weight gain following knee arthroplasty: a five-year comparative cohort study. Riddle DL, Singh JA, Harmsen WS, Schleck CD, Lewallen DG. PMID: 23203539
...METHODS: We used one of the largest US-based knee arthroplasty registries and a population-based control sample from the same geographic region to determine whether knee arthroplasty increases the risk of clinically important weight gain of ≥5% of baseline body weight over a 5-year postoperative period. RESULTS: Of the persons in the knee arthroplasty sample, 30.0% gained ≥5% of baseline body weight 5 years following surgery as compared to 19.7% of the control sample. The multivariable-adjusted (age, sex, body mass index, education, comorbidity, and presurgical weight change) odds ratio (OR) was 1.6 (95% confidence interval [95% CI] 1.2-2.2) in persons with knee arthroplasty as compared to the control sample. Additional arthroplasty procedures during followup further increased the risk for weight gain (OR 2.1, 95% CI 1.4-3.1) relative to the control sample. Specifically, among patients with knee arthroplasty, younger patients and those who lost greater amounts of weight in the 5-year preoperative period were at greater risk for clinically important weight gain. CONCLUSION: Patients who undergo knee arthroplasty are at an increased risk of clinically important weight gain following surgery. The findings potentially have broad implications to multiple members of the health care team. Future research should develop weight loss/maintenance interventions particularly for younger patients who have lost a substantial amount of weight prior to surgery, as they are most at risk for substantial postsurgical weight gain.
Bariatric Surgery Before Joint Replacement 

Bone Joint J. 2015 Nov;97-B(11):1501-5. doi: 10.1302/0301-620X.97B11.36477. Bariatric surgery does not improve outcomes in patients undergoing primary total knee arthroplasty. Martin JR, Watts CD, Taunton MJ. PMID: 26530652
Bariatric surgery has been advocated as a means of reducing body mass index (BMI) and the risks associated with total knee arthroplasty (TKA). However, this has not been proved clinically. In order to determine the impact of bariatric surgery on the outcome of TKA, we identified a cohort of 91 TKAs that were performed in patients who had undergone bariatric surgery (bariatric cohort). These were matched with two separate cohorts of patients who had not undergone bariatric surgery. One was matched 1:1 with those with a higher pre-bariatric BMI (high BMI group), and the other was matched 1:2 based on those with a lower pre-TKA BMI (low BMI group). In the bariatric group, the mean BMI before bariatric surgery was 51.1 kg/m(2) (37 to 72), which improved to 37.3 kg/m(2) (24 to 59) at the time of TKA. Patients in the bariatric group had a higher risk of, and worse survival free of re-operation (hazard ratio (HR) 2.6; 95% confidence interval (CI) 1.2 to 6.2; p = 0.02) compared with the high BMI group. Furthermore, the bariatric group had a higher risk of, and worse survival free of re-operation (HR 2.4; 95% CI 1.2 to 3.3; p = 0.2) and revision (HR 2.2; 95% CI 1.1 to 6.5; p = 0.04) compared with the low BMI group. While bariatric surgery reduced the BMI in our patients, more analysis is needed before recommending bariatric surgery before TKA in obese patients.
J Arthroplasty. 2016 Sep;31(9 Suppl):207-11. doi: 10.1016/j.arth.2016.02.075. Epub 2016 Mar 15. Lingering Risk: Bariatric Surgery Before Total Knee Arthroplasty. Nickel BT, Klement MR, Penrose CT, Green CL, Seyler TM, Bolognesi MP. PMID: 27179771
...METHODS: A total of 39,014 patients were identified in a claim-based review of the entire Medicare database with International Classification of Diseases, Ninth Revision codes to identify patients in 3 groups. Patients who underwent BS before total knee arthroplasty (group I: 5914 experimental group) and 2 control groups that did not undergo BS but had either a body mass index >40 (group II: 6480 bariatric control) or <25 (group III: 26,616 normal weight control)...RESULTS: ...Medical and surgical complication incidences were greatest in group I including: 4.98% deep vein thrombosis; 5.31% pneumonia; 10.09% heart failure; and 2-year infection, revision, and manipulation rates of 5.8%, 7.38%, and 3.13%, respectively. These values were significant elevation compared to III and slightly greater than II. CONCLUSIONS: This study demonstrates that BS before total knee arthroplasty is associated with greater risk compared to both nonobese and obese patients. This is possibly due to a higher incidence of medical or psychiatric comorbidities determined in the Medicare BS patients, wound healing difficulties secondary to gastrointestinal malabsorption, malnourishment from prolonged catabolic state, rapid weight loss before surgery, and/or age.
Bone Joint J. 2016 Sep;98-B(9):1160-6. doi: 10.1302/0301-620X.98B9.38024. Does bariatric surgery prior to total hip or knee arthroplasty reduce post-operative complications and improve clinical outcomes for obese patients? Systematic review and meta-analysis. Smith TO, Aboelmagd T, Hing CB, MacGregor A. PMID: 27587514
AIMS: Our aim was to determine whether, based on the current literature, bariatric surgery prior to total hip (THA) or total knee arthroplasty (TKA) reduces the complication rates and improves the outcome following arthroplasty in obese patients. METHODS: A systematic literature search was undertaken of published and unpublished databases on the 5 November 2015...RESULTS: From 156 potential studies, five were considered to be eligible for inclusion in the study. A total of 23 348 patients (657 who had undergone bariatric surgery, 22 691 who had not) were analysed. The evidence-base was moderate in quality. There was no statistically significant difference in outcomes such as superficial wound infection (relative risk (RR) 1.88; 95% confidence interval (CI) 0.95 to 0.37), deep wound infection (RR 1.04; 95% CI 0.65 to 1.66), DVT (RR 0.57; 95% CI 0.13 to 2.44), PE (RR 0.51; 95% CI 0.03 to 8.26), revision surgery (RR 1.24; 95% CI 0.75 to 2.05) or mortality (RR 1.25; 95% CI 0.16 to 9.89) between the two groups. CONCLUSION: For most peri-operative outcomes, bariatric surgery prior to THA or TKA does not significantly reduce the complication rates or improve the clinical outcome. This study questions the previous belief that bariatric surgery prior to arthroplasty may improve the clinical outcomes for patients who are obese or morbidly obese. This finding is based on moderate quality evidence. 
Other Possible Factors

