New York Personal Injury Attorneys Blog

Our Partner Stephen Mackauf will speak at The New York State Bar Association Seminar: Medical Malpractice to be held on Thursday, November 19, 2009 at New York Hotel Pennsylvania, 401 Seventh Avenue (at 33rd St.) New York, NY. Stephen will speak on Discovery (Plaintiff’s Perspective). For more information click here. Stephen is considered by not only malpractice lawyers in New York but by malpractice lawyers across the Country as one of the leading Medical Malpractice Attorneys in The United States. He has lectured for years to both Doctors and Medical Malpractice Lawyers in States across The Country.

By: Anthony H. Gair

Blepharoplasty basically is surgery in which excess tissue is removed from the eyelids. It is the most commonly performed cosmetic surgery on the face. Upper eyelid surgery is usually performed for removal of excess skin, muscle and fat and lower lid surgery for the removal of fat pads, so called baggy eyelids caused by herniation of periorbital fat.

The most serious complication of blepharoplasty is partial or complete loss of vision, most commonly as a result of intra-orbital hemorrhage. A widely accepted theory suggests orbital bleeding increases intraorbital and intraocular pressure, compromises the ocular circulation, and results in ischemic or optic nerve damage. Ischemic optic neuropathy and central artery occulsion are believed to be the most common final events in most cases of blindness after blepharoplasty. (Lowry JC, Bartley GB: Complications of Blepharoplasty. Surv. Ophthalmol 38:327-350, 1994).

It is thus essential, prior to surgery, for the physician to carefully assess the patient’s risk factors for bleeding. Aspirin, aspirin-containing products, other antiplatelet agents and anticoagulants should be discontinued prior to surgery. (Id. at p. 331). In this regard, the physician should obviously be aware of all medications used by the patient.

Acute orbital hemorrhage constitutes a medical and surgical emergency. Severe permanent visual impairment is likely if vascular compromise exists for more than 90 minutes. Prompt recognition and management are essential. (Id. at 332).

The following is an excerpt of a deposition of a plastic surgeon in a New York Medical Malpractice case in which the patient suffered a post-operative hemorrhage following blepharoplasty resulting in a complete loss of vision of the affected eye.

Continue reading "NEW YORK MEDICAL MALPRACTICE- BLEPHAROPLASTY" »

By Anthony H. Gair;

This discussion involves a medical malpractice case, which was tried in New York Supreme Court, New York County, in which a woman who had since birth a congenital abnormality known as an hemangioma on the left side of the face which is caused by an abnormal distribution of blood vessels. There are different types of hemangiomas such as capillary or cavernous hemangiomas which may actually cause physical impairment. The type of hemangioma the plaintiff had was an intradermal hemangioma often referred to as a port wine stain because of its color which does not cause physical impairment. Since her teenage years, she was able to cover it up with make-up. When she was 40 years old she developed what are known as blood spots or blisters, which are raised areas on the hemangioma which caused difficulty in covering it with make-up.

Being concerned about it, she consulted with the defendant-plastic surgeon. Plaintiff claimed she only went to the physician because of the blood spots. It was claimed she had lived her entire life with the birthmark and only desired treatment for the blood spots.

Plaintiff’s strategy at trial was that the defendant was solely a cosmetic surgeon, not a reconstructive plastic surgeon who dealt with devastating physical disfigurements. The idea was to portray her as highly mercenary, going so far as to advertise extensively for patients who she claimed she could make look better. Plaintiff asserted that she told the defendant she was concerned with the blood spots because she couldn’t cover them with make-up. She testified that the defendant told her not only could she get rid of the blood spots but that she could remove most if not all of the hemangioma. The plaintiff, as would be expected, became very emotional that after all these years the hemangioma could be removed.

Continue reading "NEW YORK MEDICAL MALPRACTICE, ELECTIVE PLASTIC SURGERY" »

In Parnell v Montefiore Med. Ctr. decided June 23, 2009, The New York Appellate Division, First Department, reinstated the complaint in a Medical Malpractice Case against the defendant hospital which had been dismissed by the New york Supreme Court, Bronx County. While affirming the dismissal of the complaint against the defendant doctor the Court held as to the hospital;

"However, we find that there is an issue of fact as to the hospital's negligence. It was the hospital's duty to monitor the patient postoperatively, including monitoring the chest tube and the Pleurovac closed drainage system and all its component parts. The drainage system provided continuous suction to assist in drawing air and fluids out of the pleural space. The assertion of the hospital's expert that there was no evidence that the chest tube became detached from the suction is contrary to the record. Dr. Lonner testified that he noticed that the chest tube connection, specifically the connection between the patient and the canister attached in turn to the wall suction, was detached, and that he immediately re-attached the connection and proceeded with the resuscitation. Dr. Lonner also testified that if the tube became detached, air could go back into the pleural space and create a pneumothorax. This testimony alone, that an integral part of the drainage system had become detached and increased the risk of a pneumothorax, the very harm that befell the infant plaintiff, raises an issue of fact as to the hospital's negligence.

Further, plaintiffs' expert averred that it was good and accepted medical practice to check all the component parts of the chest tube and canister every time the patient was seen, at least once every hour, and that had the tube been properly monitored, it would not have become dislodged and the infant plaintiff would not have suffered a pneumothorax. He took issue with the conclusion of the hospital's expert that a mucus plug occasioned the infant plaintiff's respiratory arrest, pointing out that while there was evidence that the tube was dislodged when Dr.Lonner found the infant plaintiff, the medical record contains no evidence of a mucus plug."

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By Anthony H. Gair

The human body contains forty six osteofacial compartments. Within these compartments are muscles, veins, arteries and nerves surrounded by tissue called fascia which is dense and unyielding.

The most common orthopedic setting for compartment syndrome is the closed tibia fracture for which the incidence is 3% to 17% 1. This discussion will be limited to compartment syndrome following tibia fractures.

