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I t is important to be aware of emergency department (ED) cases and situations that lead to lawsuits in order to avoid repeating errors and reduce personal liability. This issue highlights some recent cases that involve syncope and stroke.
On the evening of June 8, 2011, Mr. Anthony Musco, age 64, experienced a syncopal event and hit his head on the floor. He had no known past medical history. EMS were called to the scene. They performed an EKG upon arrival that demonstrated atrial fibrillation, which soon converted into normal sinus rhythm. Upon arrival to the emergency department (ED) at Lakeland Regional Medical Center, he received a CT of his head, which demonstrated no acute injury. The patient was then admitted to the hospital for further observation and evaluation. The primary inpatient team started the patient on enoxaparin every 12 hours as a prophylaxis against blood clots. While in the hospital, the patient underwent extensive testing for a possible cause of the syncope and new-onset atrial fibrillation. The inpatient cardiologist, Dr. Canto, was consulted by the primary team for new-onset atrial fibrillation. The cardiologist agreed with the primary team’s treatment plan, and no changes were made to his treatment plan. Three days after the initial syncopal event, the patient experienced a massive brain bleed and sudden clinical decline. The patient went into a coma and died 10 days later.
At trial, the plaintiff claimed that Dr. Canto, the cardiologist, should have stopped the enoxaparin due to the risk for delayed brain bleed. They stated that enoxaparin increased the rate at which the bleeding occurred, or was the cause of the bleeding. Per the medical records, the patient received three doses while in the hospital.
The defense claimed that enoxaparin could not have been the cause of the bleeding, and could have only increased an existing bleed, which was ruled out by the CT scan in the ED. They also stated that enoxaparin was not started until the day after the event. The risk of delayed bleeding due to trauma was remote, and the administration of enoxaparin for prophylaxis was clinically indicated. Dr. Canto supported this claim that enoxaparin was indicated, until all cardiac concerns were eliminated. The plaintiff requested that the jury award a verdict of $10,000,000. The hospital, Lakeland Region Medical Center, and the primary care physician settled for an undisclosed amount. A defense verdict for the cardiologist, Dr. John Canto, was returned.1
Anticoagulants represent a large portion of the $300-$610 million spent per year on medical professional liability costs associated with injectable medications.2 In a review of adverse reactions caused by anticoagulants, 24.8% resulted in an increase in bleeding.3 There is no shortage of cases in medical literature in which physicians have been liable for causing increased amounts of bleeding from anticoagulation. In Jenkins v. Willis, a patient with subarachnoid hemorrhage was given enoxaparin, and died shortly afterward.4 In another case, a patient with right-sided weakness was given enoxaparin after possible stroke and atrial fibrillation, resulting in brain death.5 Although the physicians in the preceding cases were not held liable for the patients’ deaths, the administration of the anticoagulation was linked to adverse outcome. Damages have been awarded to a patient after the administration of the anticoagulation resulted excessive bleeding and, subsequently, permanent disability.6
When evaluating a patient with syncope, it is important to screen and recognize that potential head injury has occurred. Many conditions that cause syncope, such as dysrhythmias, pulmonary embolus (PE), and coronary ischemia, will be treated with anticoagulation and worsen traumatic brain injury.
Mrs. Eliza Miller, age 67, experienced an episode of syncope on October 14, 2011, while at home. On evaluation by emergency medical technicians (EMTs), the patient was asymptomatic. She was brought by emergency medical services (EMS) to the emergency medicine department at Lawnwood Regional Medical Center in Fort Pierce, FL, where she was evaluated by the ED physician. She remained asymptomatic, and the ED physician was not able to determine the cause of syncope. The ED physician later testified that he was highly suspicious that the cause of syncope was due to her extensive cardiac history, but he also considered several other possible causes. Her primary care doctor, Dr. Dawkins, was consulted and the patient was admitted to the hospital. While in the hospital, Mrs. Miller’s cardiologist and the on-call neurologist also evaluated the patient. The three physicians could not determine an exact diagnosis despite the numerous studies and tests ordered. Throughout the initial evaluation and diagnosis, the patient remained asymptomatic.
