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Debilitated Nursing Home Patient Given Overdose of Non-ordered Anti-coagulant (“blood-thinner”), Hemorrhages to Death. New!
This patient was age 73 and living in a nursing home. She suffered from chronic pain caused by arthritis and MS (multiple sclerosis). She was bedridden and often refused to move in bed or get out of bed. Her family had a DNR (Do Not Resuscitate) order.
She had chronic constipation for which she received stool softeners, bowel stimulants and enemas. Her use of narcotics (OxyContin) would cause or contribute to her constipation. Sometimes her pain would be controlled by a placebo (nonactive “fake” medication) to lower her dose of narcotics, which may have been contributing to her hallucinations, too.
Her urine was consistently concentrated (color, odor and high specific gravity) consistent with chronic dehydration. Also contributing to dehydration: their failure to adequately hydrate her by frequent offerings of water which would be substandard care and also increase the risk of a urine infection, which she developed and was treated. She was also incontinent.
Overall, her care was reasonably good, better than most Nursing Home records I have seen.
On 11/27, because of her recent onset of delirium, she was ordered to have a head CT scan.
This showed a “chronic infarct (old stroke) on the left side…with a question of a small hemorrhage.” This was repeated on 12/7 and showed no change: “No evidence of acute infarct or bleed.”
Because of her history of a previous heart attack, she was properly receiving the low dose (81 mg) aspirin therapy to reduce the risk of another heart attack. This also protects her brain from thrombotic (blood clot) strokes.
She developed abdominal pain and alteration of her mental status (more lethargic and irrational), and was hospitalized on 12/8 and died on 12/9. She had some lower intestinal bleeding felt to be from diverticular disease (outpouchings of her large intestine, which can erode a blood vessel or become infected and even perforate). Her abdomen was generally soft, against an acute perforation with peritonitis (widespread abdominal infection).
Initially her vital signs were that her blood pressure and pulse were normal and her respiratory rate was slightly elevated to 24. I have not seen any follow-up records or therapy. Her skin had “multiple ecchymoses” (bruises) consistent with bleeding into her skin. On 12/7, her BUN (kidney blood test) was elevated to 33 but her creatinine (other kidney blood test) was normal at 0.6. This disparity is consistent with acute dehydration and/or acute bleeding with the protein from her blood being absorbed and overwhelming her kidneys’ ability to excrete it all.
Her hematocrit (HCT) was low at 31.1 on 12/8, consistent with anemia. The platelet count (clotting particles produced by bone marrow) was elevated at 573 (two times normal) consistent with an acute bleeding situation.
She did not receive any anticoagulation in the nursing home. There is no record of any Coumadin (warfarin) (a pill) ordered. HOWEVER, on 12/7 the PT (prothrombin time) test for the effect of Coumadin was markedly and dangerously elevated to 38.9 (three times normal) and the more modern test for the same effect, the INR, was greater than or equal to 7.5 (7.5 times normal). Also, the PTT (partial thromboplastin time), which monitors another clotting factor elevated from the use of the injectible anticoagulant Heparin (and Levonix), which could also become elevated from a massive overdose of Coumadin, was 95 (3.5 times normal).
It takes at least three to four days to achieve the PT and INR elevations from Coumadin. Therefore, I conclude she received that drug at the Nursing Home from negligence, or in an attempt to murder this patient (possibly an attempt of euthanasia). On 11/25 at 7:30 a.m., the Nurse’s note by #1 states: “Patient states: ‘How come I woke up alive. I was not supposed to. The Nurse in the night gave me a little white pill that would make me die.’” Was this a hallucination or a deathbed confession??
No autopsy was performed. If her body was not cremated (and preferably embalmed), an exhumation autopsy could be performed (we have Experts available), and if she had extensive internal hemorrhage from excessive anticoagulation, that visual evidence should be available. The FDA and manufacturer should be consulted to see if Coumadin can be tested postmortem too.
Based on the above, I must conclude that she was given a massive overdose of Coumadin for which she had no order for, or any doses noted on her medication record at the nursing home.
