The Story #10: The Colonoscopy

On May 12, 2005 Gastroenterologist Dr. Ronald Barkin performed a colonoscopy at Inova Alexandria Hospital. The operative report noted findings of small internal hemorrhoids and notable diffuse inflammatory change with ulceration in the descending colon, the sigmoid colon and rectum. The surgical pathology report confirmed the presence of prominent infiltrate of lymphocytes, neutrophils and eosinophils within the lamina propria and surface erosion but no actual crypt abscesses. Colonoscopy examination images showed erythema (redness of the skin caused by capillary congestion) in the descending and sigmoid colon as well as the rectum and abnormal colonic mucosa mid-sigmoid. I was puzzled to read in the pathologist’s report that the biopsies were taken from the descending colon when the abnormal mucosa was mid-sigmoid.

At the office follow up visit, reading from notes in a stenographer’s notebook, Dr. Barkin revealed that inflammation in the colon was causing swelling that severely reduced the size of the opening between the large intestines and the rectum. This condition, he said, was causing a bottleneck and back up of mucus-entwined fecal matter in the large intestines and severe constipation. The mucus-entwined fecal matter, he said, had coated the folds in the intestines. He said that fistulas were beginning to form which may be attaching the rectum to other organs. He said in light of this, it was not unusual that I was experiencing IBS symptoms and that it was possible I had Crohn’s disease. He said diagnosis of Crohn’s or the extent of the fistula activity could not be determined by colonoscopy. He also said he saw ulcerations that looked like someone had put out cigarettes in my intestines.

When I asked for a copy of the operative report, he said he changed the diagnosis from ulcerative colitis to general non-specific colitis on his written report to the insurance company (Cigna) and my primary care physician, so as not to chance my medical insurance being cancelled. By downplaying the extent of problems found during the colonoscopy on the written report, Dr. Barkin made it infeasible for me to get the necessary gastrointestinal laparoscopic surgery and intensive intravenous treatment I need to remove adhesions and correct colon swelling.

When I mentioned to Dr. Silis that Dr. Barkin told me he downplayed my diagnosis from ulcerative colitis to nonspecific colitis so that my insurance wouldn’t be cancelled, Dr. Silis said he had never heard of such a thing and dismissed the thought. It didn’t matter that the operative report is somewhat contradictory from the stated diagnosis in its description of the presence of ulcerations. Once Dr. Silis saw the diagnosis of colitis, he determined my condition was not serious, and his entire demeanor toward me changed as if I was no longer someone to be taken seriously. After all, whom would you believe? The short person who looks like a kid or the prominent doctor who you’ve known for years?

It’s baffling to me that some doctors don’t give a second thought to “doctoring” or “tailoring” their reports to reflect a malady less severe than the disease they found. Then again, this case may simply be indicative of the physician’s personality. On one office visit I found Dr. Barkin preoccupied with trying to figure out a way to keep from having to pay higher scuba insurance premiums for an upcoming trip.

Dr. Barkin prescribed Asacol, medicine typically used to treat ulcerative colitis, to reduce the inflammation. He suggested pursuing other diagnostic procedures if painful symptoms persisted. While somewhat helpful in reducing systemic inflammation, particularly in my head, the Asacol did nothing to correct the bottleneck in my large intestine — a condition that likely existed over a predominance of a lifetime but had now become intolerable. Only by reducing the consistency of fecal matter to diarrhea through the use of cascara sagrada and colon cleansers and with the use of enemas was I able to have a bowel movement. From as long ago as I can remember, nausea and painful contractions accompanied going to the bathroom. It seemed to me that a pouch had been created at the site of the stricture and no oral medication was going to do the trick alone. I needed surgery and intravenous fluids to address the infection, my electrolyte imbalance and give my intestines time to heal. I also needed someone to do a proper biopsy and sensitivity test on the identified pathogen(s) to determine optimal treatment protocol.

One possible explanation for my condition was toxic colitis, a particularly severe complication that involves damage to the entire thickness of the intestinal wall. The damage causes ileus, a condition in which the normal contractile movements of the intestinal wall temporarily stop so that the intestinal contents are not propelled along their way. Abdominal expansion or distention occurs. X-rays of the abdomen show gas inside the paralyzed sections of the intestine. Flare ups of inflammation are the same as those with Crohn’s disease.

