New York State Court of Claims

New York State Court of Claims

EYRE v. STATE OF NEW YORK, #2005-018-486, Claim No. 101532


Synopsis


Based upon the facts as found, no medical malpractice was committed. The claim is dismissed.

Case Information

UID:
2005-018-486
Claimant(s):
ARTHUR EYRE
Claimant short name:
EYRE
Footnote (claimant name) :

Defendant(s):
STATE OF NEW YORK
Footnote (defendant name) :

Third-party claimant(s):

Third-party defendant(s):

Claim number(s):
101532
Motion number(s):

Cross-motion number(s):

Judge:
DIANE L. FITZPATRICK
Claimant's attorney:
CHERUNDOLO, BOTTAR & LEONE, P.C.By: ANTHONY S. BOTTAR, ESQUIRE
Defendant's attorney:
ELIOT SPITZER
Attorney General of the State of New York
By: ROGER B. WILLIAMS, ESQUIREAssistant Attorney General
Third-party defendant's attorney:

Signature date:
September 15, 2005
City:
Syracuse
Comments:

Official citation:

Appellate results:

See also (multicaptioned case)



Decision
Claimant seeks damages from the State of New York as a result of medical malpractice. Claimant alleges that while he was a patient at the State University of New York Upstate Medical University (hereinafter University Hospital) the State medical providers negligently administered Heparin to him resulting in the amputation of several of his extremities. By stipulation, the trial was bifurcated and this decision relates solely to the issue of liability.

At trial, Claimant, who was born January 30, 1918, was 86 years old. During the trial, Claimant could not recall all of the specifics; however, he testified to the general course of events. More detail was provided by the medical records admitted into evidence, the testimony of Claimant's daughter, Ms. Amy Bleyle, and the medical providers involved in Claimant's care. Each side also provided the testimony of an expert witness.

The events leading to this claim began on September 11, 1996, when Claimant interrupted a visit to Alexandria Bay with his wife because of chest pain. According to Claimant's daughter, Ms. Bleyle, in 1996, before his hospitalization, Claimant was in good health and quite active, enjoying such activities as woodworking, gardening, mowing the lawn and setting up his model train set. On September 11
, Claimant went to Dr. Capella's office, his family physician. Claimant was sent directly to the Emergency Room of Crouse Irving Memorial Hospital (hereinafter Crouse) by ambulance. That evening he was admitted to the hospital with an acute interior wall myocardial infarction (a heart attack). While at Crouse, Claimant began a regimen of Heparin, an anticoagulant, and underwent a cardiac catheterization. Claimant's blood platelet counts while he was at Crouse were:
September 11, 1996 116,000
September 12, 1996 114,000
September 13, 1996 113,000
September 14, 1996 103,000

