Please click on the titles below to go to the corresponding sample Case Evaluation Reports.

Adrenal Gland Adrenalin-Like Secreting Tumor Not Detected in a Symptomatic Pregnant Women, Caused Death of Mother and Baby.

A pleochromocytoma is a tumor of the adrenal gland (next to the kidney) which usually secretes a catecholamine (adrenaline-like) chemical which stimulates the heart to beat faster and harder, causing hypertension which can fluctuate with the amount of catecholamine secreted during the day.

When suspected, it is common to obtain a 24-hour urine collection to measure the amount of catecholamine and its metabolic (breakdown) products. Also, an MRI examination of the upper abdomen is done to see if the tumor is present and its size and location so it can be surgically removed.

In her case, at age 33 she noted more frequent heart palpitations, her heart racing, her vision becoming black, and a severe pounding in the temporal areas of her head. These were worse with exercise. On 7/13 her blood pressure was low normal at 90/72 and she had a 24-hour cardiac monitor (Holter) test which showed episodes of rapid and irregular heartbeat that coincided with her symptoms. But no one had her check her blood pressure at home during the time she was symptomatic.

They never obtained the catecholamine urine test, despite symptoms consistent with episodic hypertension consistent with a pleochromocytoma. Even after they put her on the “beta blocker” drugs (atenolol and then inderal), which block the catecholamine effect, they were not always effective, when the amount of this chemical produced by her tumor exceeded the blocking effect of these drugs. And still no specific tests were done as noted above.

She was next seen on 10/12 and Dr. Rogers of the Hospital Clinic noted: “Since I last saw her, she has continued to experience palpitations on a frequent basis. …They can last for up to a minute in duration. They are frequently followed by some sharp pain in her face and nausea.” Her blood pressure in the office without symptoms was 90/50.

He focused on the arrhythmia, and not this potential cause in the differential diagnosis that he never noted. That, in my opinion, is a departure from the standards of care expected of an Assistant Professor of Medicine, a Cardiologist, affiliated with a medical school. He was part of the “electrophysiology service” and did not see the “big picture” beyond the electrical activity of her heart.

On 10/30 she had an echocardiogram (sound wave study of her heart) that found no anatomical or mechanical problems.

On 1/11 Dr. Rogers saw her again, and noted that the inderal was 80% to 90% effective. Her blood pressure was 114/70, which, for her, was a significant elevation, and he made no comment or follow up.

His last evaluation of her was on 5/10, and she was unchanged symptom wise and her blood pressure was 106/74. He never had her check her blood pressure at home, which is very easy to do manually, or with those semi-automatic devices. However, he did note that her symptoms lasted for 10 minutes (fatigue and lightheadedness) and concluded it was from her PUCs (premature ventricular contractions: arrhythmia), and not from the inderal. Again, he did not do the necessary tests.

Her Obstetricians would reply on the care given by the Cardiologist, and all of her blood pressure recordings on 5/22, 6/22, 7/31, 8/23, 9/22, 10/19, 11/3 and 11/20 were all “normal” between 100-120/70. On 12/1 it was 140/100. The second test of her blood pressure on 12/1 was 154/126 which is grossly abnormal and puts her and her fetus in danger. That is not a value from just rushing there, since it was the second value. Even if it was the first, it was alarming, and they should have contacted her Cardiologist that day. The third value was 140/84 and the fourth was 118/76.

Did she have an interpreter with her that day? Did she have her typical symptoms and did the doctor ask how she felt, and/or did she complain of any symptoms?

On 12/3 she arrived in the Emergency Room critically ill at 1135. She was shocky and had difficulty breathing. At 1157 she was intubated (breathing tube put into her windpipe), and at 1204 her baby was delivered by emergency caesarian section. His Apgar score was 0 out of 10 and eventually they were able to obtain a heartbeat, but he had severe effects of lack of oxygen from his mother’s severe compromised state, and died the next day.

If the Cardiologists were called on 12/1 and they obtained an emergency MRI, based on the 225 gram (7 ounce) size of this large tumor, it would have been found. Possibly urgent surgery (which could take place at the time of the C-section delivery since the fetus was almost 35 weeks [40 is “term”]), its survival would be 98%. Since this was a University Facility, such speed was possible.

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The Defense will contend that the collapse was brought about by the unanticipated hemorrhage into the adrenal gland tumor liberating a vast amount of catecholamine, which caused her collapse and death, despite excellent emergency room care. They will contend, that in their workup (testing), most likely it would take more than a few days, and she was stable and on inderal, which dose they could increase.

However, she was pregnant, and severe hypertension causes uterine arteries to go into spasm delivering less oxygen to the fetus, thus jeopardizing two patients, making the urgency even greater.

On 12/1 in the obstetrical clinic she saw Eddie, a Health Care Proffesional. Was that person a Doctor (at what level of training), a Student, or a Nurse? Was her Obstetrician even notified of her blood pressure results that day? If not, they (that person, her or his employer, and the supervising Doctor) are all negligent.

The autopsy report I saw was the “preliminary anatomic diagnoses.” Obtain the final report which will include all the physical and microscopic findings, plus any laboratory reports.

The laboratory records showed the presence of some germs in the blood, but she had needles into her body, and its pre-mortem accuracy as causation, is in doubt.

The death certificate mentions the cause of death as “Amniotic fluid embolus” (this fluid can enter the bloodstream and cause death), but that death certificate box “#29B: If yes (autopsy), were findings used to determine cause of death” is not checked off for “No” or “Yes.” Therefore the death certificate’s accuracy is questionable. The Physicians are listed as Karen, M.D., S.M. Hospital and Anthony, M.D.

I would suggest Board Certified Experts in Cardiology, Obstetrics, General Surgery, Endocrinology, and Onocology to prepare opinions on negligence, causation and damages (longevity). The Medical Review Foundation, Inc. have these Medical Expert Witnesses on our Consulting Staff and would be happy to continue assisting you with this important case. We await your written authorization to proceed.

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Hyperthyroidism Treated With Drugs Without Informed Consent Resulting in Severe Complications.

A summary of this case follows.