It may be helpful to obtain a complete copy of the hospital records from her 12/8 to 12/9 stay. I cannot tell if she went into shock (consistent with hemorrhage), and if it was not treated, since I am missing most of those records. Nor can I tell if Dr. #1 noted the abnormal laboratory test of 12/7 before her demise on 12/9 at 4:30 a.m. He should have seen it and also been called by their laboratory as an emergency “flag.”
The laboratory would be negligent if they did not call that problem to the attention of her Nurse and/or Doctor. The antidote (vitamin K and fresh blood plasma) could have corrected that blood coagulation problem in a few hours, and combined with transfusions could stabilize the patient. Also Dr. #2, a Consultant, called to see her for bleeding, on 12/8, also had a duty to check that test result from 12/7. He suggested “transfusion as needed.” Were any given?
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A Patient with Aplastic Anemia Develops Hepatitis C and Receives Unjustified Therapy for his Hepatitis Which Seriously Worsens His Anemia.
Aplastic anemia is an inability of the bone marrow to produce enough red blood cells, white blood cells, and platelets (clotting particles), and can be total or of varying degrees of severity. His was moderately severe and was controlled with GM-CSF (granulocyte monocyte colony stimulating factor) since 1991.
I have no records from his evaluation when he first was diagnosed with aplastic anemia at age 8. Sometimes it is caused by a side effect reaction to medications, and if they were not needed or not monitored properly, there may be another source of liability. Sometimes it is by a reaction to chemicals. Since he is not yet 21, you may also want to investigate this potential cause of action.
After he began his GM-CSF therapy, his aplastic anemia was under control where he no longer needed blood or blood component (platelet) transfusions.
Unfortunately he contracted Hepatitis C, which is a viral liver infection which becomes chronic. Depending on its activity, it can kill more liver cells than regenerate, resulting in scar tissue (cirrhosis), and liver failure. It can also cause liver cancer (hepatocellular carcinoma). The cause of hepatitis C infection is usually from an infected blood transfusion, or contaminated needle.
I have no information as to how and when it was first diagnosed. The blood test for hepatitis C (non-A, non-B) is a few years old. But blood from paid sources, as opposed to volunteers, had a much higher risk for hepatitis C.
Which source were his transfusions from, and how well were those donors screened? That is another potential source of liability.
The current drug therapy of choice for treating hepatitis C is Rebetron which consists of injections of interferon (Intron A) (an immune protein) and Rebetrol (ribavirin) (a drug that helps kill the virus). This combination of therapy has an approximate 40% positive response rate (significant reduction of the virus amount in the blood/liver), and decrease in liver cell destruction seen on a liver biopsy, twice as effective as interferon given alone.
However, the FDA and the drug manufacturer warn in bold print: "The primary toxicity of ribavirin is hemolytic anemia (destruction of red blood cells)." They also state: " It is recommended that a patient whose hemoglobin level falls below 10 g/ (gram per decaliter) have his/her rebetol (ribavarin) dose reduced to 600 mg (milligrams) daily…. A patient whose hemoglobin level falls below 8.5 g/dl should be permanently discontinued from Rebetol/ Itron A therapy (see WARNINGS)."
When there is active hepatitis C the "viral load" (the number of viral particles per milliliter: ml of blood) is often one million or more. And as liver cells die from viral infestation they burst and their protein enzyme contents enter the blood, and are easily measured on standard laboratory tests. These are LDH, SGPT, and SGOT.
Before a patient is started on Rebetron therapy you need a reason, and often a liver biopsy is performed to actually determine microscopically what actually has occurred (scarring: fibrosis) and is (occurring active liver disease). With the standard needle biopsy through the abdomen into the liver, the major risk is bleeding, and if a patient has a very low platelet count (under 50,000, and especially under 25,000) it is contraindicated.