The foreleg consists of four compartments known as the anterior, lateral, posterior and deep posterior compartments 2. Located within the anterior compartment are the motors for dorsiflexion of the foot and toes; the tibialis anterior, extensor halluces longus and extensor digitorum longus muscles. These muscles are innervated by the deep peroneal nerve which enters the anterior compartment after winding around the outer surface of the neck of the fibula. Located within the posterior compartment are the gastrocnemius, soleus and plantaris muscles which plantar flex the foot and flex the leg. These muscles are invervated by the tibia] nerve. The deep posterior compartment contains the flexor halluces longus, flexor digitorum longus, tibialis posterior and. popliteus muscles. These muscles plantar flex the foot (tibialis posterior), flex the leg and rotate it medially (popliteus), flex the big toe and flex and supinate the foot (flexor halluces longus) and flex the four small toes and plantar flex and supinate the foot (flexor digitorum longus). These muscles are innervated by the tibial nerve. Finally, the lateral compartment contains the peroneus longus muscle and the peroneus brevis muscle which pronate and flex the foot. These muscles are supplied by the superficial peroneal nerve 3.

Continue reading "MEDICAL MALPRACTICE: FAILURE TO DIAGNOSE COMPARTMENT SYNDROME" »

Following extensive settlement negotiations, our partner, Jeffrey Bloom, on May 8, 2009, obtained a settlement of $9,260,500 in a medical malpractice case in which it was alleged that the defendant doctors failed to timely diagnose a small bowel obstruction in a 37 year old woman. As a result of the defendant doctors' negligence, the plaintiff suffered multiorgan failure including renal failure that ultimately required a kidney transplant.

On December 20, 2003, the plaintiff presented at an emergency room complaining of vomiting and abdominal pain, but the defendants failed to do any diagnostic work-up repeatedly giving her pain medications which masked her symptoms. She was sent home with a diagnosis of a virus. She returned to the emergency room three days later with excruciating abdominal pain.

Although the doctors finally diagnosed her small bowel obstruction during this second emergency room visit, her surgery to relieve the obstruction was unnecessarily delayed for 16 hours. As a result of these delays, the plaintiff suffered extensive and severe injuries. She was hospitalized for a full year and then required in-patient rehabilitation for 6 months. She has undergone 16 surgeries and 15 hospitalizations to date.

The emergency room doctors who treated her during the two separate emergency room visits as well as their practice, the surgeon who delayed her surgery and his practice, and the hospital were named as defendants. The settlement was for the full amount of available insurance.

The names of the plaintiff and defendants have been omitted due to the confidential nature of the settlement.

Our Partner Robert L. Conason is on The Faculty of This program which will be held from October 12 - 14, 2009 at the Marriott Eastside Hotel, New York, New York.

This CME program is designed to cover clinical aspects of breast imaging including conventional and digital mammography, breast ultrasound, breast MRI, and interventional procedures, as well as medicolegal issues. The faculty consists of nine nationally and internationally recognized experts. The program of lectures and panel discussions will be filled with "take home" information that should benefit every breast imaging practice. Bob will be speaking on October 14, 2009 0n Breast Imaging Malpractice: An Attorney's Perspective. For more information click here.

Our Partner, Stephen H. Mackauf is The Co-Chair of The American Conference Institutes's 8th Annual Advanced Forum on Preventing, Managing and Defending Claims of Obstetric Malpractice. The Forum will be held on June 23 & 24, 2009 at The Union League of Philadelphia-Philadelphia, PA. Stephen will also be participating in a Post-Conference Workshop on June 24th, "The Attorney's Guide to Handling an Infant Brain Injury Case from Start to Finish." Stephen will also be speaking on Fetal Monitoring and Surveillance: Making the Right Decisions Based on the Right Information. For more information click here.

Our Partner Stephen H. Mackauf will be participating in a two day Seminar, "Defending the Delivery Team: Obstetric Malpractice" sponsored by Legal iQ. The program will be held in San Francisco on April 28th and 29th, 2009. Stephen will be discussing the Plaintiff's perspective. For more information click here.

Our partners Jeffrey Bloom and Richard Steigman have co-authored an article entitled "The Impact of Arons: A Look at the Court of Appeals' Decision to Allow Ex Parte Interviews of Treating Doctors and Where We Go from Here." The Article is in The Spring 2008 Edition of Bill Of Particulars published by The New York State Trial Lawyers Institute.

Murray v. New York City Health & Hospitals Corporation June 24th, 2008
WARNING
The 2d. Department upheld the dismissal of plaintiff's action for wrongful death resulting from medical malpractice when the plaintiff's counsel failed to appear for a final conference. The Court held;

LOSS OF VISION FOLLOWING BLEPHAROPLASTY AS A RESULT OF ORBITAL HEMORRHAGE

Blepharoplasty basically is surgery in which excess tissue is removed from the eyelids. It is the most commonly performed cosmetic surgery of the face. Upper eyelid surgery is usually performed for removal of excess skin, muscle and fat and lower lid surgery for the removal of fat pads, so called baggy eyelids caused by herniation of periorbital fat.

The most serious complication of blepharoplasty is partial or complete loss of vision, most commonly as a result of intra-orbital hemorrhage. A widely accepted theory suggests orbital bleeding increases intraorbital and intraocular pressure, compromises the ocular circulation, and results in ischemic or optic nerve damage. Ischemic optic neuropathy and central artery occulsion are believed to be the most common final events in most cases of blindness after blepharoplasty. (Lowry JC, Bartley GB: Complications of Blepharoplasty. Surv. Ophthalmol 38:327-350, 1994).