A colonoscopy confirms a diagnosis of toxic colitis and lets the doctor observe the extent and severity of the inflammation. Even during symptom-free periods, the intestine rarely appears entirely normal, and tissue samples removed for microscopic examination usually show chronic inflammation. Some people may have ulcerations from an undetected infection rather than true ulcerative colitis. Treatment aims to control the inflammation, reduce symptoms and replace lost nutrients and fluids. Surgery is performed on a non-emergency basis when precancerous changes (dysplasia) are identified or because of a narrowing of the large intestine. This description fit my situation precisely.

A second CT scan of my abdomen and pelvis taken on June 7, 2005 confirmed previous findings of a colon filled with “a moderately large amount of stool throughout the ascending, transverse and descending colon.” Dr. Carlos Artiles, the radiologist, noted that the degree of constipation was somewhat improved compared to the previous study completed March 11, 2005, but noted the presence of “a moderate to severe degree of constipation.” In his report summary, Dr. Artiles again notes: “There is stool and fluid throughout the colon…” Based on this, I found it curious that Dr. Barkin’s notes to my PCP, Dr. Silis, dated June 17, 2005 states that the June 7th CT scan “showed much less stool and less inflammatory change, the details of which are to be reviewed once study is obtained.”

When I asked Dr. Barkin to clarify the radiologist’s report, Dr. Barkin suggested I get a second opinion and recommended the Association of Alexandria Radiologists (AAR), which completed the CT scan in question. Steve Richardson, the AAR office manager, told me he needed the previous radiologist’s report in order to provide an independent second opinion of the scan. He said because radiologists don’t speak directly with patients, he would have Dr. Michael Freedman, the radiologist, call the results into Dr. Barkin. Dr. Barkin later told me that Dr. Freedman said that the original report “was about right.” This was useless information to someone seeking to understand the significance of the report’s findings and flush out the discrepancy between the radiologist’s and Dr. Barkin’s notes. The June CT scan report was not nearly as detailed and precise as the March CT scan report taken at Fairfax Radiology. In fact, I suspect the quality of the second scan was compromised based on the radiologist’s further notes, which stated he had difficulty visualizing the pelvic organs due to “very little fat planes.”

“That’s about right.” Dr. Ronald Barkin’s response to my request for an interpretation of the radiologist’s report.

I know it’s not easy comparing radiographs and picking out the changes. It takes me forever to identify the dozen or so modifications made to one of the two side-by-side photos in the Sunday Washington Post Magazine. And I know radiologists don’t get nearly that amount of time to look at patient scans. That’s why I think it’s important for radiologists to speak with patients about their scans. That radiologists aren’t permitted to speak directly with patients is wrong. So is billing the patient and medical insurer for an office visit with the radiologist in addition to the fee for the CT scan when such visits aren’t permitted and never occurred.

In July 2005, I was surprised to receive an invoice for a $15 co-pay from Computed Tomography Associates, PC (CTA), the billing service for AAR, which performed the CT scan. Lilly at CTA told me that CTA considered the radiologist’s time for reading the scan as an office visit and that Cigna had already paid its share of the fee for the fictitious office visit. An office manager at AAR confirmed that AAR regularly bills for both the scan and a separate office visit with the radiologist even though there is no actual meeting between the patient and the radiologist.

I never paid the $15 co-pay. There was no co-pay required for CT scans under my Cigna plan. It took several phone calls to Cigna and CTA customer care over a few months and various inane conversations that focused on my co-pay status rather than on AAR’s breach of contract with Cigna to get the matter rectified. All this wasted time and energy for a poorly written report that concentrated predominantly on the amount of stool and fluid in my colon and the fact that the pelvic area could not be visualized well.

I think it’s difficult for people to imagine that which they haven’t experienced firsthand. That’s why many physicians don’t consider chronic constipation a serious complication. They dismiss the condition with recommendations to use suppositories, laxatives or increase fiber and water intake. Well if you consider an obstructed intestine is like a kinked water hose, it’s not hard to see that no amount of streaming water is going to straighten out the hose so that it functions properly. More likely, you’ll end up with a bubble at the kink that bursts and springs a leak from the build up of water pressure. I think that’s what’s happening inside of me. The kink is likely my redundant cecum.

As we age, the intestinal tract lining becomes covered with hard fecal matter and mucus, which makes absorption of nutrients more difficult. Fecal deposits can irritate nerve endings in the colon which leads to spastic or inflamed colon. Both of these conditions interfere with bowel function and with proper absorption of nutrients. In addition, the impacted deposits decay after a time which releases toxins that seep into the bloodstream poisoning the organs and tissues.