  • The patient was 46 years old on May 26 when she was evaluated by Dr. #1 for complaints of tiredness, headaches and weakness. On his examination, he noted that the patient had somewhat overactive reflexes with a prominent thyroid on palpation and appropriate laboratory tests were ordered. These tests revealed an elevated T3 level (also known as triiodothyroxine) and an elevated free T4 level along with a subnormal thyroid stimulating hormone (TSH) level. These lab values are strongly supportive of the diagnosis of hyperthyroidism. Dr. #1 appropriately opted to initiate therapy for this patient at that time.
  • The treatment of hyperthyroidism, or an overactive thyroid with excessive production of thyroid hormones, can be divided into three categories. The thyroid gland can be surgically removed. It can be rendered less active by radioactive means or its hormonal production can be suppressed by medications. There are advocates for each of these forms of therapy under appropriate circumstances.
  • Beginning on May 26 Dr. #1 opted to begin tapazole or methimazole therapy for this patient. Since methimazole, besides its ability to suppress thyroid hormone levels is well known to be capable of causing significant bone marrow suppression in selected patients over the age of 40, it is standard practice to warn any patient treated with methimazole of the inherent risks of fever and infection with this drug. It is also the standard of care to warn any patient receiving this drug to immediately report symptoms such as fever or sore throat to their physician.
  • Unfortunately, Dr. #1, who is foreign born, failed to give the Patient any such warnings. Since she is also from his country and understands the English language poorly, she failed to comprehend the instructions that were written in English that she received from her Pharmacist.
  • On June 26 she returned to see Dr. #1 due to a skin rash that was a presumed food reaction to fish that the patient had eaten. Dr. #1 chose to refill the patient’s tapazole medication in the absence of any additional laboratory testing or even a temperature determination. Dr. #1 also failed, once again, to remind the patient of the risks of infection and sore throat due to the bone marrow suppression that tapazole can cause. It remains entirely speculative as to whether this rash was due to the fish allergy as opposed to other causes such as a drug reaction to the methimazole medication.
  • On July 7 she had apparently had several days of a sore throat. The antibiotic levofloxacin was prescribed following another visit to Dr. #1’s office. Again there was no temperature recorded, no blood work was obtained and there was no suspicion that the patient’s sore throat was most likely due to the tapazole therapy.
  • The Patient was admitted to the hospital on July 8 with complaints of continuing fever and sore throat. She was eventually shown to have had severe bone marrow suppression and a skin rash due to the newly introduced medication, tapazole, along with a chemical hepatitis. She had a prolonged hospital course, from July 8 to July 31 and suffered several complications. Due to the tapazole-induced bone marrow suppression, she required a prolonged course of intravenous antibiotics and anti-fungal agents.

In summary, the patient’s severe skin, liver and bone marrow suppression reactions to the drug tapazole were never properly communicated as real risks to this patient prior to her starting on this medication. Her physician should have advised her of the risk of infection from tapazole therapy and reviewed the warning signs and symptoms of infection that can accompany tapazole’s bone marrow suppression.

Furthermore, even when she was seen by Dr. #1 on July 7 this patient’s sore throat symptom was dismissed as “pharyngitis” without any additional laboratory testing or consideration that this sore throat may have been caused by tapazole-induced neutropenia (low white blood cell count). The available records indicate that this patient’s marrow suppression was most likely present since at least July 4, which was the date that she first noted her sore throat.

Dr. #1’s failure to warn her of the need to seek medical prompt attention and stop the tapazole therapy at the first sign of fever and sore throat were deviations from existing standards of care that, more likely than not, directly impacted this patient’s need for eventual prolonged hospitalization.

Her white blood cell count eventually did recover during this prolonged hospitalization. However, whether her anemia and low platelet count will ever completely recover to the normal range are not predictable from the available records. The medication tapazole is well known to be capable of causing a permanent form of anemia, known as aplastic anemia, as well as less severe, more reversible forms of bone marrow suppression.

Based upon the information in the records provided, it is anticipated that obtaining Expert opinions supporting the issue of negligence in this case should not be difficult. Nonetheless, in this specific case, Expert reports should be strongly considered in the areas of Internal Medicine, Endocrinology and Hematology.

We continue to remain available to assist you in this case and have the Expert Witness specialties you require for this case. Thank you for allowing the Medical Review Foundation, Inc. to be of assistance in reviewing this interesting case.

Our office awaits your instructions to proceed.

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Diabetic Ketoacidosis Inadequately Treated Resulting in Obvious Deterioration and Respiratory Cardiac Arrest

This case concerns the care and death of this 33-year-old female insulin-dependent diabetic.

She was seen in the office of Dr. Chuck on 9/26 for a reasonable diagnosis of bronchitis and he prescribed an antibiotic (Biaxin). She had a history of recent fever, a cough and chest pain with coughing. Her respiratory rate was not recorded, but she was not noted to be short of breath. The chest was clear. No rapid heart rate was noted. Based on all of the above and the subsequent finding of a normal chest x-ray on 10/1, I can find no fault with his office care.

When she called his office on 10/1 at 11:25 a.m. with intractable nausea, vomiting and diarrhea, she was referred promptly to the Emergency Room and they were notified she was on her way there. She was immediately seen at 14:11 and was correctly cared for by Dr. Olly. The laboratory tests revealed diabetic ketoacidosis (blood sugar of 477, which is four times normal), ketones in the urine, acid blood, dehydration with concentrated urine, and BUN (acute kidney test) elevated with the more chronic kidney blood test, creatinine, normal, and concentrated blood with the hematocrit elevated at 50.2. This was a dehydration from her acute illness.

Her blood was dangerously acid with the pH at 7.05 (almost lethal level), and she had compensated to raise it “that far” by eliminating as much carbon dioxide from her blood as possible by hyperventilating (the PCO 2 was 9 with the normal range being 35-45). Also, she used up almost all the bicarbonate in the blood by trying to buffer (neutralize) the excess acid with it at 2 (normal is 22-26). All this gave her a negative base excess of –26.4 with the normal of –2.0.

