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Friday, September 21, 2007
Anesthesia Errors: Evaluation of the Anesthesia Case – Failure to Maintain a Patent Airway
The practice of anesthesiology is broad in scope extending from the control of pain and consciousness in the operating room or elsewhere to the control of pain generally in the hospital or even in the outpatient setting. In the operating room, the anesthesiologist, in addition to having an extensive monitoring role, has independent responsibility for evaluating and supporting cardiopulmonary function. Because of their monitoring functions, anesthesiologists, as a rule, document their activities contemporaneously and more thoroughly than any healthcare provider other than perhaps the critical care nurse. In addition, because errors in the administration of anesthesia can result in catastrophic injuries (which in the past were often preventable) the specialty has evolved more thorough and rigid guidelines than most medical specialties. Anesthesiologists have also benefited from the advent of safeguards such as continuous pulse oximetry and continuous mean arterial pressure and blood pressure monitoring systems. Notwithstanding the rigid guidelines and all the technologic advances, there are still serious preventable injuries, which occur and are entirely the responsibility of anesthesiologists. The one which I choose to address in this article will be airway management.
A completely healthy human being cannot survive more than a few minutes of apnea (absent ventilation) without suffering serious injury and in some cases severe brain damage or death. Nevertheless, at the beginning of every surgical procedure where inhalation anesthesia is to be employed, there is an intentional period of apnea artificially induced by the administration of paralytic drugs to enable the anesthesiologist to pass a tube through the oral pharynx into the trachea in order to secure the patient’s airway for the administration of assisted ventilation and inhalation anesthesia. Sometimes when the patient’s spontaneous ventilation have been intentionally eliminated by the use of paralytic drugs, there is difficulty in securing the airway and the anesthesiologist then experiences what most anesthesiologists regard as their worst nightmare (though it is truly a greater nightmare for the patient’s family). A patient’s ability to self ventilate has been eliminated intentionally and routinely. An airway cannot be passed or an airway is passed but a patient cannot be ventilated through the airway. The patient cannot self ventilate because of the paralytic agent. The patients dies. Alternatively, the patient is successfully ventilated ultimately but suffers severe brain damage because of the interval of apnea. The patient then subsequently either dies or is left in a comatose state.
In 1993, the American Society of Anesthesiologist’s Task Force on management of a difficult airway, promulgated practice guidelines for the management of the difficult airway which were published in the Journal of Anesthesiology, 78:597 (1993). First and foremost, it is the anesthesiologist’s responsibility during the course of a pre-operative anesthesia evaluation to assess the likelihood that a difficult airway will be encountered. Prior records are to be examined and a careful history is to be taken. There is a wide array of frequently encountered physical anomalies, which can be assessed and identified during the course of the pre-anesthesia evaluation. For a patient in whom a difficult intubation is anticipated, a specific strategy must be developed for how the difficult airway will be managed. One alternative, when a difficult airway is anticipated prior to a surgical procedure, is to not perform the surgical procedure or to perform it under regional or other form of anesthesia. In Pennsylvania a patient’s consent to anesthesia, where the patient has a difficult airway, cannot be informed consent, if the patient is not made aware of the hazards of proceeding with the surgery in the face of a difficult airway. In one of every ten thousand inhalation anesthesias an intubation effort fails and a patient cannot be ventilated and dies. For a patient with a difficult airway, the risk is a thousand times greater.
If the surgery is to be done under inhalation anesthetic, notwithstanding the risk, short-acting paralytic agents are to be given and the patient is to be pre-oxygenated to such an extent, they are easily (like a pearl diver) able to survive without harm a prolonged period of apnea. They can then await the return of their own spontaneous respiratory function after the short-acting paralytic agent has been metabolized. Awake intubation can also be attempted where the intubation is conducted without the use of paralytic drugs. Whatever method is employed initially, the anesthesiologist must be prepared before the procedure begins to deal with the possibility that awake intubation will be unsuccessful or that spontaneous ventilation will not effectively be restored. In teaching hospitals an experienced bronchoscopist must be immediately available for the placement of a tube by fiber optic bronchoscopic guidance, transtracheal jet ventilation should be available so that a patient can be ventilated through a needle inserted through the cricoid cartilage into the trachea. It is important to remember that securing an airway surgically is not an effective viable alternative in most cases.