Resultant constipation slows down food transit time. When transit time slows, putrefied fecal material stays in the colon longer. This, in turn, can lead to a buildup of toxic material along the intestinal walls which not only reduces the absorption of nutrients and but also increases the absorption of toxins. This absorption of toxins is a form of self-poisoning or autointoxication. Decaying food ferments, forms gases as well as various digestive byproducts and toxins, which enter the bloodstream and lymphatic system, settle into tissue, hence creating many disease states including autoimmune disorders. Colon cancer, the second leading cause of death in the U.S., results from years of autointoxication.

A study, published in the Journal of the American Medical Association in 2008, suggested that more careful colorectal cancer screening is necessary. In traditional colonoscopies, long considered the gold standard test for detecting colon cancer, a doctor snakes a long, thin tube equipped with a small video camera through the large intestine to view the lining. Doctors use the device to cut away a tissue sample or remove polyps. This medical study found that flat growths on the colon wall are more likely to be cancerous than the more familiar knobby masses or polyps that gastroenterologists are used to finding.

This makes me wonder if the surface ulcerations which Dr. Barkin noted on the colonoscopy report might have been cancerous flat growths. I also find it curious that those involved don’t care that biopsies were taken from areas other than where photos indicate abnormal mucosal tissue was detected. It’s as if performing biopsies was, as one doctor put it, like playing the mechanical claw game for toys and prizes — you get what you can. I’d like to think there’s a bit more at stake here and that modern medical equipment is a bit more sophisticated.

Physicians ask me if I’m so sick, how come I’m not in the hospital? In my search for competent care, I found a pervasive belief among doctors and patients alike that seriously ill people go to the emergency room and are treated in hospitals, not by outpatient doctors. I also found in my attempt to be treated in the ER in 2003 for what I suspected was internal bleeding that the ER’s mission is to stabilize patients, not necessarily to treat them.

Doctors told me that if I had such a serious condition, I’d appear to be much sicker than I appeared to them in that instant. I suppose I could go to the doctor’s office and make all the gross sounds that sick people like me typically make at home alone in their bathrooms. Then again, there’s no pleasing some folks no matter what you do. It’s doubtful that without a double blind study backing my contentions that they’d believe me anyway. Do they really want me to delve into a dissertation on abdominal distension and painful gas formation? Should I elaborate on the feeling of incapacitating nausea, occasional vomiting and bright red blood in the feces? For one thing, there’s not enough time to impart this during your typical doctor’s office visit. I’d like a doctor to do me a favor and show me a photo of what he considers to be a sick outpatient — not someone on his deathbed now too sick to help — but someone sick who is still considered viable enough to reclaim his health.

Malcolm Gladwell, in his book, Blink, talks about the benefits and failures of rapid cognition — the decisive glance that knows in an instant. I found that medical personnel often employ this instant decision making phenomenon in deciding whether a patient is seriously ill by the way the patient looks. Many doctors place more emphasis on superficial visual observation of the patient in reaching a diagnosis than on positive test results. They equate being seriously ill with the appearance of intensive care patients on their deathbed.

Such thinking is evidenced by the wording in my medical record from a 1983 Georgetown University Hospital hospitalization for internal bleeding, which states: “Physical examination revealed a well developed, pale, white female in no apparent distress.” I was eventually admitted with gastrointestinal bleeding, lavaged and transfused with two units of packed red blood cells. With no obvious outward signs of illness or distress, ER attendants kept telling me to get up and leave. But I couldn’t walk. It didn’t matter that I had been transported to the hospital by ambulance after collapsing to the floor at work.

What they didn’t see was the pool of blood in my stomach from internal bleeding ulcers. While many people with internal bleeding also bleed from the anus, my intestinal obstruction prevented this from occurring. It wasn’t until after I nearly banged my head on some equipment and fell to the floor trying to comply with their insistence that I get up that one ER attendant decided to try “one more thing.” She ran a thin tube through one of my nostrils and down my esophagus. When it reached my stomach, blood gushed forth like gasoline flowing from a siphoned hose.

This subjective bias or rapid cognition was evident in various comments in Dr. Barkin’s reports to Dr. Silis. In his June 17, 2005 report, Dr. Barkin wrote: “The patient had previous colonoscopy revealing nonspecific colitis, which I have treated with Asacol and according to the patient she has had significant improvement in symptoms.” I wish this was true. What I said in response to his question, “Are you better?”, was that the Asacol was somewhat helpful, but that I did not want to use the word “better” because this would connote an improved status of my condition, which had not occurred. I can see now that this was too wordy for Dr. Barkin who preferred more direct, short, black and white, definitive yes or no answers.

