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Adrenal Gland Adrenalin-Like Secreting Tumor Not Detected in a Symptomatic Pregnant Women, Caused Death of Mother and Baby.
A pheochromocytoma 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 pheochromocytoma. 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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40-Year-Old Obese Male With Chest Pain Not Correctly Diagnosed Because Of Delays In Testing And Consultations, Subsequently Dies From A Pulmonary Embolus (Blood Clot To His Heart/Lung Circuit).
This patient was 40-years when he was first seen and evaluated at Hospital #1's Emergency Room for an upper respiratory tract infection beginning on or about July 7. He was treated and released, and details of this patient encounter are not fully available.
On July 4, the patient was readmitted to the emergency room where the diagnosis of congestive heart failure was made. He was treated for congestive heart failure as well as being given a prescription of Cephalexin antibiotic for reasons that appear somewhat obscure. In addition, he was told to see his internal medicine physician for further followup, and indeed this was done through Dr. #1 who ordered several studies in addition to treatment for this patient. For example, on July 25, an EKG was performed, and the patient was begun on Robitussin for his cough, as well as Lasix and an aerosolized inhaler.
The patient's wife maintains that on July 28th, she placed a call to a Dr. #2 and this call was never returned. On July 30th, the patient presented again to the Hospital #1's Emergency Ward and was cared for by the ward's physicians, including Dr. #3, Dr. #4 and Dr. #5. The patient's wife maintains that none of these physicians had sufficient expertise to be caring for such a seriously ill cardiac patient, but the qualifications of these individuals is not available for my review; nor is any of their medical management from the Emergency Room, per se, negligent.
The patient's hospital course can be described as one in which he was evaluated for an idiopathic (i.e., cause unknown) cardiomyopathy, a disorder of impaired heart contractility.
It should also be mentioned that this patient had a history of Hodgkin's disease treated with radiation therapy back in 1984, and was also being treated for thyroid dysfunction in the past.
The patient had undergone a cardiac MUGA scan which revealed decreased contractility. He also had, as mentioned a baseline abnormal EKG prior to his July 30th Hospital #1 presentation. In addition, this patient also suffered from morbid obesity.
It is clear from the foregoing that this patient being 40 years old did not have a typical medical presentation with a straightforward diagnosis. In fact, heart failure in this age group with such severely impaired heart contractility, as was shown on this patient's MUGA scan, is distinctly unusual and calls for an urgent cardiac evaluation. It is clear that this patient never had the benefit of such a cardiologist's consultation throughout his emergency room and ICU course. The treatment for congestive heart failure, because it is caused by many different etiologies, differs depending on the etiologies. For example, when heart failure is caused by high output states such as sepsis, treatment for that infection generally is indicated in addition to diuretics and a host of other conventional treatment modalities. When cardiac failure is caused by a lack of blood flow to the heart, the treatment, in addition to diuretics, must include modalities to improve heart blood vessel circulation, such as angioplasty.
Clearly, the diagnosis of congestive heart failure by itself is insufficient to optimally treat such patients. Indeed, the patient received very generic types of treatment for his congestive heart failure, including nitrates, pre- and after-load reducing agents and oxygen. In addition, he appears to have had prolonged bed rest as was noted in the discharge summary by Dr. #6 who cared for this patient.
On the evening of August 1st as well as August 2nd, the patient was observed to have had nocturnal blood oxygen desaturation, and this was felt to represent sleep apnea and the patient was scheduled for a sleep study. The patient appeared to be improved on August 2nd and was receiving oxygen with assistance without chest comfort, although chest comfort did return on the afternoon of August 2nd. The patient, at that time, received sublingual (under the tongue) nitroglycerin and the pain lasted less than a minute.
On August 3, the patient no longer had atypical chest pain, and ambulation was again attempted. At that time, the patient was walking to the elevators with the assistance of oxygen, but became diaphoretic (sweaty), and profoundly short of breath. He was noted to be in sinus tachycardia at a rate of about 130 with a respiratory rate in the 70s and an oxygen saturation in the 70s. The patient soon required a full cardiac arrest to be called, and he eventually expired on that same date.