All this means she needed lots of fluids to rehydrate her and lots of bicarbonate to return her almost lethal blood and body acid status to normal or at least near normal, and enough as tests continued to reveal defects.

She received adequate fluid at 500 cc (17 ounces) per hour, and after she had produced more than one liter (quart) of urine, it was reduced to a generous 250 cc per hour. Her hematocrit came down to a normal 42.5 by 5:55 a.m. on 10/2. Her blood sugar dropped to below 200 at midnight and remained in a safe diabetic range thereafter.

However, no one checked her arterial blood gas level (other than oxygen, which was fairly normal). No pH or PCO 2 levels were ever tested again, despite the persistently very abnormal venous blood bicarbonate values of 5 at 1508, 4 at 21:30 on 10/1, and 8 at 0200, 0555 and 1000 on 10/2. That failure to respond is somewhat ominous. In my opinion, the failure to recheck her arterial blood pH (and PCO 2) was a departure from the accepted standard of care.

Her in-hospital care was given by Dr. Maddy. He wrote most of the medical therapy orders. Dr. Liddy wrote orders at 1225 (9:25 p.m.) on 10/1 and 0305 on 3/2. Dr. Maddy ordered more bicarbonate to be given at 2225 by IV “push” and to be in her next intravenous bottle and “call next chemistries 7 (which includes the blood bicarbonate) results to Dr. Liddy.” That test was at 0200 on 10/2 and the value was very low at 8, as I noted above.

An insulin-dependent diabetic in diabetic ketoacidosis is very fragile. In my opinion, even though she was responding to her rehydration and insulin therapy and feeling somewhat better, they departed from the standards of care in not more closely following her acid blood condition and more frequently giving her more adequate doses of bicarbonate to correct her dangerously low and persistently low blood bicarbonate (acid buffer).

At 0915 on 10/2 the respiratory rate was at the upper limit of normal. At 1015 it was 27. At 1115 it was 30. At 1215 it was 55. Her hyperventilating to “blow off” carbon dioxide (acid) had markedly increased, but no one ordered any repeat arterial blood gas values (especially the pH), since the blood oximeter only measured her oxygen in her blood, which was adequate, although it should have been higher considering the fact she was on supplemental nasal oxygen.

They were watching but not interceding. That is negligent, especially since they knew her blood bicarbonate buffer was too low and with increasing hyperventilation from her decompensating acidosis, her mental state (from alert to coma) was predictable, and that put her at greater risk of aspirating (choking) on her vomitus and arresting.

The Respiratory Therapist could not finish her ordered therapy (why??), walked out of the room and she promptly arrested.

The Nurses noted that at 1005 she “complained of shortness of breath (SOB) “and her respiratory rate in mid twenties to mid thirties.” She was “anxious.” At 1020 she “developed expiratory wheezes and appears more labored in her respiratory effort,” and “Dr. Maddy has ordered a respiratory treatment and a chest x-ray (CXR).” It was performed at 1040 and at 1125 “revealed a white out of patient’s right lung. CT ordered” which she initially refused when initially presented at 1059 by a Pulmonary Specialist, Dr. Bunt, even though he told her that her lung condition was life threatening. She said: Well, that’s too bad.” He did not order urgent repeat arterial blood gases, even though it was in his specialty. He focused on the CT scan and bronchoscopy intervention (which earns him a fee and was indicated), which she refused.

His failure to order that urgent blood test is a departure from the standards of care, particularly when the Respiratory Therapist noted that her respiratory rate (RR) was 55, three to four times normal, and she was in respiratory distress. Also, he should have had the Anesthesiologist see her at that moment to electively intubate her and put her on a respirator (ventilator).

At 1140 her RR was 42 and she was “visibly labored.” She was found “nonresponsive, RR labored, irregular and decreased from previous – now in the teens.” She was going into an arrest before their eyes. At 1202 the Respiratory Therapist began positive pressure mask ventilation (bagged), the Anesthesiologist was called at 1204 to inert an endotracheal tube but despite sedative (Versed) and muscle paralyzing drugs ( succynlcholine) with two doses (20 mg and then 80 mg) her mouth could not be opened. The she was given a curane drug (Nucuron) and that released her teeth clenching jaw spasm, but he could not intubate her windpipe. This can be very difficult in an obese woman, 200 pounds in a hospital bed under emergency circumstances.

A Surgeon, Dr. Giddy, was called at 1220 to perform a tracheotomy to cut into her windpipe to insert a tube, and because of her obesity, that was not successful (but she was ventilated with the mask/bag ventilator). He tried to inert a needle into the cricothyroid membrane and again it was not successful. All of his care is not negligent, nor was the Anesthesiologist negligent under these circumstances.

She was pronounced dead at 1252 by Dr. Maddy.

The sudden change in her right lung was either a very large pleural effusion (fluid outside the lung between it and her ribs), or acute pneumonia-like changes. The central venous pressure catheter, if it punctured the vein and entered the lung outer space at the insertion, followed by all that fluid could cause that effusion. However, they were able to withdraw blood from the needle tube confirming its intravenous position. The chest x-ray showed it to be anatomically in the vena cava (large vein), and her body received the fluid because over her brief hospitalization she produced more than two liters of urine.

So the x-ray change most likely was from acute aspiration in her very ill state, which risk was significantly increased by their negligent failure to carefully retest her blood pH and give her adequate amounts of bicarbonate as her body required, not just “flying blind” or worse, doing minimal therapy in spite of her persistently dangerously low blood bicarbonate (acid buffer), which is a simple venous blood test done in a few minutes, her respiratory distress, and severe aspiration pneumonia-like acute changes.

In my opinion, if they adequately treated her acid state after she was admitted to the hospital, she would not have aspirated (and therefore also eliminated much of her lungs’ ability to “blow off” the acid carbon dioxide), and simultaneously damaging body (lung) flesh, increasing her acid production.

Was an autopsy done? If so, obtain the complete report.

The blood culture tests were negative for germs (sepsis), but the sputum culture laboratory test result is missing. It is important to see if she had lung germs (even with the initial negative chest x-ray), because I do not find that she actually received any antibiotics other than 2 grams of Rocephin intravenously at 1620 on 10/1 in the ER. So it may or may not have made a major differences in the context of all her care and death.