Clin Orthop Relat Res. 2015 Oct;473(10):3163-72. doi: 10.1007/s11999-015-4333-7. Epub 2015 May 21. Low Albumin Levels, More Than Morbid Obesity, Are Associated With Complications After TKA. Nelson CL1, Elkassabany NM, Kamath AF, Liu J. PMID: 25995174
BACKGROUND: Morbid obesity and malnutrition are thought to be associated with more frequent perioperative complications after TKA. However, morbid obesity and malnutrition often are co-occurring conditions. Therefore it is important to understand whether morbid obesity, malnutrition, or both are independently associated with more frequent perioperative complications...METHODS: The National Surgical Quality Improvement Program (NSQIP) database was analyzed from 2006 to 2013. Patients were grouped as morbidly obese (BMI ≥ 40 kg/m(2)) or nonmorbidly obese (BMI ≥ 18.5 kg/m(2) to < 40 kg/m(2)), or by low serum albumin (serum albumin level < 3.5 mg/dL) or normal serum albumin (serum albumin level ≥ 3.5 mg/dL)...RESULTS: Mortality was not increased in the morbidly obese group (0.14% vs 0.14%; p = 0.942)...The group with low serum albumin had higher mortality than the group with normal serum albumin (0.64% vs 0.15%; OR, 3.17; 95% CI, 1.58-6.35; p =0.001)... CONCLUSIONS: Morbid obesity is not independently associated with the majority of perioperative complications measured by the NSQIP and was associated only with increases in progressive renal insufficiency, superficial surgical site infection, and sepsis among the 21 perioperative variables measured. However, low serum albumin was associated with increased mortality and multiple additional major perioperative complications after TKA. Low serum albumin, more so than morbid obesity, is associated with major perioperative complications. This is an important finding, as low serum albumin may be more modifiable than morbid obesity in patients who are immobile or have advanced knee osteoarthritis.
HSS J. 2017 Feb;13(1):66-74. doi: 10.1007/s11420-016-9518-4. Epub 2016 Aug 16. Hypoalbuminemia Is a Better Predictor than Obesity of Complications After Total Knee Arthroplasty: a Propensity Score-Adjusted Observational Analysis. Fu MC, McLawhorn AS, Padgett DE, Cross MB. PMID: 2816787
...METHODS: TKA cases were identified from the National Surgical Quality Improvement Program from 2005 to 2013... Malnutrition was defined as hypoalbuminemia (<3.5 g/dL). Patients were classified by BMI as follows: non-obese (18.5-29.9), obese I (30-34.9), obese II (35-39.9), or obese III (≥40). Postoperative complications were compared across obesity and nutritional statuses. Multivariable propensity-adjusted logistic regressions were performed to determine associations between malnutrition, obesity, and 30-day outcomes. RESULTS: There were 71,599 cases identified, with 34,800 (48.6%) having albumin measurements...Malnutrition prevalence increased with BMI (6.1% in obese III vs. 3.7% in non-obese). With propensity-adjusted multivariable analysis, obese III was the only obesity class associated with any complication, wound complication, and reoperation. Hypoalbuminemia was a stronger and more consistent independent risk factor, for any complication, wound, cardiac, or respiratory complications, and death. CONCLUSIONS: Hypoalbuminemia is a more consistent independent predictor of complications after TKA than obesity. Strategies for medical optimization of these conditions should be investigated.
Antibiotic Dosing and Surgical Infections

Acta Orthop. 2016;87(2):132-8. doi: 10.3109/17453674.2015.1126157. Epub 2016 Jan 5. Body mass and weight thresholds for increased prosthetic joint infection rates after primary total joint arthroplasty. Lübbeke A1, Zingg M1, Vu D2, Miozzari HH1, Christofilopoulos P1, Uçkay I1,2, Harbarth S3, Hoffmeyer P1. PMID: 26731633
...We included all 9,061 primary hip and knee arthroplasties (mean age 70 years, 61% women) performed between March 1996 and December 2013 where the patient had received intravenous cefuroxime (1.5 g) perioperatively. The main exposures of interest were BMI (5 categories: < 24.9, 25-29.9, 30-34.9, 35-39.9, and ≥ 40) and weight (5 categories: < 60, 60-79, 80-99, 100-119, and ≥ 120 kg). Numbers of TJAs according to BMI categories (lowest to highest) were as follows: 2,956, 3,350, 1,908, 633, and 214, respectively. The main outcome was prosthetic joint infection. The mean follow-up time was 6.5 years (0.5-18 years). RESULTS: 111 prosthetic joint infections were observed: 68 postoperative, 16 hematogenous, and 27 of undetermined cause. Incidence rates were similar in the first 3 BMI categories (< 35), but they were twice as high with BMI 35-39.9 (adjusted HR = 2.1, 95% CI: 1.1-4.3) and 4 times higher with BMI ≥ 40 (adjusted HR = 4.2, 95% CI: 1.8-9.7). Weight ≥ 100 kg was identified as threshold for a significant increase in infection from the early postoperative period onward (adjusted HR = 2.1, 95% CI: 1.3-3.6). INTERPRETATION: BMI ≥ 35 or weight ≥ 100 kg may serve as a cutoff for higher perioperative dosage of antibiotics.
Media Articles on Joint Replacement Restrictions on BMI









Wednesday, July 1, 2015

Lipedema, Part 4: Possible Causes and Associated Conditions

You can read the story of this mother
and daughter with lipedema here.
We have been talking about Lipedema (also spelled Lipoedema, as to the left), sometimes known as "painful fat syndrome," as part of Lipedema Awareness Month.