Prior to the patient's acute decompensation on August 3rd, discussions were held between Dr. #6 and Dr. #7, the latter a Cardiologist. There is no documentation of this cardiovascular consultation that I have been able to uncover other than the reference in Dr. #6's note in the discharge summary. According to that discharge summary, Dr. #7 felt that unless the patient's thallium scan was markedly positive, the patient should be further evaluated at a transplant center via right heart catheterization following congestive heart failure therapy being maximized. The case was also discussed allegedly with a Dr. #8 at the Hospital #2 who supposedly agreed with the workup and management by Dr. #6. It was also mentioned in this discharge summary notation that Dr. #8 agreed to the see the patient sooner if she became acutely worse.
An autopsy performed on this patient reveals that the proximate cause of his death was a pulmonary embolus. A pulmonary embolus or blood clot is an often fatal condition that is overlooked in the workup and treatment of patients who have a number of underlying risks, such as was seen in the case of the patient. He indeed had many risk factors for pulmonary emboli, including his morbid obesity, his hypercoagulable state which would be due to his Hodgkin's disease, as well as a reference in the chart that he may have had recent travel. The diagnosis of pulmonary embolism must be kept in the forefront of a treating physician's mind in order not to allow such a treatable condition to claim a patient's life, as occurred in this case. Pulmonary emboli or clots in the lungs can be readily managed by a variety of medical and surgical techniques, including blood thinners, the use of pulmonary arterial system filters, such as the umbrella and vena cava filters, as well as other modalities.
It is well known that the condition of multiple pulmonary emboli can cause the right side of the heart strain, worsening congestive heart failure symptoms, sinus tachycardia, intermittent chest pain which may or may not be relieved with nitroglycerin, as well as poor cardiac contractility.
It is my opinion based on a review of these records that the lack of cardiology consultation with direct evaluation and examination of this patient was a departure from the standard of care. It can be grossly misleading for a cardiologist to evaluate a patient by such a telephone-type format. An adequate examination of a patient begins with an adequate history as well as a first-hand examination, and both of these steps were denied this patient, to his detriment. In addition, it is inappropriate and a deviation from the standard of care, for a cardiologist to offer his services "if the patient deteriorates." The role of a cardiologist should not only be therapeutic but preventative, and the preventative role in the management of pulmonary emboli is well established.
In addition, it is reported in the discharge summary of Dr. #6 that the patient had a guaiac- (blood) positive stool and an anemia which prevented the use of full intravenous (anticoagulant: blood thinner) heparin. Although guaiac-positive stools represent blood loss from the gastrointestinal tract, such blood loss is at most a relative contraindication to the blood thinner intravenous therapy. As a compromise, it appears that Dr. #6 was willing to give this patient subcutaneous heparin. Heparin, as a blood thinner, can be very useful in preventing blood clots, but has a very limited role when given by the subcutaneous route in treating established blood clots. For this reason, the standard of care regarding pulmonary embolus therapy remains either intravenous anticoagulants, such as heparin, or similar medications.
Although the presence of anemia with gastrointestinal bleeding would have made blood thinner medication a somewhat risky form of therapy, this again is a relative contraindication, and it is far easier in general to treat gastrointestinal bleeding than it is pulmonary emboli. Furthermore, this patient never had the benefit of a scan to rule out pulmonary emboli or an ultrasound to rule out the precursors of pulmonary embolic disease; i.e., deep venous thrombosis of the lower extremities.
The lack of performance of a V/Q scan by either the emergency room or the Intensive Care Unit physicians represented serious departures from the standard of care regarding patients such as the patient in whom a search for pulmonary emboli can be life saving. Furthermore, as mentioned in Dr. #6's note, a right heart catheterization could have given very useful information, and the lack of performance of this procedure represents another departure from the standard of care, which likely contributed to this patient's adverse outcome.