The normal range for the laboratory at Crouse Hospital was 130,000 to 396,000 per microliter. No blood tests were performed on September 15 or September 16, 1996. Claimant's platelet count, even at that time, was abnormal.
After the cardiac catheterization and other tests, it was determined that Claimant was a candidate for coronary artery bypass grafting. After consultation with Dr. Anthony L. Picone, Claimant was transferred to University Hospital on September 17, 1996, for the surgery which was performed that day by Dr. Picone.[1]
His platelet count before the surgery was 100,000 and after the surgery was 55,000, however a drop in platelet count is not unusual after bypass surgery. The normal range for the laboratory at University Hospital is 150,000 to 400,000 per microliter. Although Heparin was discontinued for preoperative procedures, Claimant was again given Heparin for the surgery and postoperatively.[2] The surgery was successful and Claimant was transferred to the Intensive Care Unit (hereinafter ICU) until September 20, 1996. Claimant's platelet count on the afternoon of September 18 was 108,000, an earlier reading was attempted but platelet clumps were present so the count could not be obtained. On September 19, Claimant's platelet count was 79,000 and on September 20 it was up to 85,000. The next test was ordered for September 22, 1996.
Claimant's wife, Mrs. Eyre,[3]
and his daughter, Mrs. Bleyle, visited Claimant daily while he was in the hospital. The length of their visits were limited while he was in the ICU because of the visitation restrictions for that unit.
On September 20, 1996, Claimant was well enough to be transferred from ICU to the Cardio-Thoracic Unit. On that day Ms. Bleyle spent most of the afternoon with Claimant, and she recalled he was quite sleepy. Ms. Bleyle noticed that Claimant's fingernails were blue. She watched the respiratory therapist attempt to get a reading by placing a clip on Claimant's finger without success. She spoke with the therapist about this because she was concerned. The next day, September 21, Ms. Bleyle was again with Claimant all afternoon. Claimant's fingertips and fingers were blue and he did not seem himself that day, he was out of it. Donna Schermerhorn, a nurse practitioner at University Hospital who treated Claimant in the Cardio-Thoracic Unit, also testified at trial. Ms. Schermerhorn first saw Claimant the morning of September 21
. She noted that Claimant had bilateral lower extremity edema, although no edema was noted on the patient observation sheet for the prior evening. Edema is not uncommon after bypass surgery. Ms. Schermerhorn also noted that when Claimant was out of bed, his gait was unsteady. She noted that although Claimant was confused in the morning, he seemed to get better as the day went by and since he had been given narcotics, she did not find this unusual.
Ms. Schermerhorn also treated Claimant on September 22
. Her notes indicate that Claimant had atrial fibrillation flutter, an abnormal heartbeat, which was not present the day before. Claimant also required the assistance of two people to be ambulatory. She also noted that the skin on Claimant's legs was mottled, and her notes[4] reflect that his fingers were mottled and blue-gray. His feet were cool and cyanotic. She reported the condition of his feet and skin to Dr. J. C. Trussel, the resident that day, because it was a change from the day before and she was concerned this seemed to indicate poor circulation. Claimant's lungs were not clear, and he had an abnormal oxygen saturation reading of 88 to 90% while on room air, so oxygen was ordered. There is no documentation that Claimant's circulatory problems were the result of his heart failing to profuse normally. His platelet count was down to 22,000 on September 22. Although laboratory reports are usually brought up to the floor at a certain time each day, when the results are abnormal the readings are called to the floor to effectuate timely intervention. Claimant's blood was drawn at 10:00 a.m. and the platelet count was called to his floor at 11:00 a.m. Ms. Schermerhorn noted concern about administering Heparin to Claimant, so she checked with the house officer, but she could not recall why she had done so. At 11:15 a.m., Dr. Sinacore, a resident on call that day, ordered that all Heparin be discontinued including the Heparin flushes for the IV lines. All the experts and medical professionals agreed that the discontinuance of Heparin, in light of Claimant's rapid decline in platelet counts, was consistent with good and accepted standards of practice. No further platelet counts were ordered that day, nor were any other tests ordered to further assess Claimant's condition.
On September 22, 1996, when Ms. Bleyle arrived to visit Claimant, he was sitting in a chair eating dinner. On that day not only were his fingers blue but also his feet and nose. Claimant complained his feet were cold and painful. Ms. Bleyle went and told a nurse's aide who came and propped Claimant's feet up with a pillow. No other hospital staff member came to examine Claimant's feet or hands during Ms. Bleyle's visit that day.

On September 23, 1996, the medical staff recognized a distinct downturn in Claimant's condition. At 1:00 a.m., Dr. Trussell was called because Claimant was complaining of severe back pain which was not relieved by the pain medication, Percocet. His extremities were mottled, and the records reflect that a nurse noted his feet and fingertips were "dusky." Upon examination, Claimant's extremities were found to be cyanotic, his abdomen distended, and he was afebrile.[5]
His platelet count had dropped to 10,000. At 3:40 a.m., radiology attempted to rule out an abdominal aortic aneurysm (hereinafter referred to as AAA) by performing an ultrasound, but the aorta could not be viewed so a CT scan was ordered. Ultimately AAA was ruled out and other consultants were called. At 7:00 a.m., a general vascular surgeon, Dr. William Marx, was consulted. At that time Claimant was still afebrile, his toes were cyanotic, but he had brisk capillary refill. Claimant had an ultrasound of his gallbladder which ruled out inflammation. A venous angiodynography revealed blood clots in Claimant's popliteal vein in his left leg and in the saphenous vein in his right leg. A transesophageal echocardiogram was performed. No blood clot was seen in Claimant's heart. Dr. Marx[6] suspected either a venous problem or disseminated intravascular coagulation (hereinafter DIC). DIC is a condition where coagulation is occurring in blood vessels throughout the body; it is usually a secondary condition, caused by a variety of primary conditions, such as a transfusion reaction, severe trauma (i.e., shock, burns, electrocution), liver disease, obstetric complications, tumors, aortic aneurism, respiratory distress syndrome, certain drugs, or an infection. Several tests were performed to determine whether Claimant had an infection (sepsis) as the primary problem causing DIC. No infection was found.
Dr. Picone called Claimant's wife, Mrs. Eyre, early to tell her that Claimant was quite ill. Mrs. Eyre and Ms. Bleyle arrived at the hospital between 8:00 and 9:00 a.m. that morning and found that Claimant had been transferred back to the ICU. Claimant was asleep at that time, but Ms. Bleyle noted that his hands and nose were still blue. Ms. Bleyle and her mother met with Dr. Picone about Claimant's condition. Ms. Bleyle did not speak with any other medical personnel at the hospital that day.

