The restoration of higher nervous activity in patients who have experienced terminal states, and the prophylaxis of secondary neurological complications that can arise during postreanimation disease are cardinal problems of clinical reanimatology.
The main factor in the development of irreversible morphologic lesions in cerebral structures is the length of time during which the central nervous system has been in conditions of oxygen starvation. At the same time the regredient or progredient character of the development of neurologic complications in the restorative period, the probability of complete functional restoration of the cerebral cortex, and the possibility of new, occasionally fatal, symptoms of organic lesions in the central nervous system not only depend on the period of clinical death, but also on the gravity of the influence of the pathophysiologic factors on the organism in the preterminal period and during postreanimation disease.
The development of clinical reanimatology has enabled us to study the neurologic disorders that inevitably develop in clinical practice during the treatment of terminal states. Comatose conditions of various depth, and their corresponding stages in the dynamics of the neurologic symptoms, in the main confirm the regular sequence of the extinction of CNS functions, and their restoration in the post-terminal period, established in our experiments.
The polymorphism of the clinical picture, and the multiple and dynamic character of the neurologic symptoms and neuro-vascular disturbances in posthypoxia encephalopathias, reflect the varying degree of resistance of the separate structures and various functional formations of the nervous system to hypoxia. Organic lesions and functional disorders occur simultaneously at different anatomic levels, within different formations located at the same level, within different sectors of one and the same functional system, and in the individual structural units of a given cerebral formation.
The functional-morphologic mosaic caused by the nonidentical sensitivity of the individual elements of the brain’s formations and systems to ischaemia, hypoxia, and disturbances of microcirculation and metabolism is clinically expressed in the phasic character of the course of the postanoxic coma and in other disorders of CNS function. The post-terminal comas, characterized by degree of unconsciousness, the state of muscle tone and of pupillary, skin, and tendon reflexes, the presence or absence of a spasm syndrome, the indices of haemodynamics and thermoregulation, cardiovascular and respiratory functions, the degree of retention of compensatory-adaptive mechanisms, etc., all in fact reflect the degree of extinction of one or another functional system or level of the central nervous system, including the cerebral cortex.
The evolution or the regression of the pathophysiological processes is expressed in the various clinical symptom complexes, that develop according to the level of the affection and the domination of signs of extinction or irritation of the individual cerebral formations. The individual syndromes have been classified as ‘first degree coma’ and ‘second degree coma’, ‘third degree coma’. When all the functions of the brain and respiration are extinct a symptom complex of ‘irreversible coma’, ‘vegetative coma’, ‘coma de passe’ is observed, in which the activity of the heart and internal organs is due to peripheral vegetative regulation and the organism’s life as a whole is preserved only in consequence of the application of artificial respiration and medication stimulating cardiac activity and increasing blood pressure.
The restoration of CNS functions in the postreanimation period may be relatively rapid, with a transition from the terminal stage of coma to the appearance of the first signs of consciousness and a subsequent progressive improvement of the activity of subcortical formations and cortex of the brain. The separate phases of the restorative period, and the various stages of coma in these cases, may be quite short; but restoration of functions can be frozen at one of the stages of coma, or deterioration of the patient’s condition may occur on a background of considerable improvement of cortical function. Delay in the regression of postreanimation disease and secondary deterioration with a fatal outcome or severe psychic defects are the result of a number of factors affecting the organism during the restorative period and essentially depend on the premorbid peculiarities of the macro-organism.
Our clinical observations of recent years in the reanimation department allow us to express certain ideas on the dynamics of the neurologic lesions in the postreanimation period.
The commonest causes of terminal states and posthypoxic neurologic damage in a multi-functional reanimation department are (a) massive blood loss due to wounding of the larger vessels, traumatic amputation of limbs, operations on organs of the abdominal cavity and true pelvis, and obstetric pathology, etc.; (b) severe cranio-cerebral trauma frequently accompanied with traumatic injuries to the bones of the pelvis and extremities; (c) eclampsia; and (d) other aetiological factors causing hypoxia, ischaemia, acute respiratory insufficiency, and comatose states.
The dynamics of neurologic lesions in the postreanimation period depend to a certain degree on the causes of the comatose condition. The direct damage to brain tissue in cranio-cerebral trauma of course has its own features as a result of the combination of general brain damage and focal lesions of the brain matter that distinguish it from the postischaemia and posthypoxic general brain damage that occupies the foreground in the clinical picture of these states. The same applies to the eclampsia in which there is marked general brain damage, which calls for correction of respiratory insufficiency and of acid-base equilibrium, and other reanimation measures. It is the general brain damage that causes severe functional disturbances of respiration and metabolism in these nosological forms and that allows them to be considered not in isolation but together with other forms of posthypoxic states.
Clinical observations indicate that the regression of the neurologic lesions caused by ischaemia and hypoxia occurs in one of three main variants: (1) full, stable restoration of all brain functions; (2) full, but temporary restoration of brain functions with subsequent relapse in neurological state; (3) incomplete restoration of brain functions with the development of irreversible impairment of higher nervous activity or a fatal outcome several days after resuscitation.
In the first variant spontaneous respiration and pupillary reflexes appear three to fifteen minutes after the restoration of cardiac activity. The phase of atonic coma is short or unnoticeable. The phase of hyperactive coma may last from two to twelve hours, and hormetonic spasms sometimes last throughout the whole of this phase; in other cases they are very brief, and in some patients are not observed at all. In the subsequent period there is a gradual restoration of the more highly organized systems of the brain, an easing of the depth of the coma to one of light degree, and then transition to a dazed, inhibited state followed by complete restoration of lucidity. Parallel with the decrease in the depth of the comatose state gradual normalization of both the somatic and the vegetative sectors of the nervous system is observed. In patients with such a course of the postreanimation period there are usually no signs of functional disturbance in the motor, reflex, and sensory spheres by the end of the first week. Hightened fatiguability, asthenia, and emotional and vegetative-vascular lability often last a long time.
Analysis of dynamic electroencephalographic research has shown that, in this variant of full, rapid, stable restoration of CNS functions, spontaneous electrical activity of the brain is also normalized relatively rapidly. The variants in the evolution of the brain’s electrical activity have been described in detail; here we need only to note that the encephalograph pattern of patients with a given variant of restoration of neurological state is often of an unstable nature in the early stages. The drop in amplitude, however, is never sufficiently marked to cause us to speak of an isoelectric variant of the EEG. On the contrary, it can be supposed, with some caution, that this spontaneous drop in amplitude, with simultaneous increase of rhythm, is a reflexion of short spells of activation of desynchronized non-specific brain systems.
After the stage of continuous cerebral electrical activity, relatively rapid restoration of alpha-activity is observed on the EEG with a progressively increasing alpha-index. Restoration of a normal EEG pattern passes through a phase of slow, unmodulated, low amplitude alpha-rhythm with a low alpha-index, then one of increase of amplitude and the index of alpha-activity, and finally a concluding phase of the formation of normal, dominant, well-modulated alpha-rhythm with clearly expressed zonal variations on the EEG. In contrast to the comparatively rapid restoration of normal background EEG, brain electrical reactivity is restored much more slowly. A lowering of the functional lability of cortical neurons can be traced for many days, occasionally for several weeks. These EEG findings correlate with the well known fact of the lengthy period of asthenia in patients who have suffered severe hypoxia of the brain.