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The Defense will argue that she was “getting better,” her blood sugar and fluid hydration levels were very acceptable and she refused the CT scan and bronchoscopy (which probably would not be done before she died anyway). One record noted that she had a BKA (below the knee amputation), which could show how precarious she was for longevity. Did she have a leg amputated, and if so, why? Since she was hospitalized two years before for pneumonia, it is important to obtain those records for review to see how it may impart on this occurrence. She also smoked cigarettes. Who made what efforts to get her to stop, especially since she had pneumonia two years before? And who made what efforts to get her to lose weight, which makes her diabetes easier to control and aids breathing ability?

I would suggest that you authorize the Medical Review Foundation, Inc. to have all the records (including the requested ones) reviewed by Board Certified Medical Experts in: Endocrinology, Infectious Disease, Pulmonary Medicine and Critical Care/Intensive Care Medicine.

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Poorly treated Diabetic For Eight Years, Increasing Risk of Heart Attack and Stroke which Occurred.

Concerning Dr. #1: Diabetes is a chronic disease and good control of blood sugar levels is essential to significantly reduce the risks of diabetes: heart attack, stroke, kidney disease, blindness, infection and advanced diffuse arteriosclerosis (hardening of all the arteries from cholesterol buildup).

When did this patient first come under the care of Dr. #1? The first record I have is from 2/10/ but is part of missing (previous) records. His fasting blood sugar (FBS) levels were periodically being monitored by Dr. #1. The first record of any blood sugar level was “FBS 160,” but the month is cut off on the copy. It was between 2/10 and 8/12. If it truly was fasting (which FBS denotes), it is way too high. It should be below 110 and ideally under 80. The only treatment was with the oral drug, “Diabenese 250 mg, 2 daily.” It was to be “checked in three months.”

The next note was 8/12 and the FBS was not recorded.

His blood pressure was not under good control either. The values eight years earlier were 150/100 – 160/110, but during that only office visit it was evaluated and decreased to 140/90 and 150/90 (borderline).

In the 8/12 note he was to be on a “stricter diet” because his FBS was too high. (This was by telephone; it was not an office visit. He should have been seen.)

The next office visit was noted to be (? month)/22 in the current time. Who was treating him for his diabetes and his blood pressure for eight years? The March 3, Emergency Room record from the Hospital said, “See your private doctor: Dr. #2.” Who is Dr. #2? Can he become a Defendant? Was he under the care of any other Doctor or Clinic those eight years? Check with his Medicare and other healthcare billing records. If he was seen, a bill certainly would have been generated.

Did the Hospital Emergency Room send a copy of their records to Dr. #1. Most Hospitals do this?

On ?/22, Dr. #1’s records note his blood pressure at 150/110, that he had “prostate surgery last year” (by whom and who evaluated him preoperatively for “clearance” for surgery, as is standard medical practice?). His blood sugar (diabetic) therapy was noted to be glyburide 5 mg b.i.d. (2 times per day). Was this now a new prescription? Who prescribed his diabetic medication for those missing eight years??? He had chest pain and no EKG was done. That is negligent, especially in a poorly controlled diabetic and hypertensive patient. It most likely would have been abnormal. Also, a cardiology referral was indicated as was an endocrinology referral (to evaluate and control his diabetes, which does not disappear with age; it gets worse, especially when subject to negligent care, which was “given” by Dr. #1).

On ?/23 (probably the next day) a FBS was 208. The only response was to increase the glyburide to three times per day. He required insulin over years since the oral therapy was not giving him good control, and whatever diet he was on was not effective with glyburide. Was he ever sent (with his wife) to a dietician by any Doctor? 

On ?/25 the right side of his body was feeling weak and he had slight chest pain. This required hospitalization, testing and therapy for an impending stroke and heart attack, was not done, and negligent.

On 1/25 (therefore all the ? months above most likely were January), his FBS was 264. 

On 1/29 his FBS was 170 (still way too high) and the only response of Dr. #1 was to prescribe two glyburide every A.M. and one and a half every P.M. and order a follow-up FBS in 30 days. This was way too long a delay.

On 2/28 the FBS was 229 and he gained five pounds in one month. Was this fluid retention? He was seen on 3/1. No physical exam for edema: pushing against the legs for indentation (“pitting”) was done. The EKG note was “neg" but no EKG is in the records (why?). And because Dr. #1 noted that the chest x-ray showed “increased hilar nodes” (enlarged lymph nodes next to the heart), he said, “consult (apparently with Dr. #3 on 3/7), but prescribed the steroid, Medrol, without any diagnosis of those nodes, in a patient who was coughing, had received antibiotics with no test for any sputum germs (culture and sensitivity), and in a diabetic where steroids markedly make the blood sugar go out of control and make control of infection very difficult. All this is negligent therapy.

On 3/3 he had nausea, vomiting and upper abdominal pain (also seen in heart attacks) and no repeat EKG was done, no Emergency Hospital Admission or Cardiology consultation arranged, and NO repeat blood sugar done. All this is negligent. He had a chance to acutely intercede and failed. He had eight years of opportunity to properly treat his diabetes, and miserably failed.

Blood clot “busting” drugs were available for years, and could significantly reduce the risk of mortality and morbidity if timely begun. Dr. #1 noted the pain began “after eating sausage,” but in this high-risk cardiac patient, did not do an EKG, which would be abnormal (as it was in the Long Hospital ER when it was taken at 1855: 6:55 p.m.) At what time had he seen Dr. #1 on 3/3? If therapy is begun within four hours of the onset of chest pain, the patient has the best chance for survival.

His blood sugar in the Hospital ER at 1752 (5:25 P.M.) was 492. That marked elevation was caused by the negligent steroid prescription by Dr. #1, and such a high blood sugar can increase the risk for a heart attack.

Dr. #1 knew his patient was at risk for arterial blockage, because on January 26 the head CT scan was abnormal showing “areas of ischemia (low arterial blood flow from partial blockage) or early infarction (total artery blockage causing death: gangrene of part of his brain).