FAILURE TO PROPERLY TREAT EXTRAVASATION OF DOXORUBICIN (Adriamycin)
By: Anthony H. Gair;

The extravasation of intravenously administered chemotherapeutic agents into the subcutaneous tissue of cancer patients undergoing chemotherapy is a known risk of treatment. The potential gravity of injury caused by extravasation is dependent upon the type of drug which extravasates. The most destructive extravasation injuries are those caused by anti-tumor drugs which bind to deoxyribonucleic acid (DNA), such as Doxorubicin, (Adriamycin) which has been a primary part of chemotherapeutic regimes since the late 1960's. Extravasation of chemotherapeutic agents which bind to nucleic acids can lead to a prolonged course of injury. The most clinical experience has been derived from the extravasation of Doxorubicin. Rudolph, R, Larson, D. Etiology and Treatment of Chemotherapeutic Agent Extravasation Injuries: A Review. J. Clin. Oncol, 1987; 5:1116-1126. Doxorubicin causes severe progressive tissue necrosis that may involve muscles and tendons. Since no specific antidote has been developed, the recommended treatment of Doxorubicin extravasation is early excission of all infiltrated tissue. Dahlstrom, KK, Chenoufi, HL, Daujard, S. Fluorescene microscopic demonstration and demarcation of Doxorubicin extravasation. Experimental and Clinical studies. Cancer, 1990 Apr. 15; 65(8): 1722-1726.

It has been postulated that infiltration of Hyaluronidase, which may serve to dilute the extravasated Doxorubicin, will decrease the amount of ulceration caused by the extravasation. Disa JJ, Chang RR, Mucci JJ, Goldberg N.H., Prevention of Adriamycin-induced full-thickness skin loss using hyaluronidase infiltration. Plast. Reconstr. Surg. 1998 Feb., 101(2):370-374. In this regard the injection of saline solution at the site of extravasation of a vesicant (blistering) chemo-therapeutic agent in order to reduce the concentration of the extravasated drug has been reported to have been effective. Scuderini, Onesti MG, Anti-tumor agents: Extravasation, Management and Surgical Treatment. Am. Plast. Surg. 1994 Jan; 32(1):39-44. However, other authors have emphatically stated not to inject saline, sodium bicarbonate or hyaluronidase into the extravasation area as to do so may increase the diffusion of the extravasated agent into surrounding tissue. Hankin FM, Louis DS, Extravasation of Chemotherapeutic Agents. Am. Fam. Phys. 1985 March; 31(3)147-150.

For some time the injection of steroids into the subcutaneous tissue at the site of Doxorubicin extravasation was recommended on the theory that steroids would reduce inflammation. However, it has been demonstrated that inflammatory cells are uncommon in tissue damaged by Doxorubicin extravasation. Rudolph R, Stein RS, Patillo R: Skin Ulcers Due to Adriamycin. Cancer 38:1087-1094, 1976; Larson DL: What is the appropriate treatment of tissue extravasation by anti-tumor agents? Plast Reconstr Surg 75:397-405, 1985. In 1996 the package insert for Adriamycin was changed. Prior thereto, the injection of steroids was recommended in the event of extravasation. In 1996 it was stated that the benefit of local administration of drugs has not been clearly established. Close observation and plastic surgery consultation were recommended. The immediate treatment of DNA-binding chemotherapy extravasation should include elevation of the effected extremity and intermittent cold. There does not seem to be any agent that, injected locally, can alter the final result from extravasation of any binding chemotherapeutic agent. Persistent swelling, erythema and pain are indications for surgical consultation, even if ulceration is not yet apparent. Such consultation is mandatory when blistering and ulceration are first seen. Rudolph and Larson, supra. Snyderman RK, Krasna MJ, Adriamycin extravasation injuries. Plast Reconstr Surg 1986 Apr; 77(4):683-684.

The following case involved a patient being treated for Non-Hodgkins Lymphoma with, among other chemotherapeutic agents, Doxorubicin. During his second round of chemotherapy, the treating oncologist administered 60mg of Doxorubicin by I.V. push via a free flowing intravenous line. The infusion site was the right upper anterior arm just above the elbow. Fifteen minutes following the infusion the "chemo line" was noted to be red and swollen. Ninety minutes later, pursuant to order of the oncologist, Hydrocortisone, 100mgs was instilled subcutaneously. Hydrocortisone ointment was also topically applied. Two days thereafter, swelling and redness of the right arm was noted to be increased. The patient complained of increased swelling and redness in the right arm. The oncologist ordered topical application of Hydrocortisone cream four times a day. The patient was discharged from the hospital five days post extravasation with the right arm still swollen and hard, to be followed on an out-patient basis by his oncologist. The patient was, 3 ½ weeks later, noted to have a still swollen right arm with a necrotic area. Two weeks thereafter, he was admitted to the hospital with a fever of 103E, a swollen and erythematous right arm with a large necrotic area with dry eschars. The patient thereafter required numerous surgical debridements of the right arm as well as a fasciotomy, repair of a pseudoaneurism of the brachial artery and extensive skin grafting. The patient was left with significant atrophy of the right arm, a 90E extension contracture at the right elbow and significant restriction of motion of the wrist, hand and fingers.

The plaintiff alleged that the oncologist failed to recognize the significance of the extravasation injury, failed to understand how to treat it, failed to seek proper consultation and failed to understand the pathology of the extravasation injury. It was alleged that, given the signs and symptoms documented in the hospital record, a consult with a surgeon experienced in treating extravasation injuries was mandated and would have avoided the extensive and permanent injuries suffered by the patient.