Dr. Picone wrote in Claimant's progress note for that date:[7]

Patient with sudden change in status yesterday/AM. Developing

pain in pelvic region and peripheral mottling. LE, "lower extremity"

greater than UE, or "upper extremity." Patient was febrile yesterday

and then AM had increased WBC to 22,000. Patient has also

developed DIC picture with severe decrease in platelet count down

to 10,000 and increased PT, PTT, decreased fibrinogin and increased

fibrin split products. Abdominal CT was negative, and echocardiogram

showed reportedly good LVE function without effusion. His physical

exam shows abdominal distention, decreased bowel sounds. Lower

extremities cyanosis with tight edema. Femoral popliteal intact, good

capillary refill. Moves feet bilaterally. Impression: Presently am

concerned with septic process/peripheral emboli with gut ischemia

with associated DIC. Will plan venous non-invasive studies to rule out

venous occlusion. Antibiotic, broad spectrum coverage.

Dr. Marx wrote in Claimant's medical records at 11:30 a.m. that he would get a hematology consult to determine if anticoagulant drugs would be contraindicated and if so, he would use a Greenfield filter. A Greenfield filter is a device which can be inserted into Claimant's vena cava[8]
to prevent blood clots in his legs from migrating to his heart.
Dr. Jonathan Wright,[9]
a hematologist, was consulted on that date at approximately 1:00 p.m. regarding Claimant's condition. Dr. Wright examined Claimant, reviewed his chart, diagnostic studies, and had his blood tested for platelet count and ordered coagulation tests for fibrinogen and fibrin split products. He also had a renal flow study performed which was negative. He arrived at a differential diagnosis of DIC (which Dr. Marx had also suspected) or Heparin Induced Thrombocytopenia with Thrombus Syndrome (hereinafter HITTS). Thrombocytopenia describes a persistent low platelet count and is not unusual in patients after heart surgery. HITTS involves an allergic reaction to the administration of Heparin causing a low platelet count and blood clots forming within the blood vessels. In 1996, according to Dr. Wright, the difficulty with this differential diagnosis was that treating a patient with Claimant's symptoms for DIC consisted not only of treating the inducing condition but also administering Heparin in low dosages, but Heparin was contraindicated in the treatment of HITTS. On cross-examination, Dr. Wright admitted that he was aware that DIC can actually be caused by Heparin, and he also agreed with a statement made by an authority on Hematology[10] that once DIC is well-established in the patient, Heparin is less effective or ineffective. Other anticoagulants were available although Dr. Wright felt that these other options were not good alternatives to Heparin. According to Dr. Wright, left untreated, DIC can be rapidly fatal; with HITTS the risk is continued clotting and tissue injury. The other problem with this differential diagnosis is that there is no definitive test to determine whether a patient has either of these conditions. For DIC is it a "spectrum test"[11] in addition to looking for a primary cause. Blood clotting tests for fibrinogen indicating a low or low-normal range and fibrin split products which are higher than normal indicating that the patient is clotting: using the clotting factors (fibrinogen) and breaking down the clotting (fibrin split products). Another is a Dediamer test,[12] which measures the number of fibrin products in the circulation which would show an increase. Other blood tests which were ordered for Claimant, include ProThrombin[13] time (PT), and Partial Thromboplastin[14] time (PTT), to test how long it takes for the blood to clot. Low platelet counts are also a factor. For HITTS, there is also no definitive test but the Heparin antiplatelet antibody test is used and indicates whether the platelets are clumping and granulating in the presence of Heparin. Dr. Wright ordered this test to be done on Claimant on September 23. However the test could not be done at University Hospital at that time, so to obtain the results it typically took a few days to a week. Dr. Picone, after consultation with Dr. Wright, ordered the resumption of Heparin in low dose at 5:15 p.m. that day, which was administered by bolus followed by IV. Dr. Wright's notation in the medical records from that day provides:
"2:00 p.m. Hematology attending . 78 year old white man status post CABG 9/17/96 - on Dopamine/epi post-op. Last night developed back pain, mottling of feet and hands. Work up. Abdominal ultrasound, CT abdomen, venous angiodynography; no arterial thrombi seen, but clot in the right proximal and distal saphenous vein. Acute occlusion of left popliteal vein, reportedly arterial flow normal. Lab shows FSP greater than twenty, fibrinogen 209, platelets, 9/17- 100[15]; 9/18 - 108; 9/19 - 79; 9/20 - 79[16]; 9/21 - 85; 9/22 - 22; 9/23 - 10. PM itch. Hemorrhoidectomy, herniorrhaphy, cerebellar hemangioblastoma. Meds on admission: Hytrin, aspirin, Tenormin, Isordil, has been on Dopamine, epi, heparin, Procan SR, Nifedipine, Albuterol, Unasyn, Morphine, Lasix, Vasotec, Zantac, Digoxin, Carafate, Ceftriaxone.
On exam, lethargic, CV regular rhythm, external incision, no evidence of infection. Lungs, rhonchi. Abdomen soft, slightly distended. Extremities: Mottling both lower legs, feet, both hands.