In addition, it seems very paradoxical for the discharge summary to document that a cardiologist agreed that this patient was sick enough to be evaluated by a transplant service team but whose illness did not appear to be of sufficient gravity to warrant an inpatient expeditious cardiac authorization.
The Hospital #1 and several of its personnel may indeed also be negligent in a similar fashion.
Expert reports are available. In this particular case, the input of a Cardiologist and possibly an Intensive Care Unit Specialist would be very valuable.
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Hypertensive young smoking patient with family history of heart disease has no cholesterol testing or therapy, had chest and shoulder pain but negative EKG and cardiac enzyme blood tests. Sent home and dies a few hours later.
In 1994, at age 37, this patient was hypertensive, had a family history of heart disease and complained of chest pain. His family physician, Dr. #1, referred him to a cardiologist, Dr. #2, who performed an echocardiogram (sound x-ray-like study) and noted his heart to be normal. The coronary artery patency was tested by a stress test but was "inconclusive" because he could not exercise enough to raise his heart rate above 92. It was no where near the target rate.
I found no blood testing for a lipid panel, which includes cholesterol and triglycerides. The failure to do such a test by either doctor is a departure from the standards of care, even in 1994. Proper long-term cholesterol-lowering therapy reduces the risk of developing a heart attack. Also, I found no documentation that a low-fat / low-cholesterol diet was recommended. His aunt died of a heart attack at age 43 and these blood tests needed to be done. His hypertension was treated, although he did not always take his medication due to the cost, yet he continued to buy and consume one to three packs of cigarettes per day which shortens life by 48 minutes per cigarette.
On August 17, 1999, he was seen at the Clinic #1and his blood pressure was elevated to 180/98. They reasonably decided to recheck it in three days. They prescribed medication for his left shoulder, which was painful to touch. He had no chest pain radiating (projecting into) his shoulder, often seen with a heart attack. And it was "tender' to touch, consistent with their diagnosis and therapy.
When they rechecked him on (?) August 20, his blood pressure was borderline elevated at 140/90 and his left shoulder still was "tender."
On August 20 he arrived at the Emergency Room with a history of severe chest pain (10 out of 10) and a blood pressure of 164/90 and repeated as 170/100. The chest x-ray was normal, as was the EKG. Also, most significantly the cardiac enzymes (proteins that enter the blood stream from dying heart muscle cells, the CK-MB) were normal at 0.
Except for 30 seconds of chest pain while in the X-ray Department, he had no chest pain, the cardiac monitor was normal and his prerelease blood pressure at 1555 (3:55 p.m.) was 145/90 (borderline and required no treatment).
He died after he arrived home, most likely from a heart attack. No autopsy was done.
Even if the cholesterol test would have been done on August 17, 1999, prescribing cholesterol-lowering medication on that date would make no difference to his survival, compared to 1994.
His cigarette smoking significantly contributed to his demise and you may want to file a claim against the cigarette manufacturer of his brand.
For all the reasons noted above, I do not find negligence against his health care providers. At age 42 and with his family history and chest pains, some physicians may have admitted him to the coronary care unit of the hospital for a one-day stay and monitoring. If that had happened, his death most likely would have been prevented by the use of anti-arrhythmic drugs and electrical shock therapy. But he had significant coronary artery disease of an unknown amount. Without an autopsy, I can only assume by statistical probability that more likely than not, he would have been amenable to angioplasty (balloon artery dilatation) or CABG (coronary artery bypass graft) surgery. Then with an intense antismoking therapy program, cholesterol-lowering drug therapy and a strict vegetarian diet, he may have had added years to his life.
The defense will contend all I noted above, plus the fact that he was disabled. Therefore, the "economic value" of his life was very limited and he had real shoulder pain, which would, to some degree, confuse his cardiac diagnosis which had a normal EKG and a cardiac enzymes (which rise within a few hours of a heart attack), and the fact that his chest pain went away.
You may want us to send these records to a cardiologist and/or Emergency Room Expert for their independent opinions, regarding negligence causation and/or longevity issues. Please advise us if you want to pursue the product liability (cigarette) aspect of this case.
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