In this condition, an abnormal overgrowth of fat cells occurs in the legs and lower trunk, sometimes also including the arms or upper body as well.

Lipedema is rarely recognized by doctors. Often it is thought to be simple obesity, or it is confused with "lymphedema," the accumulation of lymph fluid in the interstitial areas.

In Part One of this series, we discussed the typical features of lipedema and how differentiate between lipedema and lymphedema.

In Part Two of the series, we discussed how it progresses, the different Stages of progression, and why it's so important to be aware of lipedema

In Part Three of the series, we discussed the different Types of fat distribution patterns, looked at some pictures to illustrate Type and Stage of lipedema, and detailed how lipedema is diagnosed.

Today we discuss the various theories of what might cause lipedema, as well as conditions that are often associated with it.

In later installments, we will discuss treatment options, as well as practical suggestions on how to deal with lipedema.

What Causes Lipedema?

No one knows what causes lipedema, but there are several theories floating around. More than one of these theories is probably involved.

Hormonal

Since lipedema is diagnosed almost exclusively in women and usually gets worse starting around puberty, most researchers assume it is hormonal:
As lipedema appears to be expressed most commonly at puberty, it is reasonable to assume that hormonal influence underlies the marked female limitation shown in our studies to date
Since lipedema often gets worse during times of major hormonal shifts, like puberty, pregnancy, and perimenopause, many researchers suspect that estrogen somehow plays a role in its development.

The estrogen connection is logical because usually only women are affected. However, occasional case reports of males can be found in the medical literature, usually secondary to other causes like liver issues.

On the other hand, some people with lipedema believe that males are also affected by lipedema but its presentation in males simply goes under-recognized because it does not have the classic pear shape that women get. It might be that male sufferers instead have an increased tendency towards weight gain or lymphedema but avoid the pear shape or extreme leg size that women tend to get.

It is also conceivable that males might merely be carriers of the traits, even if they don't present with symptoms themselves. Either way, it would be revealing to look in more detail at the close male relatives of women with lipedema.

However, estrogen can't be the only answer to lipedema because all women go through puberty, most go through pregnancy and menopause, yet only some develop lipedema. And there are lots of women who develop pretty severe lipedema even when they are childless or have not been through menopause yet. There has to be more to the story.

Estrogen-related events may trigger a cascade of reaction that makes lipedema worse, but it seems obvious that there has to be some other underlying issue to be triggered.

Genetics

It seems clear there is a strong hereditary component to lipedema. Anecdotally, it often seems to be handed down from generation to generation. In the research, reports of family history of lipedema ranges from 16% to 45%.

The hereditary link is not 100%, of course. Few things are. Lipedema can occur without a family history of it. But just as a tendency towards certain heights tends to run strongly in families, so does lipedema.

The picture below shows a mother and a daughter with Type III (full leg) lipedema.

The mother looks to be in Stage 3, with orange-peel texture on her skin, large fat pads on the knees, and the classic bracelet of fat at the ankle.

The daughter looks like she is transitioning into Stage 2. Her skin is mostly still smooth but starting to change, she has overgrowth at the hips, and fat pads are just starting at her knees. The beginnings of a bump at the ankle can be seen if you look closely.

Attempts have been made to document the family trees of people affected by lipedema. Although not every woman in family histories is affected by lipedema, there often does seem to be a history of at least a few women with notably big legs, hips, or arms.

This led some researchers to propose that lipedema is "a genetic condition with either X-linked dominant inheritance or more likely, autosomal dominant inheritance with sex limitation."

However, this has not yet been conclusively proven. At this time, no specific genes responsible for developing lipedema have been identified.

Inflammation

Some researchers now believe that inflammation plays a key role in lipedema. This is the trendy theory on many lipedema websites now, with many women promoting "RAD" (Rare Adipose Disorder) anti-inflammatory diets in hopes of halting the progression of lipedema or lessening its symptoms. One lipedema resource states:
Lipedema is...an inflammatory reaction to our environment, processed foods, high carb diets, hormonal events such as pregnancy and menopause and chronic, everyday, or event related stress.
That seems an overstatement of the evidence to me; we do not really know yet if lipedema is caused by an inflammatory reaction. And lots of other people are also exposed to processed foods, a toxic environment, and extreme stress, yet never develop lipedema. So again, there has to be more to the picture.

However, that's not to say that an inflammatory reaction could not be part of the picture. But is it really the main source of lipedema-related issues?

Many women with lipedema report that at times they have experienced a flare, a sudden MAJOR worsening of their lipedema despite no changes in diet or exercise, sometimes also with lymphedema, infection, or a change in skin texture. Some have come to call this an "inflammatory cascade."

If the inflammation theory is true, then people with lipedema may be able to minimize their condition by avoiding foods that tend to be inflammatory (dairy, sugar, and gluten are the usual culprits named), avoiding stress, and avoiding possible environmental triggers like the chemicals in plastics.

On the other hand, the field of nutrition, weight management, and alternative medicine is filled with fad diets and nutritional trends. The anti-inflammatory diet is extremely trendy these days, so it's not surprising to see inflammation proposed as the cause du jour in various diseases. It's far from proven that inflammation is the main culprit behind lipedema flares, though it could be one piece of the puzzle.

Bottom line, we should not jump to too-broad conclusions about inflammation's role without good supporting evidence. Women with lipedema may have prematurely latched on to an anti-inflammatory diet as a "cure" because it gives them a sense of control and a magical totem against the possibility of developing severe disabling complications.