Later that evening at 10:01 p.m., Mrs. Miller experienced another episode of syncope. Subsequently, she continued to decline and experienced cardiac arrest. Despite numerous attempts at resuscitation, Mrs. Miller died shortly after midnight. At the time of autopsy, the cause of death was determined to be a PE that was blocking both pulmonary arteries.
Following Mrs. Miller’s death, her husband filed a wrongful death complaint on behalf of her estate against Dr. Dawkins as well as the ED physician and the cardiologist. The ED physician and the cardiologist settled with the plaintiff.7
Overall, there is no shortage of medical-legal cases involving the misdiagnosis of PE. One review article analyzed 160 malpractice claims involving PE. Failure of the clinician to anticipate and reduce the chance of PE was the basis for six of the claims.8 In some cases, the failure of a clinician to diagnose a PE has resulted in awards of hundreds of thousands dollars to the plaintiff. For instance, in Mabry v. County of Cook, the patient was complaining of dizziness and dyspnea. She was then treated for an asthma exacerbation and discharged from the ED after a mild decrease in shortness of breath. Several days later, the patient returned to the ED with symptoms of persistent dyspnea and continued asthma exacerbation. Shortly after being admitted, she died from a PE. The plaintiff was awarded more than $500,000.9 Recognizing the link between syncope and PE has proven to be a challenging medical-legal aspect, and does not always result in a verdict for the plaintiff. For example, in Edwards v. Alexander, the patient presented to the ED with syncope and various gastrointestinal (GI) complaints. The patient subsequently died from a pulmonary embolism in the intensive care unit (ICU), but the courts at the time ruled in favor of the defense.10
The diagnosis of PE has been proven to be difficult throughout medical literature. Notably, objective testing confirms the diagnosis of pulmonary embolism in only 20% of patients.11 Classically, PE presents with dyspnea or chest pain. Vital signs, such as tachycardia, tachypnea, low pulse oximetry, or increase in temperature, may be valuable in diagnosis, but have not proven to be reliable. Approximately 5%-8% of patients who present to the ED present with symptoms consistent with syncope, near syncope, or new-onset seizure.11 Syncope due to PE is caused by a reduction of blood flow in the pulmonary vasculature or by activation of receptors causing bradyarrythmias that lead to reduction of cardiac output.12 Patients who present asymptomatically make diagnosis challenging for the physician.
It is imperative to consider PE as an etiology in patients presenting to the ED with syncope.
Mr. Charles Coulon Jr., age 65, presented by EMS to the East Jefferson General Hospital ED (EJGH) in Metarie, Louisiana. He was aphasic and unable to provide a medical history. However, his wife informed the ED physician, Dr. Terry Creel, that at approximately 10:45 p.m. she was awakened by a loud "thump," whereupon she found her husband lying on the ground in front of a sofa where he had been seated. She noted that he was confused, had slurred speech, and was unable to move his right side. She called 911, and Mr. Coulon was transported to the EJGH, arriving at approximately 11:20 p.m., within 35 minutes of his unwitnessed fall.
Mrs. Coulon relayed to Dr. Creel that Mr. Coulon also had a facial droop, which appeared to improve en route to the ED. Upon arrival, his blood pressure was 145/95. His neurological examination showed a right facial droop and a flaccid right arm, with some slight movement of his right hand. A left cerebral vascular accident (CVA/stroke) was clinically diagnosed.
Dr. Creel ordered a non-contrast head CT scan. The radiologist noted that the CT scan did not show any evidence of hemorrhage, infarction, or discernable trauma. At 11:59 p.m., approximately one hour and 50 minutes after symptom onset, and 40 minutes after arrival in the ED, the radiologist notified Dr. Creel of the CT results.