Impression: Thrombocytopenia with poor perfusion of hand and feet. Rising creatinine, biochemical picture of DIC. Major question is whether this is DIC with distal vessel (small arterial) thrombi requiring Heparin (low dose) versus Heparin induced Thrombocytopenia. He definitely has DIC, which can cause this picture. He does not to our knowledge have large arterial thrombus. The confirmatory test: Heparin dependent anti-platelet antibodies. Will take two to three days for answer.
Recommendation: Check renal flow study. Thus far again no large arterial thrombus found. If flow study acceptable, and clearly no other major arterial thrombus, would use Heparin at 500 units per hour after 5,000 units bolus. This is a judgment call. I will not know results of Heparin dependent antibodies until later this week, but I know he is in DIC, and in this clinical picture Heparin is indicated.[17]

The next day, Claimant underwent surgery, an exploratory laparotomy performed by Dr. William Marx. Ms. Bleyle saw Claimant before and after the surgery. She could see that Claimant's fingernail beds were a deep blue which seemed to be radiating into his finger tips, but his nose did not seem to be as dark blue as it had been. Dr. Jonathan Wright, the hematologist, spoke with Ms. Bleyle and Mrs. Eyre before the surgery about Claimant's condition.

Dr. Marx's findings from the surgery were that Claimant had mesenteric venous thrombosis, or the veins in his bowel and small intestine had clotted off. Dr. Marx testified that in all probability this was caused by his reaction to the Heparin.

Ms. Bleyle recalled Claimant underwent another surgery on September 25. The surgery was another exploratory laparotomy to check Claimant's bowel and the placement of a Greenfield filter and feeding tube. This surgery was also performed by Dr. Marx. During that surgery, the results of the Heparin antiplatelet antibody test came back positive. The administration of Heparin was discontinued. For anticoagulation, Claimant was given Dextran and Ticlopidine. An effort was made, without success, to obtain the drug Hirudin, a new anticoagulant, which was available in Canada but was not available here. On that date, Claimant's bowel looked better; there was no dead bowel, and the cecum looked viable.

Without a significant change in Claimant's condition on September 24
and 25, Dr. Wright stayed the course with the administration of Heparin until the Heparin-dependent antibody test results came back.
Claimant called Dr. James M. Vogel, a hematologist/oncologist, as an expert witness. Dr. Vogel described two types of Heparin induced Thrombocytopenia. One variety, often referred to as HIT,[18]
is not particularly significant despite the fact that the administration of Heparin causes a decrease in the platelet count. The second variety, HITTS,[19] is more significant. This is where the administration of Heparin causes an interaction with platelets and causes the release of "Platelet Factor 4." Platelet Factor 4 combines with the Heparin as an antigen, inducing an immunological response: an antibody to that particular Heparin Platelet Factor 4 entity. If there is more Platelet Factor 4 than Heparin, then the antibody will attach to the platelets, causing the platelets to aggregate and clot. The risk associated with this condition, according to Dr. Vogel, is clotting throughout the body, all systems and both in the arteries and veins. Dr. Vogel testified that if there is clotting restricting circulation to the extremities this will cause ischemia,[20] which is manifested by whiteness and cyanosis[21] of the affected areas. If a patient developed a clot in the mesenteric supply system, the arteries and veins that supply the intestines, the symptoms would be pain, diarrhea, abdominal distention, and there may be inflammation evident by a temperature elevation and/or a white blood-cell count elevation.
Dr. Vogel described DIC as a secondary condition caused by another stimulus, where the equilibrium between the clotting and the dissolution of the clot is upset. He indicated that treatment is actually treatment for the underlying or primary condition. Where an infection is the cause of DIC, as was suspected by Dr. Wright in this case, Dr. Vogel testified the infection is an overwhelming infection: a life-threatening infection. Dr. Vogel also stated that some drugs, such as Heparin actually cause DIC, as a secondary condition to HITTS.