Though there are cases, to be sure, where well-prepared anesthesiologists observing every precaution have encountered an airway that could not be secured and ventilation that could not be recovered, it is in the opinion of this author most often the case that the loss of a patient before the commencement of surgery because of a failure to secure an airway is the result of the failure to have properly identified that a difficult airway existed or the failure to have properly prepared for a difficult airway in accordance with the accepted guidelines of recognized authorities in the field. For general reference on this subject look to Anesthesia, Editor, Ronald D. Miller, 5th Edition 2000, Complications in Anesthesiology, Editors Gravenstein and Kirby, 2nd Edition 1996, Clinical Anesthesia, Editors Burak, Cullen, Stoetling, 3rd Edition, 1997, and Anesthesia for Obstetrics, Editors Shnider and Levinson, 3rd Edition, 1993.
posted by Jerry Meyers at 2:08 PM
Brain Injury Cases: Evaluation of an Anoxic Brain Injury Case
Patients thankfully do not frequently suffer a brain injury during the course of a hospitalization. When such injuries do occur, medical personnel are quick to explain the occurrences as tragic but unfortunate consequences of unavoidable events. Sometimes they maintain that the cause of the brain injury is unknown. Family members come to lawyers because they are instinctively unsatisfied with the explanations that they have been given, if they have been given explanations at all. It is a daunting task to search for causes of a medical catastrophe cloaked in mystery at the time of the initial client interview.
Brain injuries result from a broad variety of cardiovascular insults. Because of limitations of time and space, this article will address only those brain injuries, which have resulted from cardiac and/or respiratory insufficiency. Hemorrhagic and/or embolic strokes and brain damage due to trauma or infection will not be addressed here.
The reason that severe metabolic (hypoxic and/or ischemic) brain injury is so rare is that the insult needed to produce such injuries invariably would result in death in most cases. The fact that a person is left brain injured rather than dead simply means that there was an effective treatment for the respiratory and/or cardiovascular insufficiency, which, though employed late, was employed in time to effectively restore vital functions. If the treatment were provided a bit later, all these patients would simply be dead.
Brain tissue is rather delicate. Other tissues of the body are far more resistant to a lack of oxygen. A person who has a normal cardio-respiratory function and suffers cardiac arrest, may be successfully resuscitated without permanent injury even though a period of six to ten minutes have elapsed from the time of initial collapse. The frequently cited time limit of four minutes prior to onset of brain damage is conventional but relates primarily to those persons suffering some protracted period of cardio-respiratory insufficiency or other metabolic deficiency prior to arrest.
One important proof that the human brain endures with regularity complete cessation of circulation longer than four minutes without permanent adverse consequence can be found in the literature describing the prognosis of patients having been successfully defibrillated from witnessed ventricular fibrillation. Such literature establishes that after six minutes the chances of successful defibrillation markedly and abruptly decline, as do neurologically intact survivors. That so many neurologically intact survivors exist, notwithstanding delays in excess of four minutes, and that patients and are neurologically intact with even greater delays prove the fallacy of the four minute convention.
The window for survival neurologically intact or otherwise, for the overwhelming majority of patients does not exceed ten minutes, except in the case of cold water drowning or other special circumstance. The fact that the window is so narrow is the reason that the survival of the brain-damaged patient automatically raises suspicion that there was a treatment adequate to prevent death, which was not employed in time.
Indeed, it has been the experience of this author that when brain injury has occurred as a result of cardio-respiratory insufficiency while a patient was being attended in a monitored unit, that a meritorious case has invariably existed. Brain damage does not occur in a normotensive patient because, as sensitive as the brain is to hypoxia, it nevertheless has the ability to resist damage so long as an adequate volume of blood is being supplied, albeit with less than the desirable quantity of oxygen.