The April 29, 2005 report stated that I had no nausea or vomiting. When Dr. Barkin asked me if I was experiencing nausea, I told him I was hospitalized with bleeding ulcers in 1983 and was treated with intravenous cimetidine. I said I’ve been eating Tagamet and Zantac tabs like candy daily ever since because just about everything I eat gives me acid indigestion and acid reflux. “Does the Tagamet stop the indigestion?” he asked. “Yes,” I said. “At least until I eat something else.” “Did you take any Tagamet or Zantac before coming here?” he asked. “Yes,” I replied. “Are you nauseous right now?” “No,” I replied.

When I asked Dr. Barkin about the repercussions from “leaky gut” syndrome or intestinal permeability, he replied that he could not address the issue because once a substance leaves the digestive tract, it was out of his realm (specialty). In “leaky gut” the intestines become porous and allow tiny particles of undigested food to enter the bloodstream.
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On June 16, 2005 the pain in my back was so severe from amassed crystals passing through the kidneys, I called Dr. Silis and asked him to prescribe a pain killer. He said no. I told Dr. Silis that both kidneys hurt with pain radiating down the legs. He told me to go to Urgent Care, have my urine tested and if needed, they would write a prescription for an antibiotic. He told me to keep my appointments with the referred nephrologist and urologist, and through the process of elimination, they would find out what is wrong with me.

When speaking with Dr. Silis, I must have insinuated something derogatory about my experiences with doctors because he told me to stop “nit picking” the doctors he referred. I had an inkling that Dr. Silis’ wife’s obstetrician to which he had referred me for endometriosis treatment had complained about me. Dr. Silis asked me where I preferred to go — Georgetown? Johns Hopkins? I told him I just wanted competent care and a comprehensive diagnosis. He said, “You have all those reports.” I said, “Yes, reports — test results — listing my deficiencies. I need a doctor who can put 2+2 together and give me a diagnosis.” He said you have a diagnosis – colitis. I told him that’s just a symptom. He said a symptom is pain; colitis is a diagnosis. I told him what’s causing the colitis is the diagnosis. I told him my mom had the exact same symptoms before she died of cancer July 3, 1997. He then pointed out that the CT scan was an excellent diagnostic tool for cancer.

I wanted to make a smart ass remark about doctors looking to radiologists and others to make the definitive diagnosis, but I kept quiet. Radiologists and lab technicians report findings. It’s not their job to analyze these findings and make definitive diagnoses. That was the physician’s responsibility. Hadn’t Dr. Schuffler’s letter warned about Dr. Berman’s CT scan finding of a suspicious, possibly cancerous mass? What about the positive test marker for colon cancer? Results forgotten by doctors too busy going through the motions their attorneys told them would protect them against malpractice claims. Results each doctor figured some other doctor was responsible for noticing and acting upon. The practice of providing medical care had been reduced to nothing more than the practice of accumulating metrics no one was evaluating or making sense of.

I could feel the tension build inside of me at the notion that Dr. Silis was leaving it up to the specialists to sift through the reports and dissect their significance and meaning. But specialists aren’t necessarily trained to read radiographs or understand the significance of a radiologist’s findings. Radiologists leave it up to the prescribing physician to determine the reason an organ is decompressed or redundant. With nothing immediately coming to mind and no time to speak to radiologists or other doctors, physicians have come to rely on the testing physicians to come up with the definitive diagnosis. The testing physicians, on the other hand, see their role as limited to describing the physical findings they can discern. And if they find something they can’t explain? Better to ignore the finding than chance losing face by not being able to explain something noted on a report — like the “large bubbly radiolucent artifact” in my pelvic cavity that Dr. Platas noted in his October 26, 1995 report to Dr. Ferrer and Cigna HealthCare that no doctor could or would explain.

Dr. Silis had forgotten the reason he’d referred me to Dr. Barkin in the first place. He’d forgotten about Dr. Schuffler’s letter indicating a possible cancerous mass in my intestines. Between all the patients, Dr. Silis was simply recalling Dr. Barkin’s latest report to him that stated the colonoscopy biopsy was nonspecific and that there were no specific organisms identified. Never mind that the biopsy was taken from the wrong section of my colon. Forget that the “doctored” colitis diagnosis didn’t match the description of ulcerations found or that the treatment with Asacol is for patients with ulcerative colitis. That required too much reading and thought, and doctors are too busy going through the motions of pretending to help patients to read or think. I was in pain, and I was pissed. The one thing the discourse with Dr. Silis did, however, was get me focused on what was causing the colitis.