Dr. Vogel opined that it was a deviation from the standard of care to have failed to take Claimant's platelet count on September 21
because his levels were abnormal up to that point and he had been on Heparin since September 11. September 21 was within the window of time for assessment of whether Heparin was producing a decrease in his platelet counts. Based upon Claimant's abnormally low platelet count of 22,000 on September 22, Dr. Vogel opined that the HITTS condition was in progress, he was thrombocytopenic, and Dr. Sinacore was correct to stop the administration of Heparin. Dr. Vogel testified that where you have a low platelet count, Heparin has been administered, and HITTS is a potential diagnosis, it is mandated that Heparin be stopped. In Dr. Vogel's opinion, it was a deviation from the standard of care to restart the Heparin on September 23 and continue it through the 25th.
Based upon the absence of bacteria in Claimant's urine sample, the results of the blood cultures being negative, the CAT scan, the transesophageal echocardiogram, and the gallbladder studies, Dr. Vogel opined that there was no infection causing DIC and the Thrombocytopenia. This was supported as well by Dr. Marx's exploratory surgery which found no abscess. Although Dr. Vogel noted Claimant did have bronchitis, caused by the irritation of the tracheal bronchial area from the inhalant anesthesia, this was not a sufficient infection to cause DIC. Another component of Dr. Vogel's opinion was Claimant's white blood-cell count. Claimant's platelet count had dropped to 22,000 by September 22;
however, his white blood-cell count had not gone up. The white blood-cell count did go up on the 23rd but Dr. Vogel opined that this was in response to the mesenteric thrombosis, the inflammation of the bowel found by Dr. Marx on September 24. Dr. Vogel felt this thrombosis was the cause of Claimant's back pain as well.
Dr. Vogel also felt that the blood tests for fibrinogen, fibrin split products (FSP), Pro-Thrombin time (PT), and Partial Thromboplastin time (PTT), needed to be assessed in light of the administration of platelet units and Heparin. The blood draw for the test for fibrin split products was first done on September 23,
within two hours of the administration of six units of platelets. Dr. Vogel testified that the administration of blood products invalidate this particular test because the blood products have circulating substances that cause positive fibrin split products. The results should not have been relied upon as an indication Claimant had DIC, secondary to an infection. The fibrinogen levels did not increase until September 24 and 25. Dr. Vogel attributed the increase to Claimant's abdominal surgery and mesenteric thrombosis; it is an acute phase reactant.[22] The PT and PTT results were also not indicative of DIC. On September 17 the PT time was 17.3 seconds immediately after his bypass surgery. On September 22 at 11:15 the PT was 15 seconds. On September 23, the blood draw was at 6:02 a.m., and the level was 15.2 seconds, and at 7:09 p.m., it was 15.8 seconds. In Dr. Vogel's opinion, if Claimant had suffered from DIC significant enough to cause the type of Thrombocytopenia he had, the PT level would be substantially elevated but it was not. Claimant's PTT level, which measures the Heparin level frequency, on September 17 was 42.2 seconds, outside the normal range. The September 23 value was 38 seconds for the blood draw at 6:02 a.m. If Claimant had DIC, the PTT levels would have been significantly elevated and this was not the case. The blood draw at 7:09 p.m. on September 23, however, was elevated to 87.4 seconds. Dr. Vogel attributed this to the fact that Heparin had been reintroduced by bolus[23] followed by hourly intravenous administration.
According to Dr. Vogel, the reintroduction of Heparin to Claimant on September 23
exacerbated the ongoing problems of Thrombocytopenia and clot formation which started on September 21. On September 23, only the studies of Claimant's legs showed the existence of clotting, all other tests were negative for clots. Placement of a Greenfield filter at that time could have prevented these clots from moving to Claimant's lungs. Dr. Vogel also mentioned that there were other techniques available to address the clots in Claimant's legs without the use of Heparin, but the use of aspirin was the only item he identified. Dr. Vogel did testify that, as of the morning of September 23, although Claimant's extremities showed impairment of circulation, any problems were reversible as evidenced by the brisk capillary refill. After the Heparin was reintroduced on the evening September 23, and continued through the 24th and 25th, during that time, capillary refill slowed until it was more than 3 to 5 seconds resulting in the damage that led to his multiple amputations.
Defendant also called an expert, Dr. Jacob Rand, a hematologist board certified in hematology and internal medicine. Dr. Rand also agreed with the differential diagnosis of DIC and HITTS, and agreed with Dr. Wright that it is a difficult determination to make because there is no single test; but rather, a doctor must evaluate the patient's history, physical findings and laboratory results to reach a diagnosis. Dr. Rand agreed that DIC is usually a secondary condition caused by many factors including infection. He testified it is a common complication of coronary bypass surgery. Dr. Rand explained that the clotting formation associated with DIC and HITTS are different. In DIC it is the body's normal clotting system which rather than formulating only at the site of injury occurs throughout the body. It is manifested by the consumption of clotting factors and platelets and developing Thrombocytopenia. In HITTS, the clotting is triggered by Heparin which binds with the blood protein Factor 4. The patient's body begins to make antibodies against the Factor 4 platelet and the antibodies attach to platelets resulting in even more Factor 4 being released and binding to the Heparin, which causes more antibodies to be made, and the cycle continues. The clotting that results, according to Dr. Rand, has been referred to as "white clot[s]" which generally form in arteries. Typically red clots, which are normally seen, form in veins. Although the clotting with HITTS can occur in arteries or veins, in 1996 it was, according to Dr. Rand, primarily considered an arterial clotting disorder. Like Dr. Wright, Dr. Rand opined that the development of HITTS occurs in patients who have been previously exposed to Heparin, with symptoms developing within three to five days. Considering Claimant's prior cardiac catheterization and angioplasty eight years earlier, with which there is always concurrent Heparin treatment, it would have been expected that the symptoms of HITTS would have normally developed early on after the reexposure to Heparin: an anamnestic response. Here, Claimant's symptoms did not begin until September 22
, 10 days after the Heparin regimen began, atypical timing according to Dr. Rand. Although Dr. Wright testified during his deposition that the interval between the administration of Heparin and the onset of Thrombocytopenia would not have assisted him in his determination of a DIC versus HITTS diagnosis.
As far as Claimant's platelet counts, Dr. Rand noted that he came into Crouse with a low-baseline platelet count of 116,000 which should have been investigated. The significant drop following the surgery on September 17,
Dr. Rand testified, was a normal decrease that occurs during open-heart surgery. The increase in platelet counts on the 18th and the decrease on the 19th to 79,000 required, according to Dr. Rand, observation but it is not unusual in the post-bypass surgery setting. Despite Dr. Rand's opinion that the low platelet counts should have been observed or investigated, on cross-examination, he acknowledged that this was not done until September 23. On September 20, when Claimant's platelet count went back up to 85,000, it was, prospectively from that time, a good sign according to Dr. Rand. Dr. Rand did not agree with Dr. Vogel that daily platelet counts were the standard of care for a patient on Heparin.
Dr. Rand also testified that with Claimant's atrial fibrillation, because the heart is not contracting properly, there is a risk of "blood stasis" where the blood does not properly exit the heart increasing the susceptibility to clotting, or thromboembolism. The treatment for this is Heparin. Atrial fibrillation also results in the heart's ineffective delivery of blood and a decrease in the efficiency of circulation. On cross-examination, Dr. Rand agreed that many people with atrial fibrillation are asymptomatic, and there was no indication from the medical records that Claimant was having a problem with profusion. Because of his atrial fibrillation, the continuation of Heparin and failure to seek a hematology consult at that time was not a deviation from the standard of care according to Dr. Rand.