A liver biopsy can be performed by threading the biopsy needle via a neck (jugular) vein, past the heart and via the inferior vena cava into a hepatic (liver) vein, which eliminates bleeding into the abdomen. That was done on 3/16/2001, 15 months after the Rebetron therapy was terminated (after two weeks of therapy), and revealed "mild to moderate chronic periportal inflammation," and "mild porotal (the vein that brings blood into the liver from the intestines) fibrosis (scarring)." "The hepatic lobules (liver cells) are otherwise unremarkable)." This is not significantly active disease.
In his case, all the liver enzyme blood test were all normal on six studies form 7/98 through 1/3/00 and also on the eight studies after his Rebetron therapy through 10/2000 (and some were even below normal). All evidence against significantly active liver disease.
The Hepatitis C viral blood levels were 564,000 on 4/97, 700,000 on 7/13/99 and 330,000 on 11/18/99.
His hemoglobin blood levels (the oxygen carrying red blood cell pigment) showed significant anemia for years, as well as on 1/3/00 at 8.1. This is obviously below the 8.5 warning threshold level to terminate the use of this drug (ribavirin).
I know of no studies that evaluate the risks and benefits of Rebetrol in patients who have hepatitis C and aplastic anemia. Therefore, this is experimental and requires a very stringent level of informed consent.
Based on the normal liver enzymes and moderate level of hepatitis C viral particles there would be a question of therapy without a liver biopsy. But in a patient also with severe anemia, I believe that it was a departure from the standards of care to begin Rebetron therapy on 1/3/00.
On 11/18/99 they noted that the HCV (hepatitis C) PCR (viral blood level) was "700,000 copies" on 7/99. But they (Dr. #1, Dr. #2 and FNP Family Nurse Practitioner #1) never noted the 330,000 HCV PCR level that was done on 11/18 until 1/3/00, and did not stop initiating the "therapy."
On 11/22 FNP #1 noted that both Drs. #1 and #2 recommended a platelet transfusion and percutaneous liver needle biopsy (into the abdomen) "before interferon therapy versus Interferon / Ribavirin therapy." They were also going to do a bone marrow aspirate biopsy. "he should also be followed by Hepatologist (Liver Specialist) for Hep C therapy." I found no such consultation. Also it was not the interferon that caused the worsening of his anemia. It was the ribavirin. Although interferon has one-half the response rate, it could be given alone. In addition, a better form of interferon, Pegasys was under development, and there was no rush in his case to begin any risky therapy.
He returned on 1/10/00 FNP #1 noted "His CBC (complete blood count) has fallen a lot since last week, but he says he forgot to take his GM-CSF last night. I emphasized to him that the Rebetron has cause some decrease in CBC and he needs to take GM-CSF every night. We will probably go up on dose next week if CBC is still decreased." There is no evidence that this negligent FNP ever brought any of this to the attention of her supervising doctors that day, or ever. His Hgb (hemoglobin) level was down to 7.7 and his white blood count was dangerously low at 1.8 (1,800) versus 2.7 the week before. He was at a serious risk for infection.
On 1/17 his Hgb was 6.0 his platelet count dropped from 16 (16,000) to 9,000 in one week. This FNP and Dr. #2 still did not stop the Rebetron therapy.
On 1/19 the Hgb was 5.6 and the platelets only 10,000. Finally the Rebetron therapy was stopped by FNP #1 and apparently some doctor (whose signature I cannot read). On 1/19 transfusions were ordered to begin with two units of RBC (red blood cells). He also was transfused two units of RBC on 2/7, 2/21, 3/14, and 4/4.
The bone marrow makes all these blood elements and some of the immature red blood cells, called reticulocytes, enter the bloodstream. His reticulocytes count pre-Rebetron on 7/12/99 was 3.0, 11/18/99 1.4 and on 1/3/00, the day of initiation of Rebetron, it was 2.6 Then it dropped to 0.6 on 1/10/00 and further decreased to 0.2 pm 1/19. On 1/31 it was 0.9. This is the opposite response of the body to hemolytic anemia where red blood cells are destroyed, and a healthy (functional) bone marrow makes more cells. This is evidence of a direct toxic effect of ribavirin on his bone marrow. Did his doctors report this to the FDA as they should have done, and did they publish their finding in any medical journals to warn other doctors of this danger?
