Evaluation of an Anoxic Brain Injury Case

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.

Severe Metabolic Brain Injuries Are Incredibly Rare

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.

The Human Brain Can Endure More Than Four Minutes Without Oxygen

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.

In Order To Cause Brain Damage, Hypoxia Must Be Present Long Enough For Hypotentsion To Occur

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.

An Important Legal Difference Between Brain Injuries Resulting From Primary Cardiac Events vs. Respiratory Events

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.

Respiratory Insufficiency Should Always Be Handled As An Emergency

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, cricothyroidotomy 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.

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