Lipedema experts these days recommend many different diets, not just anti-inflammatory ones. Take the anti-inflammatory buzz with a big grain of salt, but don't dismiss it either. An anti-inflammatory diet is mostly just common sense, and it's probably good for everyone to avoid plastics and highly processed food anyhow. It's unlikely to harm anyone if it is reasonable and moderate. Women with lipedema may want to try a RAD diet ─ not for weight loss, but to see if it helps their symptoms. But don't take it as a guarantee that it will help.

On the other hand, no one is obligated to follow an anti-inflammatory diet just because they have lipedema. Some lipedema groups lay a pretty heavy guilt trip on anyone not following an anti-inflammatory diet, despite the lack of proof of any benefit from it. Remember, at this point, its value is unproven. In the end it may be shown to have some effect, but at this point, it's all conjecture.

Inflammation is an intriguing theory and deserves to be investigated more thoroughly. However, inflammation is an unproven theory, and this must be kept in mind.

Auto-Immune System

Some people also speculate that lipedema may have an auto-immune component. This seems to tie in with the inflammation theory in that the inflammation may be an auto-immune response to insidious environmental cues around us, including food sensitivities, plastics, or estrogen-promoting foods and substances.

Although there is little proof of ANY of these theories at this time, an auto-immune connection is one theory I am inclined to take seriously, since anecdotally, many women with lipedema also report high rates of autoimmune diseases running in their families, such as thyroid issues or lupus.

Of course, the same argument made against the inflammation theory can be made here. Autoimmune is another trendy theory these days, so caution must be applied when considering it too.

Endocrine Issues

Lipedema often seems to be accompanied by endocrine issues, leading some to speculate that this may be the original trigger for the overgrowth of fat cells or inflammation cascades.

One lipedema article states, "90 per cent of...cases have accompanying diagnoses of hormonal disturbance (thyroid, pituitary, or ovarian)." And the new Dutch guidelines on lipedema encourage testing patients for various endocrine issues.

On the other hand, many lipedema resources do not pay much attention to endocrine problems as a possible cause. In my opinion, this is a vastly under-researched aspect of lipedema and I would like to see MUCH more research done on it in the future.

Honestly, lipedema reminds me a bit of acromegaly. It's not the same condition at all, but the process behind it might have some similarities. Acromegaly occurs when a benign pituitary tumor causes too much Growth Hormone to be produced, and as a result the body size increases immensely, though in different ways than lipedema (affecting bones and certain soft tissues rather than fat cells). People with acromegaly grow so much they can end up very tall, with large hands, feet, jaw, prominent forehead bulges, and enlarged organs.

What if there were something similar happening with lipedema? What if the pituitary overproduces (or underproduces!) an important hormone and this causes hypertrophy/hyperplasia of fat cells? Wouldn't that explain why some people have such overgrowth of fat, despite strict diet and exercise? And why so many people with lipedema seem to have other endocrine issues? And why people get lipedema in such differing severities?

It just seems to me that some sort of endocrine issue HAS to be involved somewhere in this condition, and pituitary seems logical since it is the "master gland" controlling the other glands.

However, as with the other theories, there is no proof of any connection between pituitary issues and lipedema, so this idea also has to be taken with a large grain of salt. 

Abnormalities of the Lymph and Vascular System

It's possible that lipedema may only develop in people with underlying abnormalities in the vascular or lymph system, as one resource notes:
Foeldi and Foeldi have proposed that microangiopathy in the area of the affected adipose tissue sets off the condition leading to increased permeability to proteins and increased capillary fragility. 
Dr. Karen Herbst, one of the most pre-eminent specialists in Rare Adipose Disorders, speculates that abnormalities in the way the body transports fluids is at the heart of the problem in lipedema. She notes:
...Fat in lipedema...[shows] copious amounts of watery fluid upon incision of lesions and of ‘free fluid fat’ in biopsy specimens. The increased fluid suggests a basic abnormality in the interstitial transport and exchange of fluid, with resulting disruption of fat and accumulation of fluid due to increased hydrostatic pressure. So this means that fluid is either entering fat at a faster rate or leaving fat at a slower rate. In fact, both are likely to be true. I think lipedema has problems in both lymphatics and blood vessels.
In other words, the capillaries that supply fat cells in lipedema women are fragile and damage easily, resulting in frequent bruising. In addition, they may be more permeable and leak proteins into the spaces around fat cells. These proteins tend to attract lymph fluids and cause swelling. The lymph system itself may also be somewhat defective, and the two of these factors (vascular permeability and lymph fluid transport issues) can add together to make things worse.

Summary

The bottom line is that nobody really knows what causes lipedema, but it's probably a combination of several things. One recent hypothesis proposes:
Lipedema is an estrogen-regulated polygenetic disease, which manifests in parallel with feminine hormonal changes and leads to vasculo- and lymphangiopathy. Inflammation of the peripheral nerves and sympathetic innervation abnormalities of the subcutaneous adipose tissue also involving estrogen may be responsible for neuropathy. Adipocyte hyperproliferation is likely to be a secondary phenomenon maintaining a vicious cycle.
This is more or less saying "all of the above." In all likelihood there is a tendency to inherit lipedema, perhaps through an underlying problem with the lymph or vascular system. Or perhaps it's underlying endocrine or autoimmune issues, with a strong sensitivity to inflammation and estrogen exposure. Or perhaps it's all of these, or something else entirely.

Whatever the combination is, it tends to create overgrowth of fat cells in certain areas. It is not yet known whether this is due to hypertrophy (an increase in size of fat cells) or hyperplasia (an increase in number of fat cells) but it's probably both.

These fatty deposits have particularly fragile capillaries that tend to leak fluids and proteins. These stress the lymph system over time, leading to the secondary development of lymphedema in some cases.

One major question that lingers in my mind is why some women do not progress very severely in their lipedema, yet other women do. Some never go beyond Stage 1 or Stage 2, yet others rapidly develop Stage 4 lipo-lymphedema. Why do some experience such severe manifestations of this condition and others do not?