Dr. #1’s negligent diabetic treatment significantly increased the risk of artery damage causing his stroke and fatal heart attack years before it would have otherwise occurred.

Obtain the missing records (EKG, Hospital #2 admission records, and from Dr. #2 as well as all other healthcare providers). Obtain copies of all pharmacy prescription from ten years through his death. Was an autopsy performed? Obtain the complete report. 

What specialty, if any, is Dr. #1? Supply his resume. Has he ever failed any Board Certification testing?

I also suggest review (after missing records are supplied) by an Expert in Endocrinology (diabetes management), Cardiology, and of the specialty, if any, of Dr. #1. How does he advertise in the Yellow Pages now and eight years earlier?

We look forward to continue assisting you and your Clients in this interesting case.

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Hyperthyroidism and Graves disease (thyrotoxicosis) causing exophthalmos (bulging eyes), and treatment.

Before I discuss the specific facts of this case, let me discuss the function of the thyroid gland and its hormones. The thyroid gland, sitting at the uppermost part of the trachea (windpipe), produces two hormones: T3 and T4. T3 is very active in regulating the body's burning of calories and the normal function of all the cells of the body. T4 also serves in that same manner, but is less active. However, it is converted into T3 in the cells, to meet the demands of the body.

The pituitary (master) gland in the brain measures the blood level of those hormones. When their level decreases, it produces thyroid-stimulating hormone (TSH), to increase the hormone output of the thyroid gland. Likewise, when the blood thyroid hormone (T3 and T4) levels rise too high, there is very little TSH produced. TSH is a very sensitive measure of thyroid gland hormone blood levels.

When the thyroid gland is overactive and does not respond to a reduction of TSH, it is called hyperthyroidism. When it is symptomatic, it is called thyrotoxicosis (Graves' disease). One of its consequences can be a bulging of the eyes, even beyond the point where the normal closure of the eyelids during sleep do not meet, and the cornea (clear outer "lens," or window into the eye), can dry out and develop an ulcer.

When the patient is symptomatic, the usual initial therapy is with a drug such as Tapazole, to decrease the thyroid hormone production. This sometimes results in a permanent remission (cure) of their Graves' disease. Also, a "beta blocker" drug such as Inderal (propranolol) can be used to control the symptoms (physiological effects) of the excess thyroid hormone in their body.

Often this is not successful and definitive therapy is required, which can either be from surgery, to remove 75-85 percent of the gland, or radioactive iodine. Surgery, which has immediate results, may or may not remove enough of the gland, and has risks of permanent hoarseness from damage to one of the two small nerves (recurrent laryngeal nerves) that sit adjacent to the thyroid gland. It can also cause permanent tetany (painful diffuse muscle spasms) from damage to the three to five tiny parathyroid glands that lie on or within the thyroid gland's surface layer.

Radioactive iodine, which takes months to have its full effects, is selectively absorbed by the thyroid gland and destroys those functioning cells that make the T3 and T4 hormone. However, it will turn an overactive gland into an underactive (hypothyroid) gland in almost all cases. Therefore, it is critical to monitor the thyroid function tests (T3, T4, and TSH levels) and to add thyroid in pill form. This is either dried out (desiccated) animal thyroid, or synthetic thyroid (Synthroid or Levoxyl).

In most cases, those patients who develop bulging of their eyes (exophthalmos), eye muscle spasm and pain secondary to their Graves' disease, will have either some improvement or no further progression once their disease has been successfully treated. But a small percentage of patients may actually develop the condition during or shortly after their Graves' disease has been resolved (based on thyroid function tests). Graves' disease is an auto-immune condition, where the body will react against its own flesh, just like rheumatoid arthritis is an auto-immune disease against its own joints, and fibromyalgia is the body's reaction against its connective tissue and muscles. Sometimes x-ray therapy directed at their eyes may be needed to treat that bulging eye and eye muscle spasm condition.

In the case of this patient, she had a very strong family history of rheumatoid arthritis (mother and two siblings) and she had a positive blood test for this disease. She responded to therapy for rheumatoid arthritis.

She also had a mass in her chest, found on a chest x-ray and CT scan, which required surgery. She also had findings of fibromyalgia (connective tissue disease causing fatigue and muscle pain), consistent with her chest mass (thymoma: a benign thymus gland tumor) and her Graves' disease.

I will outline the facts in her case as they evolved sequentially, and make comments as appropriate:

On 12/31/96 she had normal thyroid blood tests. The normal (reference) range will be in T3 27 (22-35), T4 6.8 (4.5-12.5), TSH 2.3 (0.4-5.5). They vary slightly from laboratory to laboratory, and I will not repeat these ranges unless they used a different type of test with a major difference in "normal."

On 1/3/97 the cardiologist Dr. #1 evaluated her with a stress treadmill test and echocardiogram (sound-like study of her heart), and concluded that her fatigue was secondary to "deconditioning and depression."

On 10/16/97 a CT scan of her chest confirmed the presence of the thymus gland tumor (thymoma).

On 10/24/97 neurologist Dr. #2 diagnosed her as having "myopathy (muscle disease and pain) symptoms in presence of rheumatoid arthritis and thymoma."

10/27/97: T3 37 (high), T4 13.2 (high). 11/3/97: TSH less than 0.1 (very low). Also, the thyroglobulin antibody test level was high at 10.6 (normal less than 1.0). All of these are consistent with Graves' disease. On 11/3/97 she had a thyroid radioactive uptake scan (not therapy), and this was also high at 53% in 24 hours (5-35%). All this confirmed her overactive thyroid gland (hyperthyroidism) condition.

On 11/14/97 she came under the care of Dr. #3, an Endocrinologist. Her pulse was very elevated to 130 and she had "no sign of exophthalmos." Dr. #3 ordered laboratory tests: The thyroid autoantibodies were high at 9.9 (less than 1.0), T3 314 (60-181), T4 2.7 (high), and TSH less than 0.005 (very low). All this confirmed the diagnosis he made of Graves' disease. On 12/5/97 her pulse was moderately elevated to 96 and he started her on the antithyroid drug Tapazole and the beta blocker Inderal (propranolol) to help control her symptoms. All this is good, standard care.