Thankfully, the severe pain eased on its own by the next day. My mid-back still hurt, but not unbearably. My guess is that radiographic dyes from the CT scans recently taken or a build up of calcium oxalate from the high doses of vitamin C in my intravenous solution precipitated the crystals. Then again, any of the following medical conditions I suspected I had could have caused kidney stone formation: arthritis (bone degeneration), colitis (causes dehydration and electrolyte imbalances from malabsorption), Crohn’s disease (causes dehydration and low citrate), hypertension (causes arterial plaque buildup), renal tubular acidosis and urinary tract infections (both cause crystal precipitation). I later even heard that administering radiographic dyes to a dehydrated patient can cause life threatening complications.

Fortunately, I had an appointment with Dr. Barkin the next day. At my request, he wrote a seven-day script for Pen VK. I asked if he recommended a different antibiotic for urinary/kidney infection. He said it didn’t make any difference which medicine was used since all target the entire body. He said meds don’t discriminate by area of the body treated. There seemed to be something very wrong with this last statement. Not that it wasn’t accurate, it’s just that — don’t doctors perform drug sensitivity tests on pathogens to determine which drug is most effective in eradicating the offending pathogen? I guess that assumes that an offending pathogen had been identified. I guess I assumed there was a notorious common bug typically associated with urinary tract/kidney infections.

When I talked to my various doctors about the possibility of developing kidney stones, they told me that there was nothing from the urinalysis, the CT scan or sonogram to indicate that I had kidney stones. I guess they didn’t know sonograms and CT scans usually cannot detect small stones or that it is not uncommon for abnormalities to be missed by the standard urinalysis conducted in the doctor’s office.

I found that it’s common practice to conduct a dipstick test on a room temperature urine sample only after any debris or casts settle. There are problems with this delayed testing. Urine ph of an uncovered specimen becomes alkaline as it sits because carbon dioxide vaporizes into the air. Crystals and casts break up as urine sits, and hence, elements essential for making an accurate diagnosis are lost. The presence of certain types of casts in the sediment is a sign that the kidneys may be malfunctioning.

I found many offices now only refrigerate and culture specimen sediment for microscopic examination if the dipstick test indicates infection. Other offices that perform routine urine cultures come up with an inordinate number of false negative results for a variety of reasons.

One need only go online to dozens of forums discussing today’s conventional “urinalysis” to discern the extent of the problem. Like me, many of the forum participants, who are experiencing real symptoms of infection or dysfunction, are dismissed by their care providers once their urinalysis test results state: ‘Mixed urogenital flora, less than 10,000 CFU/mL isolated. No further testing performed.” The statement is said to indicate the urine sample was contaminated with epithelial skin cells and needs to be repeated. (I can tell you I was never once asked to repeat the test after results for countless specimens stated the aforesaid.) The statement is also said to indicate that not one of the bacteria colonies present grew in numbers large enough to be identified. Perhaps the labs would have greater success with different culture media as urogenital flora, particularly the sediment, contain the clues vital for accurate diagnosis and effective treatment.

One study found samples from individuals suffering from interstitial cystitis (chronic bladder infection), whose routine urinalysis tested negative, tested positive for enterococcus, a gram-positive bacteria, doing “broth” culture testing.(Enterococcus along with S epidermidis and diphtheroids are among the types of bacteria frequently found in the anterior urethra of humans.) In contrast to the routine urinalysis culture, the broth culturing method allows all microbial strains from the specimens to emerge. By transferring representative strains to appropriate differential media, the disease-causing agent can then be isolated for further study and reported to the physician along with the appropriate antibiotic sensitivity pattern. Evidence shows that many doctors’ common practice of prescribing broad spectrum antibiotics for such bacterial infections is of no therapeutic benefit.

My point is that those who continue to regard the sediment from urine specimens as contamination that needs to be separated from the less dense urine that is siphoned and sent to a lab for culture and microscopic examination are compromising test results. Casts are composed of certain proteins, white blood cells, red blood cells and epithelial cells. Increased amounts of albumin and other proteins in urine can signify damage to the microscopic kidney tubules, and when renal casts are visible, excess albumin is likely. Diseases in which protein in urine reaches high levels include glomerulonephritis (an inflammatory condition), lupus (an autoimmune disorder) and diabetes. Minor elevations of protein occur with hypertension and during pregnancy.

~ by doctorblue on December 17, 2008.