If we can figure this out, I believe we will find many of our answers about the base cause of lipedema and how to treat it.

Possible Associated Conditions

Many women with lipedema also have other conditions, commonly referred to as "co-morbidities." Here are a few that are commonly seen.

Hypothyroidism or Other Endocrine Issues

As noted above, there may be a connection between lipedema and endocrine issues.

Two of the leading experts in the field note that many women with lipedema have thyroid issues. If you think you have lipedema and have not been diagnosed with hypothyroidism, you might want to have your thyroid levels checked periodically.

Please note that it's important to read up on the controversies of thyroid testing before having these labs drawn. Have the Free T3 and Free T4 levels checked as well as the TSH levels.

Get your exact numbers, and know how your lab defines normal and abnormal results.  Compare your results to various cut-off recommendations; don't accept just "normal" or "borderline" from your care provider. Different doctors and labs use different cut-off recommendations; the same reading can get you an "abnormal" flag from one provider and a "normal" flag from another provider.

Although not all "borderline" numbers need treatment, many people with borderline thyroid numbers and symptoms find they benefit significantly from treatment. In my non-professional opinion, the presence of lipedema plus a TSH around 2.5 or more and symptoms of thyroid issues deserves consideration of a careful trial of meds, especially if there is a history of autoimmune issues in your family. You may need to seek out a naturopath, integrative medicine specialist, or other "alternative" practitioner in order to get this treatment, however, as many traditional doctors will not treat unless the TSH number is well above 5.5.

Some women with lipedema also find that they have adrenal issues, especially adrenal fatigue. This seems not uncommon in women with thyroid or other endocrine issues. Some lipedema doctors recommend getting adrenal testing to check adrenal functioning. However, whether adrenal fatigue is real is controversial in some circles.

Again, some speculate there is a connection between lipedema and pituitary issues. Since the pituitary is the "master gland" controlling all the other glands, perhaps that is the real source of the thyroid or adrenal issues, rather than something limited only to those specific glands. 

Polycystic Ovarian Syndrome (PCOS)

PCOS seems to be a common co-condition with lipedema, although many women with PCOS do not have lipedema. Since women with PCOS tend to have an excess of estrogen compared to progesterone, and since lipedema seems to be associated with estrogen-related life changes (puberty, pregnancy, perimenopause), it seems logical that there could be a crossover between PCOS and lipedema.

Typically, women with PCOS have "apple-shaped" bodies (lots of abdominal fat but average-sized legs and hips), which doesn't fit the lipedema body type at all. However, some women with PCOS have more of a pear-shaped body and might want to look at the symptoms of lipedema more closely.

Many women with lipedema have symptoms of PCOS and borderline thyroid levels. It's my own unscientific observation that these women often have fibromyalgia as well.

Not much research has been done on a possible connection between PCOS and lipedema, but this is an area ripe for exploration in the future. Best guess is that many women who have both PCOS and lipedema will benefit from treating their PCOS. It won't make the lipedema go away, but it might help lessen its impact and progression.

Insulin Resistance

Many women with lipedema also have strong insulin resistance, perhaps related to concurrent PCOS.

On the other hand, most doctors would blame the obesity common with lipedema as the reason for insulin resistance. But insulin resistance and obesity is a chicken-and-egg question ─ which causes which? Was there an underlying insulin resistance which predisposed the woman to gain a lot of weight and worsen the lipedema? Or did the person gain a lot of weight first and then develop insulin resistance and worsening lipedema?

Women's experiences suggest that the insulin resistance usually comes first and predisposes to everything else later, but it's hard to prove that. And of course, weight gain may make everything worse in a vicious circle.

Either way, if you have lipedema, you should check your insulin levels. If they are high, it would probably benefit you to try to normalize them. It might not affect the lipedema much, but it might help lessen further weight gain, and it probably would lessen the risk for diabetes, stroke, and heart disease later on.

Nutritional Deficiencies

Some resources note that many women with lipedema have very low levels of Vitamin D, iron, and Vitamin B12. No one is sure why this might be, but there are a couple of theories around.

Vitamin D is fat-soluble, so most doctors assume that extra fat sequesters Vitamin D in the body, making it less available in the blood. However, other doctors point out that there is actually no proof of this theory and it's often promoted as fact when it is really just a theory with no supporting evidence. Whatever the reason, many doctors now believe that high-BMI people need higher doses of Vitamin D supplementation than average-sized people.

Low iron levels (or low ferritin levels, which lead to iron-deficiency anemia) may be associated with hypothyroidism. This may particularly be a problem for women in perimenopause, when some experience very heavy periods before their bodies shut down menstrual cycles altogether.

People with hypothyroidism can tend to have lower stomach acid, which may be one reason why they don't absorb dietary iron or Vitamin B12 very well. Low stomach acid can also predispose to intestinal yeast overgrowth, which may also inhibit absorption of nutrients.

If women with lipedema have higher rates of hypothyroidism, and if hypothyroidism tends to lower stomach acid and make it harder to absorb certain nutrients, then it makes sense that women with lipedema might have more nutritional deficiencies. On top of that, years of restrictive dieting and bariatric surgeries like gastric bypass put some women even more at risk.

Some women with lipedema report improvement with an anti-inflammatory diet, as noted above. This diet often involves leaving out dairy and gluten, among other things. Interestingly enough, people with low stomach acid often report having trouble with dairy and gluten. So perhaps there is a connection.

None of these connections have been proven conclusively, but they certainly are interesting. Perhaps taking out dairy and gluten can help, or perhaps increasing stomach acid levels (via daily apple cider vinegar or Betaine consumption) makes it possible to process those foods more easily and improve levels of ferritin, Vitamin D, and Vitamin B12.

