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Brain damage can occur following bariatric surgery, which is often done to help patients lose a lot of weight and, hopefully, keep it off. The damage is due to a lack of thiamine, also called vitamin B1.
Patients who have had bariatric surgery may not be able to get enough nutrients from their diet due to their limited ability to eat. In addition, their ability to absorb nutrients may be impaired, and their reserves of vitamin B1 (thiamine) may become severely depleted.
They may go to emergency departments due to mental confusion, vomiting, impaired balance or movement (ataxia), and eye movement problems (typically, nystagmus, in which the eyes move repetitively).
If an emergency room doctor fails to diagnose and treat a patient quickly in the right way, immediately administering high doses of vitamin B1, that person could suffer irreversible brain damage.
Weitz & Luxenberg P.C. is now accepting cases of adults or adolescents who underwent bariatric surgery and were later diagnosed with Wernicke’s encephalopathy (also called Wernicke encephalopathy). We are helping clients with cases of hospitalization due to brain injury or death after being misdiagnosed or receiving a delayed diagnosis of Wernicke’s encephalopathy by an emergency room physician.
Bariatric surgery, including procedures such as Roux-en-Y gastric bypass, laparoscopic adjustable gastric banding (“lap band” surgery), sleeve gastrectomy, and duodenal switch with biliopancreatic diversion, can lead to a state of nutrient starvation.(1) (2)
Patients may not appear to be starving after bariatric surgery, as patients are typically severely overweight or obese when having these types of surgical procedures. However, due to lower food consumption necessitated by their bariatric surgery, impaired ability to absorb nutrients, or these combined with other risk factors, they may not actually be getting and absorbing adequate vitamins. Deficits in certain vitamins, such as vitamin B1 (thiamine) can lead to serious, life-threatening problems.(3)
Patients with Wernicke’s encephalopathy may develop serious neurological impairments and defects that can be life-threatening. This condition typically can be treated if the patient begins receiving adequate thiamine supplementation right away. However, it is often missed because many emergency room physicians fail to recognize and correctly diagnose and quickly treat this subset of patients.(4)
Timely and correct diagnosis and treatment of Wernicke’s encephalopathy are critical. Patients who have undergone bariatric surgery typically develop symptoms of Wernicke’s encephalopathy within six months postoperatively, but there are some cases reported in the literature with much longer latencies.(6) (7)
Any diagnostic delay can result in irreversible brain damage. The longer the delay in diagnosing a patient with Wernicke’s encephalopathy, the greater the risk of life-long brain damage or death.(8)
The most common symptom of Wernicke’s encephalopathy is ataxia, which may appear as “gait abnormalities up to the full inability to walk or move.” The second most common is altered mental status, “presenting itself as delirium, confusion, and problems in alertness or cognition.” The third is eye movement disorders, typically nystagmus, in which the eyes move repetitively, or ophthalmoplegia, which is paralysis or weakness of the eye muscles. Often patients will have all three of these symptoms.(9)
When patients arrive at an emergency department with the abovementioned symptoms and a history of bariatric surgery, physicians should have a high degree of suspicion for a diagnosis of Wernicke’s encephalopathy.
Without timely and appropriate administration of thiamine, patients with Wernicke’s encephalopathy could become comatose, die, or be left with lifelong debilitating cognitive and motor impairments.(10)
If a misdiagnosis or delayed diagnosis of Wernicke’s encephalopathy happened to you or a love one, contact us. We can serve as your Wernicke’s encephalopathy lawyer in your medical malpractice lawsuit.
Wernicke’s encephalopathy is a severe but preventable syndrome. It can be a life-threatening medical condition that impairs how the brain works.
This syndrome results from vitamin B1 deficiency.(11) If not diagnosed and treated promptly, a patient may experience irreversible, lifelong brain impairment.(12)
Wernicke’s encephalopathy is a possible complication following gastric bypass surgery.(13)
Although patients who have undergone bariatric surgery may develop Wernicke’s encephalopathy within just weeks or months of having the surgery, the risk of developing the condition is possible for many years postoperatively.(14)
There has been at least one case where a patient developed Wernicke’s encephalopathy 28 years after undergoing a gastrectomy.(15)
Some patients who are treated for Wernicke’s encephalopathy show improvement shortly after receiving a regimen of vitamin B1. Sometimes, even if a patient receives treatment of vitamin B1 to treat thiamine deficiency, neurological deficits may persist.
In fact, as many as nearly one out of two patients with Wernicke’s encephalopathy may never fully recover.(16)
Many patients who undergo gastric bypass surgery may also have diabetes. Diabetes has unique complications of its own in relation to Wernicke’s encephalopathy.(17)
In cases of a patient with Wernicke’s encephalopathy who has diabetes, medical personnel who miss the diagnosis or Wernicke’s encephalopathy may treat patients with intravenous fluids, including dextrose. However, “providing dextrose-containing fluids without thiamine supplementation to at-risk populations” may pose significant dangers to these patients and further complicate the clinical course of the Wernicke’s encephalopathy.(18)
Glucose, or sugar, metabolism requires thiamine; “increasing glucose levels can deplete already-low thiamine stores.” When treating patients with diabetes who have undergone bariatric surgery and are showing symptoms of Wernicke’s encephalopathy, physicians must make sure patients receive appropriate amounts of glucose along with appropriate thiamine supplementation. This is critical so the increases in circulating blood sugar do not further deplete the patient’s already low thiamine levels.(19)
Both Wernicke’s encephalopathy and Korsakoff syndrome seem to arise from deficient thiamine levels. Most healthy adults need about one milligram of thiamine per day. A person’s body holds roughly 20 days’ worth of thiamine in reserve.(20)
If thiamine reserves are depleted, patients may show signs of Wernicke’s encephalopathy shortly thereafter. If people with Wernicke’s encephalopathy are not treated immediately, their condition may continue to worsen and progress to a chronic syndrome, known as Korsakoff syndrome.(21)
Korsakoff syndrome patients may have persistent, severe memory impairment. Patients may confabulate, which means they may not remember experiences fully or accurately, and they may invent or try to fill in the blanks by fabricating memories.(22)
Sadly, by the time a person has been diagnosed with Korsakoff syndrome, the condition likely will not respond to thiamine supplement. Specific neurons in the brain may have been damaged beyond repair. This brain injury and impairment may be permanent.(23)