On 12/15/97 her T4 was normal at 2.3. On 12/17 and 12/31 her pulse was normal at 80. On 1/8/98 her T4 was again normal at 1.5. He concluded it was safe for her to go ahead with her chest surgery for the thymoma tumor.

Her chest surgery took place on 1/29/98. The tumor was large (weighed 66 grams), and because it partially surrounded the left phrenic nerve (that controls the left half of the diaphragm, or breathing muscle), it had to be cut in order to remove the whole tumor without cutting into it. If it had been malignant (cancer), cutting into this tumor would have decreased her chance for a cure. Fortunately, after it was removed, the pathologist noted that it was benign (not cancer), and had an unusual pattern of cells: "Follicular B-cell hyperplasia associated with Graves' disease and auto-immune connective tissue disorders," (fibromyalgia and rheumatoid arthritis, both of which she also had). Because the left phrenic nerve had to be cut, she may experience some increased shortness of breath, with part of that "bellows" (muscle) non-functional.

On 3/2/98 the T4 0.8 and TSH 4.3 tests were normal. On 4/7/98: T4 1.01 (normal), and TSH - 0.13 (low). On 4/15 her pulse was 88.

On 5/5/98: T4 0.39 (low) and TSH 31.5 (high), caused by the Tapazole blocking thyroid hormone production. However, she developed a severe rash and Dr. #3 properly discontinued both the Tapazole and Inderal drugs, and she received 12 mCi of radioactive iodine. This would destroy her thyroid gland.

Because she would no longer have a functioning thyroid gland, she was begun on Synthroid (synthetic T4) on 5/13/98 at 0.1 mg (milligrams) = 100 mcg (micrograms). On 5/27/98 her pulse was normal at 80 and she was receiving 0.1 mg of Synthroid.

On 6/9/98: T4 0.8, TSH 21 (high). The thyroid gland was not yet fully suppressed, because her pituitary gland did not sense enough thyroid hormone in her blood (from the Synthroid and any residual from her thyroid gland) to stop making its thyroid-stimulating hormone (TSH).

On 6/24/98 she complained that her eyes were bulging, she had fatigue, had arm and leg pains and muscle weakness.

On 7/21/98 her TSH was 0.519 (low normal).

On 7/31/98 her TSH was noted to be 0.519 and her pulse was 88 (high normal). She also had "very mild exophthalmos" and was taking 0.15 of Synthroid per day. This is proper therapy. She was referred to an ophthalmologist specializing in this problem. This is also good care.

Dr. #4 first saw her on 8/20/98. He noted she had thyroid eye disease and dry eye syndrome (also seen in some connective tissue diseases), and exposure keratopathy (from drying of her cornea). He prescribed proper medical therapy and she improved, but developed a progression of her thyroid eye disease. He recommended radiation (x-ray) therapy to her eyes to try to control that condition. Dr. #5, a radiation therapist at the Hospital #1, administered 2000 rads over 10 days, which was completed on 2/24/99. She had some improvement in her symptoms, according to his letter.

Referring back to her thyroid tests and therapy on 8/31/98: TSH 0.45 (0.4-4.0). This is ideal, based on her disease.

On 9/3/98 she was "feeling strange," had severe fatigue and was taking 0.15 mg of Synthroid.

On 9/10/98 Dr. #6, her primary care physician, noted, "On Synthroid 0.45 mg apparently and endocrinologist reports her level is doing well." I found no other records supporting that three-times-the-daily-dosage value. Are there any prescriptions for that 0.45 mg total per day dose? If so, by whom? Was she taking it on her own?

On 9/28/98 Dr. #6's record says, "rapid (heart) rate with regular rhythm." However, the nurse recorded a heart rate of only 68 on the office "Vital Signs Flow Sheet." She was wheezing and he treated her with an Albuterol nebulizer for "asthmatic bronchitis." That was proper care and it relieved her wheezing caused by spasm of the bronchial tubes in her lungs. It can also temporarily speed up her heart rate. On that day the laboratory T3 was normal at 32, the T4 was slightly high at 11.2 (4-11), and the TSH was low at 0.1.

On 10/2/98 an office note of Dr. #6's said that she finished her last refill of Synthroid 0.15 mg daily per Dr. #3, and she was not happy with Dr. #3, "who told patient current thyroid dosage too high; prescribed (Rx) Synthroid 0.10 but when at this lower dose in the past felt like it did her no good." Dr. #6 told her to decrease it to 0.125 mg.

On 10/1/98 Dr. #6 wanted to decrease the Synthroid to 0.1 (the TSH was 0.4), but Dr. #3 said to keep it at 0.15.

On 10/21/98 her Synthroid dosage was decreased to 0.1 mg (100 micrograms).

On 11/2/98 she had fatigue, probably secondary to fibromyalgia.

On 12/14/98 the TSH was 0.876 (0.35-5.5).

On 3/18/99: T3 = 34, T4 = 10.2, and TSH = 0.86 (all normal).

On 4/6/99 she twisted her body and developed a limp, probably from a pinched nerve.

On 6/15/99 her TSH was 0.77, and on 8/30/99 her TSH was 3.06 (all in the normal range).

It is generally recommended that the TSH level should be suppressed to below normal levels, to assure no failure of thyroid suppression, which could stimulate any residual thyroid tissues (flesh = cells), and cause the eye disease to worsen.

Based on the voluminous records I reviewed, mostly summarized above, it appears that she received very good care by her first Endocrinologist. After her radioactive iodine therapy, Dr. #3 attempted to suppress her TSH levels to the lower limit of normal, or just below normal, as he should have done. When her eye disease was symptomatic, he referred her to an ophthalmology specialist in that condition. That physician gave her good eye care, and had to recommend the radiation therapy to her eyes to try to control her exophthalmos (bulging eyes) and the symptoms of pain and light sensitivity (photophobia) she was experiencing.

Unfortunately, she developed exophthalmos, which persisted, as noted in the enclosed photographs. Perhaps she would be recommended to see a physician specializing in plastic surgery of the eyes for his opinion on any potential operative therapy.