Either way, women with lipedema (especially those with hypothyroidism) should watch for nutritional deficiencies and treat if needed.

Eating Disorders

A number of lipedema resources note the possibility of eating-disorders. One clinic in Germany found that 74% of their patients with lipedema had eating-disordered behaviors.

This is probably an overestimate. Most women with lipedema do not have true eating disorders, but some have flirted with them. Others clearly do have eating disorders, and that must be addressed in order to improve health.

Eating disorders can occur with lipedema because people have spent years being shamed and lectured into trying to lose weight. Yet lipedemic fat is extremely resistant. Often their approaches get more and more extreme as each diet fails. Is it any wonder, then, that some develop eating-disordered behaviors?

Some do truly develop into the binge-eating, housebound stereotype that TV programs love to feature. Some overeat for emotional reasons. Some learn to binge and purge to try and control their weight. Others become fat anorexics, following rigid diet restrictions and extreme over-exercising in a futile effort to control their size. The study from Germany found that 16% of their lipedema patients were actually anorexic in their behaviors, more than were bulimic or binge-eaters.

Although most people with lipedema do not have eating disorders, it's important to recognize that some do, and that this is a recipe for serious difficulties. Care providers shouldn't automatically assume that a woman with lipedema has an eating disorder, but if one exists, it is vitally important that it get treated too.

Immune System

Some resources describe a generally depressed immune system in women with lipedema. This may make you prone to easily getting illnesses and having a hard time healing from them.

Whether this is a function of the lipedema itself or the possible accompanying issues (i.e. hypothyroidism, auto-immune issues, chronic nutritional deficiencies) is not clear, but it is probably a good idea to be very proactive about avoiding illness.

Fibromyalgia

Anecdotally, there seem to be a lot of women with lipedema who also experience fibromyalgia. Since some believe that fibromyalgia is an autoimmune issue, the possibility that lipedema also has autoimmune components might explain a connection.

Fibromyalgia is not the same as lipedema, of course, since fibromyalgia patients have tremendous sensitivity to touch/pressure all over their bodies, and pain is mostly limited to the legs in lipedema.

However, perhaps difficulty with efficient lymph drainage explains similar symptoms. One Manual Lymph Drainage (MLD) therapist notes that many women with fibromyalgia find some relief from their pain levels with MLD therapy. Research does seem to support that MLD can be an effective treatment both for lipedema and for fibromyalgia.

Varicose Veins

Many women with lipedema develop telangiectasias, or spider veins.

In spider veins, small red spidery capillaries are visible just beneath the surface of the skin, spreading out like a spider web. This is not dangerous, but some people are bothered by its looks.

If you look very closely you can see spider veins in the picture to the left. Look just above and to the inside of the knees at the faint red lines. (You can see other pictures of spider veins here.)

Varicose veins and Venous Insufficiency can also be a problem for some people with lipedema. Good blood flow can be impeded by the extra fat deposits and the fragility and permeability issues. This may lead to blood pooling in some areas instead of circulating efficiently.

Hypermobility

Some resources have noted that many women with lipedema tend to be hypermobile, that is, their ligaments tend to be looser than average and therefore the women more flexible, at least in childhood.

This seems to be borne out in anecdotal evidence, though the hypermobility can vary from mild to significant. This can then lead to joint issues later in life.

Fallen Arches

Some lipedema resources report that "flat feet" (a.k.a. fallen arches) is more common in women with lipedema.

Is this just a function of a typically higher weight, or is this related to the lax ligaments and hypermobility that some have noted with lipedema? No one is sure, but it does seem logical that if lipedema women have hypermobility and joint issues, they might also tend to have fallen arches.

Joint Issues

Knee osteoarthritis is another issue common to women with lipedema. One 2009 study found that more than half of their patients diagnosed with lipedema also experienced significant knee pain.

Knee osteoarthritis seems to be common as people with lipedema age, and at a fairly early onset compared with the general population. One resource notes "early onset of degenerative joint changes and arthritis" among the symptoms commonly associated with lipedema. 

Of course, some providers question whether knee arthritis is more common simply because women with lipedema tend to be heavier. However, the authors of the 2009 study noted (my emphasis):
Knee pain is a feature of lipedema, but can also be found in simple obesity. Nevertheless, it appears to be a phenotypic feature and is often a complaint in pure lipedema where the BMI is normal.
Doctors think that this increased rate of joint issues is probably because of three different factors. First, because the fat deposits tend to have pockets of fluid around them and because lymph flow is inhibited, this excess fluid will tend to flow to areas of least resistance ─ the joints. This can irritate the joints and cause pain.

Second, as lipedema progresses, fat pads around the knees build up and can alter the mechanics of the knees. The gait may be thrown off and stress the knees.

Third, hypermobility issues may exacerbate joint issues. As women with lipedema age, this hypermobility combines with gait changes and fluid irritation in the knee to result in significant knee pain and rapid development of arthritis, especially in the face of an injury or trauma to the area.

Muscle Weakness

In addition to joint issues, there may be an increased level of muscle weakness, as well as weak connective tissue and joint laxity in those with lipedema.

This is a significant finding because one way to treat knee issues is to strengthen the muscles around the knees. However, if these muscles weaken as lipedema worsens (and do not respond to physical therapy and strengthening exercises), that may be another reason why mobility can be so affected.

Mobility Issues

Between the joint issues, hypermobility, muscle weakness, pain, and lipo-lymphedema, mobility issues often become very significant in people with lipedema as they age. 

Unfortunately, many people with lipedema are denied joint replacement surgery because they have elevated BMIs and doctors refuse to operate on them until they lose weight. But significant weight loss to "acceptable" BMIs is nearly impossible for people with lipedema, so they are never able to get their knees or hips replaced, and their increasing pain levels continues to decrease their mobility. Some end up in wheelchairs or scooters, and this lack of mobility creates even more lymphedema and fat deposits in a vicious feedback loop.