Apparently, he will undergo a bone marrow transplant. That will complicate his hepatitis C depending on which additional drugs he will receive. Immuno-suppressive drugs do interfere with the body's ability to fight infection, including viruses. And with a damaged liver, many drugs are more toxic to his liver.
He is at risk from bleeding internally and externally from a very low platelet count. He is also at risk from complications from blood transfusions including infections and transfusion reactions.
The Defense will content that he was fully informed of all the risks, but what known risks are there with aplastic anemia, to fully inform a patient about? I now of no information on that subject. You may want to conduct a Medline search (with the National Library of Medicine)
Using the key words ribavirin and aplastic anemia.
The Defense will try to claim "contributory negligence for him missing one dose of GM-CSF on 1/9/00. I doubt it made the difference to his persistent bone marrow suppression.
Since 3/4/96 has he ever missed taking any of his daily 250 mcg (microgram) injections? If so, there did not appear to be any profound effect on his bone marrow and anemia.
In my opinion Dr. #1, Dr. #2, FNP #1, their hematology clinic, and Hospital #1 (which appears to be their employer or created agents of them) are all negligent for all the reasons stated above.
You need to know that there are nutritional (herbal) alternatives to aid the liver including milk thistle (containing silymarin), and combinations of Chinese herbs. Was this option with no side effects ever discussed with him?
I would suggest that you authorize our office to obtain Board Certified Experts in Hematology, Infectious Disease and Gastroenterology to give you their opinion on negligence, causation, and damages.
He also was noted to have a "probable panic attack" in 3/00. Has he been under a Psychologist or Psychiatrist's care?
Thank you for allowing our organization to assist you with this interesting case. We continue to remain available on this case to obtain Expert Witness opinions.
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Problems with anticoagulation (blood thinner) and neck bleeding.
This patient had been diagnosed with a "hypercoagulable state," which means increased risk from excessive blood clotting. Because of that problem she developed deep vein thrombophlebitis (DVT) which required anticoagulation (blood "thinner") therapy on a long?term basis using the oral drug, Coumadin.
Because the condition recurred, her physicians offered her the surgical option of inserting a Greenfield vena cava filter. This is placed through a large neck vein, threaded downward past her heart and "fired open" into the inferior vena cava just below where her kidney veins enter. This looks like an umbrella with multiple small perforations to allow blood through, but blocks life-threatening clots from the pelvic and leg veins. However, with a Greenfield filter and her hypercoagulable state, chronic anticoagulation therapy is needed to prevent clots from forming on that filter, breaking loose and also passing into the venous system and then heart lung circulation (pulmonary embolus), which can be fatal.
The Doppler (ultrasound blood flow study) venous examination of 2/26/94 showed old and possibly new clots in her leg veins. On 2/27/95 there was some improvement.
The letter by Dr. #1 of 7/12/96 noted a history of pulmonary embolism in addition to her hypercoagulable state. That would justify her remaining on Coumadin. Its dose is adjusted according to the results of the Prothrombin (PT) time and the INR tests, usually done every two weeks.
On 12/18/96, a Doctor #2 noted, "…seen at Hospital #1 at request of Dr. #3 for upper airway obstruction. History of deep vein thrombosis, was admitted for anticoagulation and possible insertion of filter or vein stent. She developed massive hematoma of the right neck and upper airway compromise requiring emergency intubation (putting a tube through the mouth into the windpipe [trachea] to maintain an open breathing passageway) at approximately 3:00 a.m. several days ago." I have not seen any of those records to see if she was over anticoagulated or if some surgical (invasive) procedure took place while she was under the effect of anticoagulation, which usually is negligent, and can cause excessive bleeding.
On 12/18, she was hoarse and had swelling in her larynx (voice box). There was ecchymosis (black and blue discoloration from bleeding into her flesh) in the posterior and side of her throat (pharynx).