Her physical symptoms of incapacity (fatigue) are not related to her thyroid disease care, but as her doctors noted, probably related to fibromyalgia, deconditioning, and depression.

Based on all of the above, it appears that she wanted to have a higher dose of Synthroid than Dr. #3 prescribed. His dose was reasonable, based on the TSH blood levels and her diagnosis, as I noted. I do not find an "overdose" of Synthroid prescribed by her treating Physicians as the cause of her exophthalmos (bulging eyes).

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An insulin dependent diabetic is sent home from an Emergency Room, and then hospitalized in a coma for weeks and has numerous complications including infections and bleeding.

This 39-year-old patient was an insulin-dependent diabetic with many of the problems common to a diabetic, including eye, kidney, artery and nerve damage and marked increased susceptibility to infection.

She had many previous trips to the Emergency Room. She was seen on 1/18 and had a negative head (brain) CT scan, but was diagnosed with a sinus infection (the CT scan did not note any sinus problem). She was given a pain medication (narcotic, Demerol) injection. It was believed she was lethargic from this injection. She was given a prescription for an antihistamine (Claritin) and an antibiotic, which she never filled. I am missing the records from that critical Emergency Room visit.

On 1/19 she was comatose at home and taken to the hospital again. She remained unconscious her entire stay at Hospital #1 from 1/19 through 2/10. Her diabetes was out of control and was properly stabilized. She had a history of high blood pressure and on arrival at the emergency room it was very high at 210/120. It came down quickly to 190/100 although it was initially difficult to control despite proper intravenous drug therapy. The CT scan on 1/19 was normal, as was the CT scan of 1/21.

Her out-of-control diabetes was properly treated. The spinal tap was negative for meningitis. She had a severe bladder infection, which was treated. She was admitted to the Intensive Care Unit where she remained unconscious the entire hospital stay of three and one half weeks.

Multiple Specialists saw her and the Neurologist thought she had a stroke involving damage to her brain stem and other areas of her brain. Time is the only treatment. She also had diffuse pneumonia, which was treated correctly. Her chronic diabetic kidney failure worsened but stabilized.

She had an endotracheal tube inserted for ventilation and suctioning of her trachea (windpipe) and bronchial tree. Usually after five to seven days, if the patient is still comatose, a tracheostomy operation is done to gain direct access for a ventilation tube to be inserted. This was finally done on 2/4. Because of that previous indwelling endotracheal tube there was inflamed scar (granulation) tissue build up above her vocal cords which were not directly damaged. After a few months, that healed without any problem for her voice.

Because of her multiple problems and the negative brain CT scans, it was hoped that her comatose state would resolve when her diabetic state and all her infections would be fully stabilized (when the metabolic encephalopathy would be resolved). Therefore, there was some justification for the delay in doing the tracheostomy operation.

That operation was more difficult because of bleeding from her thyroid gland that was controlled with sutures. Afterward she developed bleeding at that site, which was very difficult to control and required insertion of an endotracheal tube and gauze packing, which was proper care. She developed DIC (disseminated intravascular coagulopathy, a free bleeding state from her infections) and received proper blood clotting fraction therapy and blood.

The family requested she be transferred to Hospital #2 where she remained from 2/10 - 4/7. She remained comatose for weeks. Their MRI was consistent with strokes, most likely caused by her high blood pressure weeks before. She had a severe diabetic problem with impaired emptying of her stomach (gastroparesis) which required the insertion of a feeding tube into her small intestine: J tube jejunostomy operation (on 3/12). That was removed a few months later.

When they evaluated her throat and trachea, they found only easily bleeding scar tissue in her larynx/posterior pharynx (throat above the vocal cords) and that healed spontaneously. The previous tracheostomy operation was correctly done. They did not "cut too deep."

Her pneumonia and fungal blood infection was very difficult to cure, but finally resolved. Her swallowing problem resolved. It was related to her diabetic nerve damage and stroke.

After she finally awakened and her overall condition properly stabilized, she was transferred to their Rehabilitation Hospital for physical therapy to help her regain her strength.

She developed severe lower intestinal bleeding and was transferred back to the main hospital where she was evaluated and treated from 4/8 - 4/21. No source of that hemorrhage was found despite detailed examinations. She was stabilized and properly treated.

She was again treated in rehabilitation therapy for the residual effects of her stroke and finally discharged on 5/13 after the jejunostomy tube had been removed. All of their care was good.

I have not seen all of the 1/18 Emergency Room records from the Hospital #1, other than the CT scan report. All of those Emergency Room records including the Nurses notes and laboratory reports need to be obtained in order for me to be able to give you my final opinion on that critical aspect of her care. The only information I had was what they say occurred there after she was hospitalized on 1/19.

If they should not have discharged her and/or improperly treated her on 1/18, then it probably was the proximate cause of her condition going out of control. This would also have been responsible for her entire lengthy Hospital stays where she eventually was brought back to most of her pre - 1/18 condition.

Her overall health status was precarious because she did not eat (and probably did not take her insulin) and her diabetes was out of control contributing to her coma and severe infections. Because she probably did not take her medication for her high blood pressure secondary to her nausea from her out-of-control diabetes, her blood pressure was dangerously high at 210/120. This directly contributed to her brain damage and prolonged coma, which caused her pneumonia requiring the tracheostomy (that bled) and the need for the prolonged bladder catheter that resulted in further bacterial and fungal infections, which were very difficult to cure. It also contributed to a temporary worsening of her chronic diabetic nephropathy (kidney failure).

Therefore, please obtain all those missing 1/18 records from her Emergency Room visit and care at Hospital #1.

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Woman 40 years old develops spontaneous hip fracture and then spine and pelvis fractures, all from non-diagnosed and non-treated severe osteoporosis.

The issue in this case is was there a negligent delay in diagnosis of the pubic bone (front of the pelvis) fracture in this 52-year-old woman, and what difference did it make? I will discuss her entire medical condition and care prospectively.