That's why it's so important to stay as active as your circumstances permit. It slows the progression of lipedema and lymphedema, as well as being good for your heart and other systems.

Mobility issues is another reason why it's so important that lipedema becomes more recognized as a medical condition deserving treatment.

At this point, the medical stigma of obesity among many doctors means that this condition often goes undiagnosed, with unrealistic weight loss prescribed when symptoms arise. Sufferers are often denied access to the treatments that do work until they become progressively more disabled and immobile, and then are made fun of in society when they use mobility aids like scooters.

It's only by raising awareness of lipedema and its treatments that more women will get the treatments that will help most and the stigma surrounding this condition will diminish.

Skin Infections

Cellulitis infection with lipo-lymphedema;
notice the foot swelling from secondary lymphedema
Another common problem in the latter stages of lipedema is skin infections.

This is usually not a serious issue until Stage 3 lipedema, or if secondary lymphedema starts to develop. However, sometimes things like bug bites or a seemingly minor cuts or burn can result in serious swelling, redness, and infection, even in the earlier stages of lipedema.

This means that all people with lipedema need to be very vigilant in caring for their legs and watch for minor problems before they develop into major ones.

Erysipelas and cellulitis (bacterial infections of the skin and underlying tissues) are a problem in some people as lipedema becomes severe, and it can be hard to treat because decreased lymph flow inhibits healing.

Infections secondary to lipolymphedema are hard to heal. Many care providers prescribe inadequate dosages of antibiotics in heavier people with skin infections, not realizing that weight-based dosing is needed with some types of antibiotics, or unnecessarily worrying about overloading the person's kidney function.

If not stopped with antibiotics, a skin infection can spread to deeper layers and become necrotizing fasciitis. If it gets into the blood system, a person can get sepsis and even die. Therefore, preventing, watching for and early treatment of any skin infections is an important part of care in people with lipedema, especially in the later stages.


When high BMI people go to the E.R. with cellulitis or other skin infections, they are often under-dosed with antibiotics, even in hospitals that specialize in treating heavier people. 

This is a MAJOR problem. Research shows that high BMI people, especially people with a BMI over 50, are often given an antibiotic dose that does not reach full inhibitory response. This may result in an initial improvement of symptoms, but a drastic relapse later on as the bacteria mutate and adapt to the inadequate dosage of antibiotics.

If you have lipedema and develop a serious skin infection, you may need to be very proactive in advocating for yourself. Ask for a wound infection specialist, ask if the type of antibiotic they are prescribing should have weight-based dosing (some do and some don't).

If the wound does not respond well, ask about more proactive wound care, including IV antibiotics, more frequent dosing, and larger doses, as research shows that proactive care like this can improve outcomes better than traditional care.

Summary

As we have discussed in this series, lipedema is a condition that is often mistaken for simple obesity. Diets and weight loss do not substantially reduce its presence, and lipedema often gets worse as people age, sometimes leading to significant mobility issues and life-threatening infections.

Many fat people with lipedema go undiagnosed for years because physicians either have not been taught about this condition (despite it having been discovered in 1940), or have so much weight stigma that they do not recognize the condition as anything other than obesity. Some even deny it is a real clinical entity, despite the fact that is recognized as one by many groups, including the NHS in the U.K.

Fat disorders are only now beginning to get the research attention needed to expand our knowledge but recognition of this disorder still has a long way to go in many parts of the world. Thus many people with lipedema will likely continue to go undiagnosed for some time to come.

Many women discover their condition via massage therapists or physical therapists rather than doctors because doctors are so under-informed about lipedema. Even today, women are being told that there is "no such thing" as lipedema, that they just need to lose weight, to exercise more, or that they are just making excuses for being fat and lazy.

Others are accused of lying about their food intake or exercise habits. Friends, family, and acquaintances may harass them about their weight and think that "lipedema" is just making excuses for bad habits.

Some lipedema sufferers are diagnosed with lymphedema without any mention of lipedema. Some are only diagnosed with lipedema once significant lipo-lymphedema develops and their condition becomes very severe. The fact that many cases of lipedema are only diagnosed after severe lipo-lymphedema develops is a sad statement about the ignorance of lipedema among most doctors.

Even once a woman has a diagnosis of lipedema, care providers can be very apathetic about managing it, or overly pessimistic about its progression so they don't bother providing much care. Women with lipedema often have to fight for adequate care or insurance coverage of needed treatments.

No one really knows what causes lipedema but it likely is hereditary in many cases. It may involve some sort of endocrine, inflammation, and/or auto-immune disorder, and there may also be underlying abnormalities in the lymph or vascular system. As one resource puts it:
Often mistaken for obesity or unusual weight gain, lipedema is a fat-storage disease that almost exclusively affects women...This chronic disorder affects the legs and arms, causing an abnormal accumulation of fat cells that produce a noticeably disproportionate appearance. There's a genetic component in approximately half of all lipedema cases, and it's not just being overweight or out of shape -- it's truly a disproportion in the affected areas of the body. It's a condition that is not only an overgrowth of fat tissue, but it also has a vascular or lymphatic component with swelling.
In other words, it's really NOT about diet and exercise, but about something we don't completely understand yet. Hopefully, finding and treating the hormone or endocrine issues and/or reducing inflammation as much as possible will help. It likely won't make the lipedema go away, but it might help minimize it or slow the progression.

More care providers need to familiarize themselves with lipedema so women get diagnosed and treated earlier to keep the condition from progressing. Furthermore, if complications such as knee pain, cellulitis, or lymphedema occur, care providers need to know how to treat them appropriately, instead of just telling the patient to lose weight, as so often happens now.