Prior to hypoxia causing brain damage, it must persist for a sufficient length of time for hypotension to occur. The initial response of the heart to hypoxia is an increased heart rate (tachycardia) which is followed after a time by a decreasing heart rate (bradycardia). The heart beats faster to attempt to compensate for the decreased quantity of oxygen. As the heart, notwithstanding increased rate, eventually is unable to meet its own metabolic needs, the heart rate falls and with the fall of the heart rate comes a simultaneous fall in blood pressure. After shock ensues, hypoxia risks brain injury but there is a window of time remaining during which a restoration of adequate oxygen will permit resuscitation without brain injury.
Though there are similarities in the effects of brain injuries resulting from primary cardiac events (myocardial infarction) and those resulting from respiratory events, there are important differences medical-legally. For example, all of the measures needed to prevent the death of a patient from respiratory insufficiency can be employed in any general hospital in time in a patient with a healthy heart, to prevent brain injury. No patient should be permitted to go without respiratory support long enough to produce a predisposition for a brain injury. The signs of respiratory dysfunction are obvious as they are demonstrated by changes in color, respiratory rate and pattern of breathing.
In monitored hospital beds, pulse oximetry is routine. A pulse oximeter is attached to a finger or toe. It looks a bit like a large thimble and has a spring-like device, which secures it to the digit. Pulse oximeters measure oxygen saturation. They are all set to alarm audibly if a decline in oxygen saturation occurs. The alarm limits are always to be set at a level far above where any damage from lack of oxygen might ensue. In addition, in intensive care units and in many step-down units, all patients have cardiac monitoring as well. As mentioned earlier hypoxia causes an elevation in pulse and tachycardia invariably well before a patient’s brain tissue would be threatened.
The response to respiratory insufficiency should not be casual. It is to be regarded as an emergency. Nurses at every hospital are permitted to employ oxygen without a doctor’s order. Nurses also can assist ventilation mechanically without a doctor’s order in cases of extreme shortness of breath where supplemental oxygen has not resolved the problem. Nursing personnel are required, simultaneous with their provision of respiratory support, to request in-house physicians or anesthetists, who can within seconds after arrival restore ventilation by means of the placement of an endotracheal tube in the event that simple bag-mask ventilation does not resolve the problem. If an endotracheal tube cannot be placed, cricoidthyroidotomy can be performed in thirty to forty seconds. A needle-like device is inserted through the cricoid cartilage in the anterior neck. The patient is ventilated through the large bore needle. This technique is employed in cases of respiratory obstruction or in other circumstances where a tube cannot be placed.
The cases of brain injury following sudden cardiac failure should be viewed with a similar skepticism. Such events often occur in a monitored setting. If not, the event would not be recognized and the patient would be dead rather than brain damaged. A patient does not usually suffer brain damage because they have had a heart attack. They suffer such damage because the treatment which restored cardiac function was not given in time. Sudden treatable cardiogenic shock or arrest is therefore, without more, an insufficient excuse for brain injury.
When a patient survives a cardiac or respiratory event with brain damage, it is certain that a means of treatment was available which, if provided at some earlier point in time, would have avoided the brain damage. For that reason, an investigation into why the damage occurred is mandatory. Most often, one will find that brain damage occurred because of an untimely and inadequate response to earlier signs of deterioration. Though it may not be possible to prove negligence, a search for such proofs represents one of the most challenging and rewarding tasks that we, as trial lawyers, can undertake.
posted by Jerry Meyers at 1:59 PM
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The Pittsburgh, Pennsylvania attorneys at the law office of Meyers Kenrick Giuffre & Evans, LLC focus on medical malpractice and personal injury cases
in the following cities and counties in Western and Central Pennsylvania: Allegheny,
Altoona, Armstrong,
Beaver County, Blair County,
Butler, Cambria,
Clarion, Clearfield,
Crawford, Elk, Erie,
Fayette, Indiana,
Jefferson, Lawrence, McKean,
Mercer, Somerset, Venango, Warren,
Washington, and Westmoreland.
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