Although Mr. Coulon’s CVA was diagnosed within the three-hour "window" in which tissue plasminogen activator (tPA) should be considered in the treatment of an ischemic CVA, Dr. Creel concluded that he was not a tPA candidate, as his fall was unwitnessed, his facial asymmetry was improving, and he had slight use of his arm. There is a factual dispute as to whether Dr. Creel discussed the possibility of administering tPA with Mrs. Coulon. At deposition, he testified that he offered tPA but she declined, stating that, "I do not want any further harm done to my husband." Mrs. Creel denied that such a conversation had ever transpired. Dr. Creel admittedly failed to document this conversation. At deposition, Dr. Creel admitted that he never specifically informed her about the benefits and risks of tPA (e.g., the 12% chance of neurologic improvement at three months versus a 6% risk of intercranial hemorrhaging). Because he deemed that Mr. Coulon was not a tPA candidate, Dr. Creel did not consult a neurologist.
At trial, the jury awarded Mr. Coulon $150,000 in damages, but denied future medical expenses. This is clearly a small award that is not consistent with compensating the effects of a missed CVA. During post-trial jury interviews, jury members expressed concerns regarding the issue of informed consent. They were concerned that there was a lack of discussion and clearly no documentation on the chart that Dr. Creel had ever reviewed the risks and benefits of tPA with Mrs. Coulon. Clearly, the jury, via the size of the award, did not think a case was made that tPA should have been unequivocally administered, but were willing to give compensation on the undocumented or lack of informed discussion on the administration of tPA.13
Multiple other recent court cases have mandated that informed consent is warranted when discussing treatment, admission versus discharge, and even test ordering in stroke-related conditions. In one case, a patient was discharged for outpatient treatment of TIA and had a CVA.14 In another case, a patient discharged with a diagnosis of Bell’s palsy was not informed that CVA was in the differential diagnosis, and that a CT scan was a test consideration.15
There is no doubt that issues regarding tPA administration frequently arise in ED litigation. In a recent review of ED legal malpractice suits, seven legal databases were used to examine lawsuits from the ED associated with tPA and stroke. Thirty-three cases were found involving tPA ischemic stroke therapy. In 29 (88%) of these cases, patient injury was claimed to have resulted from failure to treat with tPA. Emergency physicians were the most common physician defendants. Defendants prevailed in 21 (64%) cases, and among the 12 with results favorable to the plaintiff, 10 (83%) involved failure to treat and two (17%) claimed injury from treatment with tPA.16 The study noted that more lawsuits are filed for failure to give tPA in ED stroke patients rather than complications from its administration.
In a recently settled Kentucky case, Sparks v Bokhari, a 43-year-old woman was celebrating on Christmas Eve with her family. There was no family discord or stress. She was witnessed to suddenly fall to the ground. The family noted that she could not speak and was unable to use her right arm at approximately 9:30 p.m. They brought her immediately to the ED. Upon arrival, she was evaluated by Dr. Bokhari at 10 p.m. A CT scan of the brain was performed and read by the radiologist as normal at 10:48 p.m. Nursing notes commented on the patient’s "unwillingness" to communicate and also that she moved her extremities when the family was not present. The physician failed to document a neurologic exam on the chart. At one point, the family testified that Dr. Bokhari stated, "Your daughter is having a nervous breakdown because of how you raised her." Mrs. Sparks was admitted to the hospitalist with a diagnosis of conversion disorder. No neurologist was consulted, and administration of tPA was not considered. The next morning, a repeat CT scan revealed a large left middle cerebral artery infarct. The patient was left with dense motor and speech deficits. The case was settled for an undisclosed sum.17
It is imperative that ED providers be aware that other illnesses may mimic a stroke. A study looked at what other diagnoses are often labeled as CVA. In 65 cases of definite stroke mimic and 44 cases that were likely mimics, the following were the most common etiologies: Seizure accounted for 21.1 %, followed by sepsis (12.8%), toxic/metabolic (11.0%), syncope (9.2%), confusional state (6.4%), vestibular problems (6.4%), mono-neuropathy (5.5%), and migraine (2.8%).18
Conversion orders often present with neurologic-type symptoms. These include: non-epileptic seizures, weakness and paralysis, movement disorders, speech disturbances, globus sensation, sensory complaints, visual symptoms, and cognitive symptoms.7 The ED provider must be very cautious in making this diagnosis in the ED. Between 2% and 50% of patients diagnosed with conversion disorders later develop severe organic disease. One study of 85 patients with the diagnosis of conversion disorder found 12% had neurologic disease.19
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