As one research summary notes:
Lipedema is a genetically mediated disorder of fat deposition. It results in a characteristic pattern of lower-extremity enlargement that is resistant to diet and thus very demoralizing. It can eventually lead to lymphedema but should not be mistaken for lymphedema in its early stages...This frustrating genetic disorder of fatty deposition is not particularly rare, but is rarely diagnosed because clinicians fail to recognize it.
Hopefully, once more doctors get past their stigma and prejudices about obesity, more research will be done into how to treat (and hopefully prevent) lipedema.

*Next post: Treatment options



References and Resources

If you think you have lipedema and need help in getting it diagnosed, see this resource. Also print out some of the papers from the links below and take those to your appointment with you. Remind your doctor that this condition is now recognized by the National Health Service in the U.K. and that there is information online about how to diagnose and treat it.

Resources

*Trigger Warning: Many of these sites are not size-friendly. However, because they also contain valuable information about lipedema and its treatment, they are included here.
Blogs, Websites, and Facebook Pages from Those Dealing with Lipedema
Possible Causes of Lipedema

Child AH, Gordon KD, Sharpe P, Brice G, Ostergaard P, Jeffery S, Mortimer PS. 2010. Lipedema: An inherited condition. Am J Med Genet Part A 152A:970–976. PMID: 20358611 Free full text available here.
Lipedema is a condition characterized by swelling and enlargement of the lower limbs due to abnormal deposition of subcutaneous fat. Lipedema is an under-recognized condition, often misdiagnosed as lymphedema or dismissed as simple obesity. We present a series of pedigrees and propose that lipedema is a genetic condition with either X-linked dominant inheritance or more likely, autosomal dominant inheritance with sex limitation. Lipedema appears to be a condition almost exclusively affecting females, presumably estrogen-requiring as it usually manifests at puberty. Lipedema is an entity distinct from obesity, but may be wrongly diagnosed as primary obesity, due to clinical overlap. The phenotype suggests a condition distinct from obesity and associated with pain, tenderness, and easy bruising in affected areas.
Med Hypotheses. 2014 Aug 23. pii: S0306-9877(14)00295-3. doi: 10.1016/j.mehy.2014.08.011. [Epub ahead of print] Pathophysiological dilemmas of lipedema. Szél E1, Kemény L2, Groma G2, Szolnoky G2. PMID: 25200646
Lipedema is a common, but often underdiagnosed masquerading disease of obesity, which almost exclusively affects females. There are many debates regarding the diagnosis as well as the treatment strategies of the disease. The clinical diagnosis is relatively simple, however, knowledge regarding the pathomechanism is less than limited and curative therapy does not exist at all demanding an urgent need for extensive research. According to our hypothesis, lipedema is an estrogen-regulated polygenetic disease, which manifests in parallel with feminine hormonal changes and leads to vasculo- and lymphangiopathy. Inflammation of the peripheral nerves and sympathetic innervation abnormalities of the subcutaneous adipose tissue also involving estrogen may be responsible for neuropathy. Adipocyte hyperproliferation is likely to be a secondary phenomenon maintaining a vicious cycle. Herein, the relevant articles are reviewed from 1913 until now and discussed in context of the most likely mechanisms leading to the disease, which could serve as a starting point for further research.
Lipedema and Undertreatment of Skin Infections

Am J Emerg Med. 2012 Sep;30(7):1212-4. doi: 10.1016/j.ajem.2011.05.027. Epub 2011 Dec 12. Underdosing of common antibiotics for obese patients in the ED. Roe JL1, Fuentes JM, Mullins ME. PMID: 22169576
BACKGROUND: ...Obesity alters the pharmacokinetic profiles of various drugs. Although there are guidelines for dose adjustments for many of the antibiotics commonly used in the emergency department (ED), they are seldom used. METHODS: This is an institutional review board-approved retrospective study at an American Society of Metabolic and Bariatric Surgery Center of Excellence and a level I trauma center with annual ED volumes of more than 80,000 visits. Data were retrospectively collected from ED pharmacy records during a 3-month period in 2008. Any first dose of cefepime, cefazolin, or ciprofloxacin administered in our ED to a patient recorded as both more than 100 kg and with a body mass index greater than 40 kg/m(2) was compared with our hospital guidelines and found to either adhere or not adhere to those guidelines. RESULTS: ...Adherence rates for first dose of cefepime, cefazolin, and ciprofloxacin administered, respectively, were 8.0%, 3.0%, and 1.2%. CONCLUSION: Emergency physicians frequently underdose cefepime, cefazolin, and ciprofloxacin in obese patients. Underdosing antimicrobials presents risk of treatment failure and may promote antimicrobial resistance. Education is necessary to improve early antibiotic administration to obese patients.
J Prim Care Community Health. 2015 Apr 29. pii: 2150131915583659. [Epub ahead of print] Cellulitis in Obesity: Adverse Outcomes Affected by Increases in Body Mass Index. Theofiles M1, Maxson J2, Herges L2, Marcelin A3, Angstman KB2. PMID: 25925834
...This study was a retrospective chart review of 637 adult primary care patients designed to evaluate rates of treatment failure of outpatient cellulitis among patients of varying BMI. Treatment failure was defined as (a) hospital admission for intravenous antibiotics, (b) prolonged antibiotic course, or (c) requiring a different antibiotic after initial course. RESULTS: Adverse outcomes were not statistically significant between normal BMI and those with BMI ≥40 kg/m2. A subset of patients with a BMI ≥50 kg/m2 was noted to have approximately twice the rate of adverse outcomes as the normal BMI group...CONCLUSIONS: Patients with cellulitis weighing >120 kg or with a BMI ≥50 kg/m2 were at greatest risk for treatment failure in the outpatient setting, even when controlling for comorbid diabetes and tobacco use. As morbid obesity continues to become more prevalent, it becomes imperative that primary care physicians have better antibiotic dosing guidelines to account for the physiologic effects of obesity to minimize the risk of increased morbidity, health care costs, and antibiotic resistance.