In 1984 she had a wrist (Colles') fracture, which was properly set. How did it occur? In 1987 she had a right hip fracture at age 40, which occurred when she "turned while getting out of bed and sustained an intracapsular fracture of the right femoral neck." This was reduced and held together by surgery, performed by Dr. #1 using five Knowles pins for internal fixation. After it healed, those pins were removed ten months later. All that is good care and not directly related to her pelvic fracture.

In 1990, at age 44, x-rays showed a healed right hip fracture but also: "the body of L1 with diminished vertical height (approximately 20%). The change is consistent with a degenerative compression deformity primarily."

It is most unusual for a woman in her young forties to develop a spontaneous hip fracture from turning getting out of bed, and also lose 20% of the height of the first lumbar vertebra. Her treating physician, who is unknown, and the orthopedic surgeon who performed the two hip operations, in my opinion had a duty to investigate directly, or by consultation with other physicians, why her bones were so fragile. This was not done and in my opinion, was negligent.

There are many causes of osteoporosis and reliable, safe and often effective treatments are available. This was not offered to her, and put her at higher risk for more fractures and the sometimes-chronic pain that may result.

In 1991 and 1992 she had episodes of back pain and sciatica (pinched nerve), which was treated with narcotics (Vicodin) and steroids. Steroids increase the risk of bone degeneration. In 1992 she also had "cervical syndrome" and "tennis elbow" for which she received more steroids and pain medication.

In 1995, Dr. #1 operated on her right hand for "trigger thumb," a tendon problem, and that care was good.

In 1996 she complained of severe left shoulder pain without trauma, for which she received more narcotics and steroids (another Medrol Dosepak).

On 6/2/98 she slipped on a concrete floor and sustained rib fractures which eventually healed under the care of Dr. #2, and time. One week later she experienced back pain.

On 7/9/98 she had right hip pain diagnosed as bursitis. On 8/6/98 she had back pain, was limping and also had left groin pain. They believed it was because she had favored her left hip secondary to right hip pain that also occurred when she fell on 6/2/98.

On 8/13/98 she had a "massive hematoma (blood clot in the flesh), left inner thigh, has grown since yesterday." They did not know its cause. No bleeding or clotting studies were done, and that would be negligent. However, they may have been normal, as some were thereafter.

On 8/13 she also correctly had x-rays of her pelvis, which showed no fracture and her back x-rays were unchanged from 1990. She also had a MRI of her lumbar spine, including her sacrum (tail bone area of the posterior pelvis), which was normal, but did not mention the rest of her pelvis. Perhaps it was misread by Dr. #3, the Radiologist at Hospital #1.

A whole body bone scan was done on 9/9/98 and revealed the healing rib fractures and no other fractures. Therefore, based on all the 8/13 reports and this study, most likely she did NOT have a pelvic fracture at that time.

On 10/1/98 she had continued back and left hip pain. Physical therapy was given. By 10/19 "patient is improving, and by 10/21 "walking much better." Physical therapy continued.

Because of the concern for cancer causing a spontaneous fracture of her pubic bone she had a needle biopsy on 12/23/98, which initially was suspicious for cancer. She saw Dr. #4, an Oncologist on 1/7/99, who concluded that it was not cancer. He noted that she saw Dr. #5 on 11/10/98 for the first time, a CT of her pelvis on 11/23/98 showed "she was found to have a left parapubic fracture," and an MRI on 12/17/98 of her pelvis showed "loss of bone about the left pubic symphysis" (the left half of the center of her pubic bone).

On 1/7/99 she was in so much pain, that she was unable to get on the examining table. "Any type of weight-bearing causes obvious severe pain."

On 1/15/99 Dr. #4 noted the patient and her daughter were surprised to learn for the first time that she had a pubic bone fracture.

On 1/21/99 Dr. #5, an Orthopedic Surgeon, believed that she had an "insufficiency fracture," was taking the female estrogen hormone Premarin (which is supposed to decrease the risk for osteoporosis which causes an insufficiency fracture), and that she had a hysterectomy. He ordered a bone density study (which should have first been done in 1987). This showed osteopenia of her lumbar spine and osteoporosis of her left hip (femoral neck), and severe osteoporosis of L4 (fourth lumbar vertebra). She was -2.71 standard deviations below normal for hip done density. The Radiologist recommended calcium with Vitamin D supplementation, weight-bearing exercise, estrogen replacement therapy (she was receiving this but at what dose and for how long?), and to avoid nicotine, and limit caffeine and alcohol.

On 2/17/2000 Dr. #6 at Hospital #2 noted that her pubic bone fracture was healing ("interval consolidation") and she was "undergoing strengthening and aquatic therapy," which is good care.

The records suggest that she had numerous cortisone (steroid) injections. What drug, what doses, when, for what reason, and by whom? They may be negligent, especially in a woman who was at much higher risk based on her hip fracture in 1987.

The concern for her "pelvic floor symptoms" from "long term weakness of the pelvic floor" (inside her vagina) would be related to vaginal deliveries and the hysterectomy, and not the pelvic fracture.

Pelvic fractures usually heal spontaneously in three months. No surgery or other therapy is used, just time and pain relief. So the fact that she did not know that she had this stress fracture from osteoporosis for a few months is irrelevant.

The fact that the bone scan was negative supports the absence of any pubic bone fracture on the pelvic x-rays and MRI from 8/13/98. She most likely developed it later, but either way, there is no direct therapy to heal it faster, just therapy to prevent it from occurring, as I noted.

The fact that she may have not had proper instructions and therapy to avoid osteoporosis and strengthen her bones, to reduce the risk of all fractures, including this pubic fracture is relevant, and negligent. Who was the Family Physician, Internist and/or Gynecologist who was treating her all this time and who wrote all those office notes without any identification? That should be the focus of this case.

I would suggest Experts in Orthopedic Surgery, Endocrinology and the same specialty as that unknown treating Physician.

I suggest that the patient be evaluated by a local Clinical Psychologist with courtroom experience for any residual emotional (psychological) damages. Administration of standardized tests such as the M.M.P.I. (Minnesota Muliphasic Inventory) which have been given to millions of people would further support that opinion before a jury.

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