The following is excerpted from the deposition of the oncologist:

Q. You have had training, have you, in the administration of chemotherapeutic agents such as doxorubicin?
A. Yes.
Q. Adriamycin is doxorubicin; correct?
A. Yes.
Q. Doxorubicin is a chemo-therapeutic agent which binds to nucleic acid, correct?
A. Yes.
Q. Binds to DNA, true?
A. Correct.
Q. In fact, that’s the mechanism by which it fights cancer cells, true?
A. Correct.
Q. What is the significance of the fact that doxorubicin binds to nucleic acid with regard to the progression of injury which may be caused by extravasation of doxorubicin into subcutaneous tissue?
A. It makes the damage irreversible.
Q. During the patient’s admission to the hospital did he suffer an extravasation of intravenously administered chemotherapeutic agents?
A. The answer is yes.
Q. Doctor, by extravasation we mean the escape of intravenous fluids into subcutaneous tissues, correct?
A. Correct.
Q. Do you recall what you did then?
A. I went straight back to the patient to see what happened.
Q. What did you observe or what did you find out?
A. I noticed that there was redness in the upper arm, a streak, along the long vein.
Q. Do you recall what you did next?
A. I took insulin syringes and first I aspirated around. Then I injected decadron a corticosteroid.
Q. Why did you do that?
A. To minimize the inflammatory process.
Q. Why did you want to do that?
A. This is a chemical irritant and to reduce the impact, the inflammatory impact.
Q. What is a chemical irritant?
A. Adriamycin.
Q. Adriamycin is not an irritant, it is a vesicant, isn’t it?
A. It’s a vesicant.
Q. A vesicant agent by definition is a blistering agent; is that right?
A. Correct.
Q. Doctor, I believe you stated that you administered the steroids to combat the inflammation, if you will; is that right?
A. To limit.
Q. Would you agree that severe local tissue necrosis may occur following doxorubicin extravasation?
A. Correct.
Q. Would you agree that the necrosis is progressive following extravasation?
A. Correct.
Q. And would you agree that the extravasation of a DNA binding vesicant agent leads to a more prolonged course of injury than a non-binding agent?
A. Correct.
Q. That’s because the pathogenesis of injury with a DNA binding agent is that, in this case, when the agent extravasates, it starts being up taken by healthy cells?
A. Correct.
Q. And it progresses and progresses as a result of that?
A. Right.
Q. Doctor, the cause of injury as a result of doxorubicin extravasation is not an inflammatory process; is it?
A. Inflammation follows.
Q. See if you can answer this question: We are talking about an agent, a vesicant agent that binds to nucleic acid. The injury caused by the extravasation of such agent is not caused by an inflammatory process; is it?
A. The initial injury is not an inflammatory – inflammation follows.
Q. I would like an answer to this question: In the face of extravasation of a vesicant chemo-therapeutic agent such as doxorubicin, which is a nucleic acid binding agent, it binds to DNA, how would the injection of steroids prevent the process of injury?
A. As I said before, the secondary process – I cannot remove the Adriamycin which is already bound to the nucleic acid. But the secondary process is the inflammation and I can do everything to limit that.
Q. But the progress of the injury I think we agree, is caused by the doxorubicin being up taken by healthy cells?
A. Yes.
Q. It progresses and progresses, correct?
A. Yes.
Q. Would you agree that doxorubicin, when extravasated into subcutaneous tissue, produces a permanent loss of that tissue’s ability to heal itself?
A. I don’t think it’s permanent to heal itself. It is a lasting damage. But I don’t think it’s permanent to heal itself.
Q. You think eventually it could heal itself?
A. Yes.
Q. Doctor, would you agree that there is no agent, that when injected locally, can alter the final result from extravasation of doxorubicin?
A. I believe so.
Q. You believe there is no agent or your believe there is an agent?
A. There is no agent that has been proven to reverse the damage produced by Adriamycin.
Q. Given the fact that you had no experience in treating a patient who had sustained an extravasation of doxorubicin, do you think it would have been a good idea for you to have talked to a physician who had experience in treating such patients; "yes" of "no"?
A. As I have stated before, I have discussed it with some colleagues and the conclusion was it’s not severe enough. Just monitor it carefully.
Q. Those are the people you don’t remember who they were, right?
A. Correct.
Q. The ones you made no note of, correct?
A. Correct.
Q. Would you agree that the only effective remedy for doxorubicin extravasation is the complete excision of the tissue containing the doxorubicin?
A. Yes.
Q. Well, if that’s so, why didn’t you obtain a surgical consult?
A. I thought it was improving. The arm was improving.
Q. As far as this patient’s arm was concerned and the effect of the possibility of extravasated chemo-therapeutic agents, that was your responsibility, correct, that was your expertise as an oncologist; wasn’t it?
A. I believe we all were involved, had this responsibility.
Q. But you were the attending oncologist, true?
A. Yes.
Q. That was in your particular area of expertise, correct?
A. Yes.
Q. Certainly when you are an oncologist and you are using chemotherapeutic agents such as doxorubicin, you should be aware of the effects of extravasation of such a drug, correct?
A. Correct.
Q. You should be aware of how to treat it, correct?
A. Correct.
Q. That is within your responsibility as the oncologist administering those drugs, true?
A. True.
Q. Is it the responsibility of the oncologist to determine when surgery should be performed in a given patient?
A. It is usually a team approach between the oncologist and vascular surgeon.
Q. Or a plastic reconstructive surgeon?
A. Plastic reconstructive surgeon.
Q. And a plastic reconstructive surgeon should be part of the team?
A. Yes.
Q. Doctor, you never ordered a plastic surgical, vascular surgical or any type of surgical consult for the patient at any time during your treatment of this man, true or not true?
A. I have not ordered the initial consult.

The deposition of the treating oncologist demonstrated a complete failure to understand the significance of the extravasation. Further, it was apparent that the physician did not understand how to treat the extravasation injury either acutely or long term. The deposition left no doubt that the physician had no understanding regarding the pathology of an extravasation injury caused by doxorubicin, had no training in treating same and had no knowledge as to the indications for injecting steroids into an extravasation.

Based on the total lack of knowledge of this physician, undeniably confirmed by the deposition testimony, the case settled for a substantial sum prior to trial. Further, it demonstrates that the plaintiff’s attorney must, prior to the deposition of the defendant physician in a malpractice case, be fully versed in the area of medicine involved as would be the case at trial.

A Study To End the Frivolous Malpractice Lawsuit Myth
This article written by our partner Jeffrey B. Bloom in 2006 is just as relevant today as it was then.

"Last week, within days of the U.S. Senate performing its annual rite of taking up and then denying cloture to a bill to limit the rights of medical malpractice victims and cap damages in medical malpractice cases, a study was released which clearly demonstrates that our current tort system is working quite well in ensuring that the vast majority of cases are valid claims and that frivolous or non-meritorious malpractice cases are rarely brought and hardly ever result in damages being unjustly paid.