When Claimant's platelet count dropped to 22,000 on September 22
, Dr. Rand testified, at that point it was necessary to obtain the consultation of a hematologist. However, this was not done until September 23 when the hematologist, Dr. Wright, was consulted. Dr. Rand agreed that it was appropriate to stop the Heparin as Dr. Sinacore directed.
On September 23,
when Claimant's platelet count dropped to 10,000, he had Thrombocytopenia, venous thrombosis, elevation in his fibrin split products, which Dr. Rand, unlike Dr. Vogel, did not feel was affected by his earlier transfusion, and a slight increase in his PTT, all consistent with the diagnosis of DIC. Dr. Rand also noted Claimant's fibrinogen was within the normal range; however, with someone as ill as Claimant, the fibrinogen is typically significantly higher than normal. Because it wasn't, his fibrinogen level could reasonably be viewed as low which also was consistent with DIC.
With the differential diagnoses of DIC and HITTS, it was appropriate for Dr. Wright to order the Heparin-dependent antibody test. Dr. Rand, on direct examination, testified that the resumption of low-dose Heparin at that point, until the result of the Heparin-dependent antibody test was available, was appropriate given the differential diagnosis of DIC and the atypical onset of HITTS symptoms. To discontinue the Heparin with the diagnosis of DIC on the table would have risked patient's continued clotting and possible death. Unfortunately, as Dr. Rand acknowledged, the problem was that the two conditions, DIC and HITTS, required opposite treatments, and to continue to treat with Heparin with HITTS could result in thrombosis, limb gangrene and possible death as well. Once the antibody test came back positive, the standard of care required the discontinuation of Heparin.