This had improved by 12/21 and markedly improved by 12/26. This does not appear to have caused any permanent physical damage, but was very upsetting psychologically. I do not know the degree and persistency. I have not seen any psychological evaluations regarding this post?traumatic stress disorder. However, she subsequently refused the insertion of a Greenfield filter on the basis of this harrowing experience.
On 1/4 she told a Doctor at the Clinic #1, that "she was recently hospitalized from 12/13/96 - 12/23/96 for a recurrent right iliac (vein) deep vein thrombophlebitis." She told this Doctor that she suffered "severe throat trauma" from the physician at Hospital #1. "going in the wrong place." She apparently had an infusion of the blood clot dissolving drug, urokinase, that she claimed "leaked in the neck, causing swelling and bruising, stripped vocal cords, if that is the concern in this case (I have not seen any "statement of facts"), all these records should be obtained, including the discharge summary, admitting history and physical, doctor and nurses progress notes, all medical orders and medication index (what she received and when), consultation reports and the laboratory tests for an Addendum Report review.
She complained that she had trouble taking a breath and subsequently had a number of complaints they called "hyperventilation syndrome," which would be a psychological adverse reaction to that problem if she did not have it prior to that neck hemorrhage and almost-death event. For example, she was hospitalized for "problems breathing" on 2/20/97, and this was noted on 4/28/98 with hypersensitivity to the left side of her face. She was taking the drug, Paxil (like Prozac), and this dose was increased at that time.
Subsequently, most of the time, they properly adjusted her Coumadin dosage in accordance with her PT and INR tests. They properly stopped it before dental work on 8/11/98.
On 2/13/97, she again refused the Greenfield filter and was noted to have a "larger ROM (range of motion) in turning neck to the left." This may be related to the hemorrhage three months earlier. Has this persisted?
On 8/7/97, they negligently increased her Coumadin to 10 mg per day from 7.5 mg despite a therapeutic range of the PT at 20.4 seconds and the INR at 3.2. On 8/7, the laboratory tests (which came back on 8/8) again showed a good therapeutic value of 21.4 for the PT and 3.2 for the INR.
On the follow-up office visit on 8/14, they noted she was "presently on 10 mg Coumadin" but failed to note the previous change in dosage despite a good therapeutic blood test range at 7.5 mg of Coumadin. The next day she was called to stop the Coumadin for two days and decrease it to 5 mg per day. The reason was that the PT was 30.1 and the INR was 6.5, both dangerously elevated. However, she did not develop any bleeding problems from that negligent error.
On 11/17, the tests showed dangerously high values of 23 for the PT and 4.3 for the INR. She was not called when the results returned on 11/18 and, due to their negligence, she developed bloody stools on 11/25. They stopped the Coumadin and had a gastroenterologist evaluate her by colonoscopy (the passage of a hose-like lighted telescopic device up her rectum and into the full length of her large intestine). The result of this uncomfortable study is not in their records (if it was done).
On 1/29/98, an upper gastrointestinal x-ray (UGI) study showed an 8 mm (1/3 inch) mass in the duodenum (the first part of her small intestine). I see no follow-up biopsy despite such a recommendation by the Radiologist. On 12/1/97 she was referred to Dr. #4 for her "GI bleed." I have not seen his records.
She had visits on 12/1, 1/7/98, 1/27, 2/12, and 3/17. All of the INR and PT values were consistent with no use of Coumadin. No one commented. On 4/20 their note says, "Patient is on Coumadin," which is impossible. The INR test from that date was 0.8 (which is low, meaning hypercoagulable). She was seen on 4/28, and nothing was said about that problem.
Finally on 6/2, they noted the "subtherapeutic anticoagulation" and "patient's Coumadin is to be restarted." I see no problem developing in her condition from those seven months without proper anticoagulation. The last records I have show therapeutic values for her PT and INR on 11/12/98.
The only area of potential negligence with resulting physical and emotional damages occurred from her neck hemorrhage in 12/96. I have not seen those records, which should be evaluated.
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