The study,“ Claims, Errors, and Compensation Payments in Medical Malpractice Litigation,” was conducted by a prestigious group from the Harvard School of Public Health and the Harvard Risk Management Foundation and was published in the May 11, 2006 issue of the New England Journal of Medicine. Physicians trained in reviewing malpractice claims were assigned malpractice files randomly selected from 1452 closed medical malpractice files provided to the group by five malpractice insurance companies in four regions in the U.S. The goal of the study was to determine if so-called tort-reformers are correct when they claim that frivolous malpractice claims are common and costly and are a substantial source of waste in the health care and legal system. The study supports what lawyers involved in malpractice litigation have been stating for years: the vast majority of malpractice cases brought are valid and the claimants are rightfully entitled compensation.

In the study, meritorious cases outnumbered non-meritorious case by 2 to 1. Presumably, in many of the cases deemed by the reviewers to be “non-error,” issues of credibility were resolved in the medical providers favor without the benefit of seeing the witnesses testify and be cross examined in order to make a fair appraisal as to which party is telling the truth. Of the claims that these reviewers opined were not caused by medical error, the vast majority received no recovery at all. Eighty percent of the claims examined involved injuries deemed to have caused significant or major disability or death. In only 3 percent of the claims, no adverse outcome from medical care was evident. Of the 37 claims which were deemed to involve no injury, only a handful of these claimants received any monetary award.

The authors of the study also found, “[T]he malpractice system performs reasonably well in its function of separating claims without merit from those with merit and compensating the latter.” As further proof of how well the system works, most meritorious cases were settled without the need for a jury verdict. Malpractice insurers and hospital risk managers are well trained to recognize valid claims and often choose to resolve those claims by settlement, thereby reducing defense costs and the risk of larger damage awards from a jury. For these reasons, settlements were reached in 85% of all the malpractice claims evaluated. Of the remaining 15% of cases which went to verdict, plaintiffs rarely won. According to the study, 79% of the verdicts of the cases reviewed which went to trial resulted in no award for the plaintiff, including a significant number of meritorious claims which resulted in verdicts for the defendant-medical provider. While the study found that non-error claims were more likely to reach trial than error claims, 27% of claims in which the claimants suffered injuries resulting from medical errors received no compensation. In other words, if there is an injustice in the system, it’s more likely that the victims of malpractice suffer the inequitable result rather than medical providers Perhaps we should label this injustice a successful “frivolous defense.”

The study also dispelled the proclamations of President Bush, Senator Frist, et al. that our tort system is overrun by greedy trial lawyers bringing meritless malpractice lawsuits. The authors of the study wrote: “The profile of non-error claims we observed does not square with the notion of opportunistic trial lawyers pursuing questionable lawsuits in circumstances in which their chances of winning are reasonable and prospective returns in the event of a win are high. Rather, our findings underscore how difficult it may be for plaintiffs and their attorneys to discern what has happened before the initiation of a claim and the acquisition of knowledge that comes from the investigations, consultations with experts, and sharing of information that litigation triggers.” In sum, the authors found that “portraits of a malpractice system that is stricken with frivolous litigation are overblown.” Furthermore, if the costs of malpractice litigation including compensation paid, attorney’s fees, litigation and court costs in all the cases the reviewers labeled as non-error were eliminated, the total savings for the system would amount to 13% of the total cost– a far cry from the savings promised by Bush-minded tort reformers.

Rather than engaging in an honest debate and seeking ways to reduce medical errors and to provide malpractice insurance premium relief for physicians, these tort reformers instead have perpetrated the myth that frivolous malpractice lawsuits are the root cause of our country’s rising medical costs. Senator John Ensign (R.-NV), the chief sponsor of the latest attempt by the U.S. Senate to have the Federal government usurp the power of the states and, in a clear affront to federalism, put in place a nation-wide cap in malpractice cases, stated in support of his bill (S.22), “The number of frivolous lawsuits clogging our system is what we need to deal with.” Likewise, Senator Tom Coburn (R-OK), a co-sponsor of the bill and a physician made the following outrageous statement on the floor of the Senate: “Only 16 percent of the lawsuits that are filed across the entire country have any merit whatsoever.” Similarly disingenuous, Senator Conrad Burns (R-MT), another co-sponsor, proclaimed on the Senate floor that the only people who would be hurt by caps on damages are not the severely injured victims of malpractice but rather: “the folks who make a living in frivolous lawsuits.”

Not only does this Harvard study clearly disprove the notion that frivolous lawsuits are frequent, let alone “clogging the system,” the argument that capping damages in cases involving significantly injured malpractice victims will somehow reduce frivolous claims is patently absurd. . Perhaps now that there is documentation that number of so-called frivolous cases brought is quite few with a rather small cost to the system, the debate about medical malpractice litigation will turn honest and the President, Senators Frist, Ensign,Coburn, Burns and like-minded so-called tort-reformers will reveal to the public their true agenda–they seek to save money for the insurance industry at the expense of victims of medical negligence.

Hopefully, this non-partisan study, undertaken by one of the nation’s most prestigious schools studying public health issues will put to rest the nonsensical notion that plaintiff’s trial lawyers are flooding the courts with meritless malpractice cases which usually result in no compensation being awarded and from which a contingent fee could be earned. To the contrary, before bringing a medical malpractice lawsuit, plaintiff s lawyers are well aware that only meritorious claims with significant injuries are likely to result in a recovery. As the study proves, when an attorney working for a contingent fee agrees to assume the risk of bringing a costly and time consuming medical malpractice case, it’s likely to be a valid claim with significant injuries. Furthermore, when a claimant in a malpractice case receives an award of damages, either by settlement or verdict, he or she was likely to have been a victim of true malpractice.