On cross-examination Dr. Rand acknowledged that DIC is always a secondary condition, and although many primary conditions can cause DIC, the only one considered by the medical staff at University Hospital was an infection, sepsis. There was, however, no indication that Claimant was suffering from an infection. Dr. Rand acknowledged that there was no indication of an infection or abscess from the CAT scan of Claimant's abdomen or ultrasound of his gallbladder. There was also no sign of an infection from the urine tests or blood tests. Claimant's platelet count had dropped to 10,000 before there was any elevation in his white blood-cell count on September 23
. Claimant also had no temperature until mid-morning on September 23, and even then, his temperature was only slightly above normal.
Legal Analysis
In a medical malpractice case, it is the Claimant's burden to show that the medical professionals involved either did not possess the requisite knowledge and skill ordinarily possessed by practitioners in the field, or neglected to use reasonable care in the application of the requisite knowledge and skill, or failed to exercise their best judgment (
Pike v Honsinger, 155 NY 201; Hale v State of New York, 53 AD2d 1025, lv denied 40 NY2d 804). For liability to be imposed, there must be a showing that the medical provider's treatment decision was "something less than a professional medical determination" (Darren v Safier, 207 AD2d 473, 474; Ibguy v State of New York, 261 AD2d 510). A physician's duty is to provide the level of care acceptable in the professional community; he is not required to "achieve success in every case and cannot be liable for mere errors of professional judgment" where a choice is made between medically acceptable alternatives or diagnoses (Schrempf v State of New York, 66 NY2d 289, 295; see also Oelsner v State of New York, 66 NY2d 636; Nestorowich v Ricotta, 97 NY2d 393, 399).
Claimant argues that the medical professionals involved failed to use reasonable care in their decision to readminister Heparin. The question is whether Dr. Wright and Dr. Picone deviated from the standard of care when, on September 23,
they ordered the readministration of Heparin to Claimant given his condition and the information available and accessible to them at that time.
Both experts and the treating physicians all agreed that on September 23
, the differential diagnoses of DIC and HITTS were appropriate given Claimant's symptoms and test results. These two very serious, potentially life-threatening, conditions presented a conundrum for medical staff. According to Dr. Rand and Dr. Wright, the preferred medication for DIC was Heparin and all agreed that the continuation of Heparin in a patient with HITTS unquestionably increased the risk of complications of that condition. It is clear that Claimant did not present with an entirely consistent case of either condition. It is also equally clear that the doctors at University Hospital were diligently working to determine the cause of Claimant's deteriorating condition on September 23.
Although Claimant argued that it was a deviation from the standard of care for the medical staff not to have ordered a blood test, specifically a platelet count on September 21, the Court does not find this to be the case given the conflicting opinions of the experts and Claimant's seemingly improving condition on September 20,
with an increasing platelet count.
Yet, the medical staff did fail to investigate Claimant's deteriorating condition on September 22
, when his platelet count had dropped to 22,000, which is significantly low, even when viewed in light of his low-baseline of 116,000 upon admission to Crouse. Dr. Sinacore stopped the Heparin but did nothing else to try to determine what was causing this patient's symptoms. There is also no indication from the medical records that any other physician checked Claimant's condition later on that day. Yet it would be speculative to presume that if the evaluative tests, specifically the Heparin-dependent platelet antibody test, had been ordered on that date the results would have been received a day earlier, at a time when permanent damage could have been prevented.
On September 23
evaluative tests were performed, and armed with the results from the blood tests, the transesophageal electrocardiogram, ultrasound of his gallbladder, and a CAT scan of his abdomen, Dr. Wright diagnosed Claimant as definitively having DIC with the possibility of HITTS and directed that a low-dosage of Heparin be administered to Claimant. Dr. Vogel disagreed with Dr. Wright's definitive diagnosis at that time and strenuously disagreed with the readministration of Heparin. Dr. Vogel opined that once HITTS was considered a potential diagnosis, all Heparin had to be discontinued. Both Dr. Rand and Dr. Wright indicated that the treatment of choice for DIC was Heparin. Dr. Vogel's position was that the treatment for DIC was to treat the underlying condition.
Undisputedly, DIC is a condition that is always secondary to some other primary condition. Also undisputedly, the only primary condition considered in Claimant's case was infection, or sepsis. Typically, when an infection is the precipitating cause for DIC it is readily evident, meaning the signs of infection are apparent. However, Dr. Rand testified that this is not always the case and he did not agree that the infectious process would manifest within a very short period of time. The test results on September 23
did not support an ongoing significant infection. Claimant's white blood-cell count, which would typically be elevated if there was an infection present, was slightly elevated on September 17 and consistently thereafter, but it did not significantly increase until later on September 23. He did not have a fever until midmorning on September 23, and then his fever was only slightly above normal.
The other tests relied upon were also not exclusive to the diagnosis of DIC over HITTS as Dr. Wright acknowledged. With the fibrinogen split products and the fibrinogen levels there was no way to distinguish between DIC and HITTS, because as Dr. Wright testified during his deposition, a person can have both with these values. Between September 17, 1996,
and the 6:02 a.m. blood draw on September 23, the PT was not significantly elevated and actually decreased. The PTT also decreased, although both values were higher than the normal low-high range. Simply put, the blood-coagulant test results were not inconsistent with either diagnosis.
Further complicating this picture, both Dr. Rand and Dr. Wright testified that typically with HITTS the onset of symptoms begins within 3 to 5 days, although the experts and Dr. Wright agreed it can be longer. Also, in 1996, HITTS was primarily considered an arterial clotting problem. Here, the blood clots were found in the veins of Claimant's legs. It was Dr. Vogel's opinion that HITTS could involve both arterial and venous clots.