By Anthony H. Gair, Gair Gair Conason Steigman & Mackauf

The popliteal artery is the major source of blood supply to the lower leg. The femoral artery becomes the popliteal artery as it passes through the hiatus of the adductor magnus muscle and enters the popliteal fossa. It generally ends at the inferior border of the popliteus muscle where it divides into the anterior and posterior tibial arteries. It lies directly behind the posterior horn of the lateral meniscus.1 Injuries to the popliteal artery during anterior cruciate ligament reconstruction or arthroscopic meniscectomy are extremely rare.2 The popliteal artery is closely related to the posterior capsule of the knee joint, being separated from it only by a small amount of fat. The artery also kinks forward when the knee is flexed, placing it close to the posterior horn of the medial meniscus. It is thus imperative that surgery in the posterior aspects of the knee is performed under direct visualization. If an arterial injury is suspected following surgery of the knee an opinion from a vascular surgeon should be sought urgently.3

Delayed recognition of a popliteal artery lesion is a major cause of amputation of the affected extremity. Further, true spasm of the popliteal artery is rare. It is thus dangerous to diagnose arterial spasms since in reality thrombosis is usually present. It is further, axiomatic that the absence of pulses in an extremity is due to arterial injury until proven otherwise. Additionally, compartment syndrome may accompany vascular injury secondary to prolonged ischemia, venous injury or partial laceration to the artery with bleeding into the compartments.4

The following case involved a young woman who was diagnosed with a tear of the anterior cruciate ligament and of the posterior horn of the medial meniscus of the right knee. Subsequently, the orthopedic surgeon performed arthroscopic assisted surgery for the repair of the ACL and partial medial meniscectomy. On the afternoon following surgery the patient complained of pain behind the knee and decreased sensation in the foot. The foot was noted to be swollen. On post-op day one swelling to the right thigh and foot was noted as persisting. On post-op day two she complained of pain behind the knee and swelling. The leg and foot were edematous, there was no sensation of the toes and an inability to move the toes or foot was noted. The skin was colorless with some mottling at the foot. The surgeon was called and changed her pain medication to percocet. On post-op day three the surgeon was again called and examined the patient. Despite the above symptoms indicative of vascular injury, together with the presence of foot drop, he did not request a vascular consultation. He sent her to the emergency room for an ultrasound to rule out a deep venous thrombosis. The popliteal artery was not studied. The compartment pressures were measured and compartment syndrome ruled out as a cause of the patient’s symptoms, as was deep venous thrombosis. On post-op day four, the patient continued with complaints of severe pain behind her knee. The surgeon was once again called and met the patient at the emergency room. Compartment pressures were measured and were elevated in the anterior compartment only. A fasciotomy was performed at which time the muscles of all compartments were noted to be viable and should have indicated to the surgeon the elevated pressures in the anterior compartment could not have been present for more than eight hours and hence did not explain the patient’s prior symptoms. The post-anesthesia care record noted the right foot to be cold, blanched and mottled at the ball of the foot with decreased movement. A pulse of the right foot was not palpable or obtainable with doppler. Nurses notes for post-op day five noted the toes of the right foot to be cold to touch and non-mobile. No pedal pulses were noted. The knee, calf and foot were edematous. The patient complained of swelling and burning of the leg. A vascular consultation was finally obtained on post-op day six. An angiogram was performed which demonstrated a 2cm pseudoaneurysm of the mid popliteal artery with occlusion just distal to the pseudoaneurysm. Surgery was immediately performed for repair of the artery. However, as a result of prolonged ischemia and resulting necrosis, the patient’s right leg was required to be amputated below the knee.

Plaintiff claimed several departures from proper practice. First was the iatrogenic injury to the popliteal artery at the time of the initial surgery. Secondly, and most glaring, was plaintiff’s claim as to the failure to obtain a vascular consult between the time of the ACL repair and post-op day six despite obvious signs of vascular compromise. It was claimed that had a prompt vascular consult been obtained the arterial injury would have been diagnosed and the leg saved by prompt repair by the vascular surgeon.

It was anticipated, as a result of review of the surgeon’s records, that it would be claimed that this was an unusual presentation, that the symptoms were more likely caused by arterial spasm and/or compartment syndrome and thus the failure to obtain a vascular consult was not negligence. Hence, a good portion of the defendant’s deposition was directed at eliminating these claims as valid defenses.
The surgeon was first questioned as to whether the injury occurred at the time of surgery:

"Q. In your opinion, with a reasonable degree of medical probability, did the patient’s popliteal artery sustain some type of injury during the surgery that you performed?
A. It may have.
Q. Do you believe that the popliteal artery may have been injured prior to your surgery?
A. Not that I am aware of."
* * *
"Q. Doctor, her blood work before surgery was normal, correct?
A. Yes.
Q. Her clotting factors were all normal, and we went over that.
A. Yes.
Q. The MRI, the cuts that showed the popliteal artery, other than the anatomical position that you mentioned, show no abnormality; is that correct?
A. None that I detected.
Q. No vascular compromise?
A. It wasn’t a full vascular study, but, no, it didn’t show any.
Q. And it showed no popliteal cysts; is that correct?
A. Correct."
* * *
Q. Certainly, you did not diagnose such an injury before the surgery you performed?
A. Correct.
The surgeon was thereafter questioned with regard to his examination of the patient on post-op day three at which time she displayed as stated above, obvious signs of vascular compromise.
"Q. With regard to physical examination, it says, physical examination, right leg, and you dictated, there is deformity in terms of soft tissue swelling.
The compartments are full in the leg but they are compressible and not tense. She has no active extension to the toes and ankle, though sensation is intact. When dependent her foot reddens nicely and has nice refill. When she is supine, it starts to blanch and becomes mild and the refill is sluggish.
She is two plus, two plus dorsalis pedis pulses, and then you wrote in, with dependency.
Q. And then you wrote in wound is well healed?
A. Right."
* * *
"Q. When you wrote in this note or when you dictated in this note that there was no active extension to the toes and ankle, you mean she couldn’t move her foot?
A. Yes.
Q. What was the significance of the fact that when the patient was supine her right foot starts to blanch?
A. That the blood was not circulating distally when she was not with gravity.
Q. By blanching, you mean it became whiter or pale?
A. Yes.
Q. In layman’s terms, she wasn’t getting proper blood supply to the foot, true?
A. In that position, the blood supply was compromised.
Q. Under physical examination, the second to last full sentence, where you dictated when she is supine it starts to blanch and becomes mild and the refill is sluggish, what do you mean by mild?
A. I think it was a typo. It is supposed to be mottled and I didn’t check it.
Q. Mottling, under these circumstances, is also an indication of a diminution in the blood supply to the effected area, true?
A. Yes, it can be from that.
Q. So, can we agree that based upon the findings of your physical examination something was causing a compromise of the blood supply to the foot?
A. That is what I was concerned about.
Q. So, the answer is yes, correct?
A. Correct."
* * *
"Q. Would you agree that the findings of swelling of the leg and foot, no active extension of the toes and ankle, blanching of the foot and sluggish capillary refill indicate a vascular injury?
A. It could happen from compartment syndrome also.
Q. So, would you agree that the findings of swelling of the leg and foot, no active extension of the toes and ankle, blanching of the foot and sluggish capillary refill indicate vascular compromise?
A. Yes.
Q. Just so I am clear on this, when we refer to vascular compromise, we are referring to an inadequate blood supply to the effected area?
A. Yes.
Q. Doctor, is it fair to say that you considered some type of vascular problem as a cause of the positive findings you made?
A. I considered as a secondary effect, I thought, and I mention it in here, I thought it was more likely compartment pressure from fluid extravasation causing the problem.
Q. When you say compartment syndrome, it does cause a vascular problem, correct, as a result of increased pressures and ischemia occurs, correct?
A. Yes, as a secondary effect.
* * *
"Q. Doctor, when you asked them to rule out deep venous thrombosis, you were referring to a clot in a vein; yes or no?
A. To rule out a DVT, yes, that is what you are trying to do.
Q. When you told us before that people can develop blood clots following surgery, what you were referring to is a venous blood clot, a blood clot in a vein; yes or no?
A. Yes.
Q. Did you at this point in time consider obtaining a consult with a vascular surgeon?
A. No, I did not.
Q. Why not?
A. My working diagnosis was primarily compartment syndrome or development thereof.
Q. Did you consider ordering an angiogram?
A. At that point, no.
Q. You also note in your plan that you were going to get compartment pressures there and that was because you were concerned about either compartment syndrome or that she was developing compartment syndrome, true?
A. Yes."
The surgeon was next forced to admit, that whatever the cause, the patient was obviously suffering from vascular compromise which was an emergent situation:
"Q. When you wrote that you thought that there was a spasm of the artery, what artery were you referring to?
A. Well, primarily, I was thinking of the popliteal artery."
* * *
"Q. How would spasm of the artery cause a lack of active flexion of the toes and ankle?
A. I feel, if it persisted long enough to interrupt the blood supply to the foot, they would have less ability to function.
Q. So, it must have been present for a while?
A. Yes, I would say it could have been present for a while."
* * *
"Q. So, according to you, it was your opinion or thought process that this was being caused by a spasm of the artery and therefore a compromise to the lower leg and foot?
A. At this point in time I wasn’t 100 percent sure what was causing it. I was worried about a fluid compression causing it, possible vasospasm, compartment syndrome.
Q. Whatever the cause, you knew she wasn’t getting enough blood to the lower leg and foot, true?
A. I knew she was having problem with the blood supply specifically when she was supine, as I say in my exam.
Q. Doctor, the finding that she had no active flexion of the toes and ankle, is that an indication that she was suffering a significant compromise of the blood supply to her lower leg and foot; yes or no?
A. Yes, it does mean that.
Q. And if that blood supply is compromised long enough, ischemia results, correct?
A. Yes.
Q. Eventually, the muscles of the lower leg and the nerves and the muscles of the foot, they are going to die? They are going to necrose, true?
A. They could, yes.
Q. They will if it is unrelieved? It is not that they could --
A. If it is completely unrelieved, if the pressure is completely unrelieved, if it is not successful, yes, they will die.
Q. In point of fact, when one is dealing with compartment syndrome, if elevated compartment pressures are allowed to exist for more than eight hours, the result -- and when I say persist for more than eight hours until decompressive surgery is performed -- the result will be some loss of function, true?
A. Most of the time, yes. I am not saying it is 100 percent, but yes.
Q. So, this was an emergent situation, true?
A. It was clearly an urgent situation.
Q. Something had to be done to relieve this impairment of the blood supply to this young lady’s lower leg and foot, true or not true?
A. I think something had to be done to change her condition, whatever that might be.
Q. And you knew at the time that there was some type of vascular problem here, whether secondary to compartment syndrome or to a vasospasm of the artery, she was having a vascular problem, true?
A. At this point in time she was having a compromise to he blood supply to the leg.
Q. Which is the vascular system?
A. Right."
The physician then admitted that vasospasm absent other arterial injury is rare. He further admitted that prompt diagnosis of an arterial injury is crucial in order to salvage the affected extremity.
"Q. Doctor, would you agree that a true spasm of the popliteal artery without other injury to the artery seldom occurs?
A. It is not a usual finding."
* * *
"Q. Would you agree that delayed recognition of a popliteal artery lesion is known to be a major cause of limb loss?
A. Yes.
Q. Because we agree, do we, that time is of the essence when dealing with an injury to the popliteal artery?
A. Dealing with any arterial injury, yes."
The Doctor was next asked to explain what he thought was causing the patient’s problems since he was able to rule out compartment syndrome and deep venous thrombosis and also why he still did not order a vascular consult:
"Q. You measured the compartment pressures?
A. Yes."
* * *
"Q. Going over these figures, is it fair to say that the pressure in the anterior compartment was normal?
A. Yes.
Q. And the pressure in the lateral compartment was normal?
A. Yes.
Q. And the pressure in the deep posterior compartment was normal?
A. Yes.
Q. And the pressure in the superficial posterior compartment was either normal or slightly elevated?
Q. Yes, it was elevated.
Q. Slightly?
A. Yes.
A. In fact, based upon the recorded pressures, you ruled out compartment syndrome, true?
A. At that point I didn’t feel she had compartment syndrome, though she was fairly swollen.
Q. It says compartment syndrome ruled out. That is your writing?
A. Yes.
Q. So, you ruled it out at that time based upon the pressures you took?
A. Yes.
Q. And you also ruled out deep venous thrombosis?
A. Yes.
Q. There’s a triage note by a nurse that says patient to E.R. by wheelchair with complaint of swollen right leg and discoloration of right foot. It goes on to say, right leg swollen, blanched from ankle to toes?
A. Yes.
Q. And she had leg and foot pain, correct; that is, according to the first page of the record.
A. Yes.
Q. And according to your findings she had no active extension of the toes or ankle, correct?
A. Correct.
Q. And she had diminished capillary refill?
A. Yes.
Q. And you had ruled out deep venous thrombosis, correct?
A. Yes.
Q. And you had ruled out compartment syndrome, true?
A. Yes.
Q. So, what did you think was causing the vascular compromise and these resulting problems?
A. Well, at this point I basically attributed it to spasm from the arteries just within the leg without being overt compartment syndrome because the pressures weren’t high enough. That was my working diagnosis then.
Q. Just so I am clear, you thought that the popliteal artery was in some type of spasm which involuntarily contracted resulting in a diminution of blood supply to the lower leg, true?
A. More or less that is what I was working on."
* * *
"Q. Did you at this point in time, having ruled out compartment syndrome and having ruled out deep venous thrombosis, consider obtaining a vascular consult?
A. I didn’t.
Q. Why not?
A. Basically, for the same reasons I had mentioned before. I was hopeful with edema control the situation would resolve itself."
* * *
"Q. Prior to your discharging the patient from the emergency room, did you consider that the findings of swelling of the right leg, blanching of the leg from ankle to toes, the lack of active extension of the toes or ankle and pain of the leg and foot might be caused by ischemia as a result of injury to the popliteal artery?
A. That was not a primary diagnosis of mine.
Q. I didn’t ask you whether it was a primary diagnosis. I asked you whether you considered it.
A. At that point I wasn’t considering it.
Q. Why was that?
A. Because of the length of time from the surgery, I felt, if she had an arterial injury, it would have presented a lot sooner than 72 hours later, or whatever the time frame was at that point in time, and that was the main reason why.
Q. That was a thought process that went through your mind at that time?
A. Well, piecing everything else together that I knew, yes.
Q. In thinking about that and thinking about in your mind that you would have assumed that an arterial injury would have manifested itself somehow differently at an earlier point in time, did you think, as you were thinking about that, about getting a vascular consult?
A. I did not at that point in time.
Q. Do you think you should have?
A. Knowing what the end result was now?
Q. Yes.
A. Of course."
Finally, the Doctor was confronted with the findings on fasciotomy which unequivocally eliminated compartment syndrome as a cause of the patient’s symptoms and mandated a vascular consult:
"Q. The surgery that you performed according to this was a four compartment fasciotomy of the right leg?
A. Correct."
* * *
"Q. Would you agree that based upon these findings with regard to the muscles in the anterior compartment, the pressures within that compartment had to have been elevated for a period of less than eight hours?
A. It is hard to say, but I was surprised that the muscles looked in good condition at that point in time?
Q. Why?
A. Because my thought process was that this was probably going on since the day before and I didn’t know what the muscles would look like, quite honestly, when I went in there.
Q. The fact is this: If the patient had the elevated compartment pressures within the anterior compartment for a period of more than eight hours, wouldn’t you have expected to find a loss of contractility of the muscles together with at least some discoloration?
A. Yes, you would think that would have happened.
Q. And the findings that you made of good contractility, color and consistency of the muscles indicates that she couldn’t have been suffering from compartment syndrome for over eight hours, true?
A. Basically, I agree with that."
* * *
"Q. Based upon these findings that you made with regard to the muscules within the compartments, is it fair to say that compartment syndrome was not causing the loss of movement of her ankle and foot?
A. The compartment syndrome directly was not the cause of it."
The inexcusable failure of the surgeon to obtain a vascular consult despite his admission that the patient was suffering from a vascular compromise was irrefutable following his deposition. Once again, this demonstrates the detailed knowledge the plaintiff’s attorney must acquire about the area of medicine involved in order to conduct a meaningful deposition of the defendant physician.