Dr. Wright interpreted the test results and Claimant's symptoms and diagnosed DIC . He testified that he had to treat the condition that he knew existed rather than attempt to treat the potentiality of HITTS until the Heparin-dependent platelet antibody test results were obtained. This diagnosis was consistent with the information available, although it was not exclusive to that diagnosis, as the same information can also be indicative of HITTS.

Under these circumstances, the Court cannot find that Dr. Wright and Dr. Picone failed to exercise reasonable care when the order to readminister the Heparin was made on September 23. The conflicting evidence as to how the various test results should have been interpreted and whether Heparin should have been readministered does not establish the State's liability (
Oelsner, 66 NY2d at 636, 638; Ibguy, 261 AD2d at 510). A difference of opinion among medical providers does not establish a prima facie case of medical malpractice (Ibguy, 261 AD2d at 510). Dr. Wright utilized the information available, applied his professional knowledge and skill, and arrived at an appropriate differential diagnosis. Relying on the tests results and Claimant's condition, he determined that Claimant definitely had DIC. This exercise of his professional medical judgment was reached with reasonable care based upon the information he had available. Unfortunately, he was wrong. However, an error in judgment does not establish liability, for medical providers are not held to the position of an insurer guaranteeing the success the benefit of hindsight can provide. It is unfortunate that Claimant was caused to suffer such pain and permanent disfiguration, and the Court has struggled with this decision. Yet based upon the facts as found, no medical malpractice was committed despite the unpropitious results.
The claim must be DISMISSED. LET JUDGMENT BE ENTERED ACCORDINGLY.


September 15, 2005
Syracuse, New York

HON. DIANE L. FITZPATRICK
Judge of the Court of Claims




[1] Dr. Picone was Claimant's attending physician for his hospital stay at University Hospital. Dr. Picone's deposition transcript was admitted into evidence as Claimant's Exhibit 1.
[2] Postoperatively, Claimant received Heparin at the rate of 5,000 units subcutaneously Q 12, with Heparin flushes for all central IV lines and locks.
[3] Mrs. Eyre was deceased at the time of trial.
[4] Exhibit 3A, pp. 381-382.
[5]Meaning normal body temperature; without fever.
[6] Dr. Marx did not testify at trial; however, his deposition testimony was admitted into evidence as Defendant's Exhibit B.
[7]This quote is from Dr. Picone's deposition testimony, Exhibit 1, where he read his September 23, 1996 progress note into the record, interpreting his abbreviations.
[8] "Either of two large veins by which the blood is returned to the right atrium of the heart." (Merriam Webster's Medical Desk Dictionary [1996] p. 856.)
[9] Dr. Wright testified at trial and the transcript of his deposition testimony also was admitted into evidence as Exhibit A.
[10] Trial Transcript, March 31, 2004, p. 87, l. 13-25, p. 88, l. 1-14. The authority was Dr. Yuri Sellason, Williams Hematology, 5th ed., Chapter 141, entitled "Disseminated Intra-Vascular Coagulation."
[11] All quotes are from the trial transcript unless specifically noted otherwise.
[12] This test was not actually ordered until September 25, 1996.
[13] Prothrombin is a plasma protein produced in the liver in the presence of vitamin K and converted into thrombin by the action of various activators in the clotting of blood (Merriam Webster's Medical Desk Dictionary [1996] p. 660).
[14]Thromboplastin is a complex enzyme found in the brain, lung and other tissues and especially blood platelets which functions in the conversion of prothrombin to thrombin in the clotting of blood (Merriam Webster's Medical Desk Dictionary [1996] p. 814).
[15] These values are in the thousands.
[16] The platelet count for 9/20 was actually 85,000 and there was no platelet count done on 9/21.
[17]Claimant's Exhibit 3-A p. 392, 393; Deposition transcript of Dr. Wright (Defendant's Exhibit A, p. 6, l.13-p. 8, l. 14).
[18] Dr. Vogel indicated that this is sometimes also referred to as HITT I.
[19] Dr. Vogel testified that this is also referred to as HITTS or HITT II.
[20] Localized tissue anemia due to an obstruction of the inflow of arterial blood (Merriam Webster's Medical Desk Dictionary [1996] p.402).
[21] A bluish or purplish discoloration of the skin, for instance, due to deficient oxygenation of the blood (Merriam Webster's Medical Desk Dictionary [1996] p. 180).
[22] Acute phase reactant means an inflammation. Infection can be responsible for an elevation in a particular test (Dr. Vogel trial testimony p.42, l. 9-11). Dr. Wright in discussing the fibrinogen levels agreed that higher levels were an acute phase reactant to Claimant's grave illness, and since his levels on the 23rd were not elevated he considered the fibrinogen low in support of his DIC diagnosis (see Dr. Wright deposition transcript Exhibit A, p 33, l. 18- p.34, l. 3).
[23] A large amount of something given over a short period of time as a direct push into a vein (Dr. Vogel trial testimony p.28, l. 7-11).