1. Colburn GL, Lumsden MB, Taylor BS, Skandalakis, JE. The Surgical anatomy of the Popliteal Artery. AM Surg 1994 Apr; 60(4) 238-46.
2. Potter D, Morris-Jones W. Popliteal Artery Injury Complicating Arthroscopic Menisectomy. Arthroscopy 1995 Dec; 11(6) 723-6. Roth J.H.; Bray R.C. Popliteal Artery Injury During Anterior Cruciate Ligament Reconstruction: Brief Report. J Bone Joint Surg. Br. 1988 Nov. (70)(5): 840
3. Potter D, Morris-Jones W. Supra. Tawes R.L. SR, Etheredge SN, Webb R.L., Enloe LJ, Stallone RJ Popliteal Artery Injury Complicating Arthroscopic Menisectomy. Am J Surg. 1988 Aug; 156(2):136-8. Jeffries JT, Gainor BJ, Allen WC, Cikrit D. Injury to the Popliteal Artery as a Complication of Arthroscopic Surgery. A Report of Two Cases. J Bone Joint Surg. [AM] 1987 Jun; 60(5):783-5.
4. Seybold EA, Busconi BD. Traumatic popliteal artery thrombosis and compartment syndrome of the leg following blunt trauma to the knee: a discussion of treatment and complications. J Orthop Trauma 1996; 10(2):138-41