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Advances in resuscitation create the risk that patients may be saved with a brain so damaged that they can never recover cognition. It is imperative that those who provide intensive care facilities determine the prognosis of such patients at a relatively early stage. This review suggests ways in which such predictions may be derived for patients in medical coma.
An analysis of 752 cases of severe diabetic coma during the period 1931 to 1973 showed that infections were present in one or more organs in 58% of the cases. The incidence of infections showed an increase from 53% (1931 to 1940 to 57% (1961 to 1970), with a further rise to 61%(1971 to 1973). A decrease in pulmonary infections from 40% to 17% and a distinct increase in urogenitial tract infections from 6% to 20% and in multiple infective complications from 3% to 7% were the most striking findings. The incidence of infections in other organs (abdominal, dermatological, laryngological and miscellaneous) remained virtually constant over the individual decades. Mortality was altogether higher in patients with infections (30% versus 20% in patients without infections). The highest mortality (35%) was recorded in the period 1951 to 1960; THE latest figure was 29%(1971 to 1973). Antibiotics are presumeably responsible for the decrease in the initially high mortality rate of 41% to 50% in urogenitial tract infections to 23% for the decade 1961-1970, with a further drop to 18% in the most recent period (1971 to 1973). Similarly, with multiple infections the mortality of 100% up till 1950 decreased to a recent figure of 63%, partly on account of the introduction of intensive care therapy during the past years. In abdominal infections there was also a distinct decrease in mortality form 43% to 14%, whilst in pulmonary infections the mortality remained at about the same level (24% to 28%).
Diabetic hyperosmolar coma is characterized by the appearance of a diabetic metabolic state in middle age, lack of ketosis, osmolarity of the plasma greater than 350 milliosmoles, psychic and neurological disturbances, increased occurrence of secondary diseases, arterial thromboses, azotemia. The mortality is 30-60%. The pathogenesis is still uncertain in many respects, consequently the suggestions for therapy are varied. The authors have found the following procedure useful: rapid compensation of sodium deficit, restoration of water balance, normalization of the composition of body fluids by reference to continuous laboratory investigation.
Authors report one case of HENOCH-SCHONLEIN syndrome particular by the association of two serious complications of good prognosis: neurological signs with coma and necrosing enteritis necessitating an intestinal resection of 60 cm of small bowel.
The Authors describe the clinical course of 331 cases of post-traumatic coma, studied during the two-year period 1970-1971 at the 2nd Division of Neurosurgery (Ospedale Maggiore, Bologna). Among them, 42% died from trauma-related causes; 40% survived and had a complete reintegration into society; 18% survived at a lower social level or remained totally excluded from society. The quality of survival does not depend on the presence and degree of organic sequelae only, but also on psycho-social factors.
Eight patients were seen within 15 minutes of intranasal self-administration of large amounts of pure D-lysergic acid diethylamide (LSD) tartrate powder. Emesis and collapse occurred along with signs of sympathetic overactivity, hyperthermia, coma and respiratory arrest. Mild generalized bleeding occurred in several patients and evidence of platelet dysfunction was present in all. Serum and gastric concentrations of LSD tartrate ranged from 2.1 to 26 nanograms per ml and 1,000 to 7,000 mug per 100 ml, respectively. With supportive care, all patients recovered. Massive LSD overdose in man is life-threatening and produces striking and distinctive manifestations.
Although the frequency of recognition of the syndrome of non-ketotic hyperosmolar coma is increasing in all age groups the mortality rate remains high. This paper reports the occurrence of this syndrome in a 12-year-old girl. The pathogenesis is discussed and a planned approach to the management of circulatory collapse, hypokalemia, hyperglycemia and hyperosmolarity over the initial 24 hours is proposed. The phenomenon of insulin resistance which was observed in this case is a rare complication of this syndrome. Awareness of the occurrence of this syndrome in all age groups, early recognition of its features and a planned approach to management are mandatory to reduce the very high mortality rate.
Using observation in a number of patients with severe closed head injuries followed by prolonged coma and of which three are reported in detail, the authors present an analysis of the resulting psychiatric problems. After a brief review of the literature they suggest a central psychopathological "core" common to such head injuries beneath their seemingly diverse symptomatology. This "core" seems to be built up around the following disturbances: 1) Memory disorders; 2) Perceptual problems and difficulties with the association of ideas; 3) Excessive tiredness and concomitant reduction in the powers of concentration.
Report on a case of cardiac arrest and coma lasting 10 hours secondary to the i.v. administration of 2 mg Flunitrazepam. The possible cardiorespiratory depressant respectively cerebral side-effects of Flunitrazepam are discussed. The high concentration of Flunitrazepam in the registered ampules is misleading to overdosage.
The diabetic coma presents a metabolic derangement which is initiated by a lack of insulin but is markedly enhanced by intracellular insulin resistance. The most essential points of insulin, fluid and electrolyte substitution are presented in this publication. Intensive care treatment is recommended not only because of the severe metabolic defect but also because of disturbances coming up in the course of treatment.
Sustained upgaze is a rare phenomenon that is observed primarily in those patients with coma secondary to cardiac arrest or prolonged hypotension. Because of "selective vulnerability" of the brain, cardiac arrest or prolonged hypotension may produce both cerebral and cerebellar cortical damage sparing the brain stem vestibulo-ocular reflex (VOR) pathways. This selective damage may be responsible for the generation of sustained upgaze. The VORs receive their selective inhibition from the cerebellar flocculus. This inhibition is exerted on only one of the two VOR pathways converging on each extra-ocular muscle, so that total disinhibition of the VOR pathway activities will result in a tonic upward bias. The underlying neuronal mechanism of sustained upgaze appears to be due to total floccular disinhibition resulting in upward drift produced by the biased VOR and the lack of correcting saccades due to cerebral dysfunction releasing the brain stem ocular motor systems from their control.
Fifteen patients with prolonged coma after craniocerebral injury were observed for a year or more, and their communicative functions were evaluated. Nine of them showed a considerable degree of recovery, while 6 remained in a vegative state. Of the 9 with recovery, 6 showed complete recovery of semantic functions, while 3 remained with aphasic deficits. Eight out of these 9 remained dysarthric. Communicative recovery began as late as 5.7 months after injury, and it roughly paralleled recovery in locomotion and A.D.L. Restlessness and sweating were favorable prognostic factors. Excessive salivation, snout reflex, corneomandibular reflex, retractory nystagmus and stereotypic movements were unfavorable. The 8 patients who remained dysarthric showed marked diminution of their expiratory and inspiratory reserves, and of their forced vital capacity.
In a 20 year old female nurse prolonged recovery (4 hours) unexpectedly followed to Rohypnol intoxication, the oral intake of which was realised only in the later period of postanaesthetic coma. Naloxone and physostigmine failed to achieve improvement but 4-aminopyridine was immediately successful.
A 3-year-old White child was admitted to the critical care unit in a coma after a generalized convulsion. Codeine and salicylic acid were present in his plasma. The possible aetiology and management are discussed.
In 1946, Mendelson described 66 cases of gastric juice inhalation during obstetrical work with no mortality. Other studies studying different populations (essentially in post-operative condition) denounced a mortality from 19 to 64%. In Forensic Medicine, a bronchial regurgitation of gastric juice is denounced in 1/3 lethal toxic comas. This regurgitation can be the direct cause of the death, it also can be an epiphenomena, as suggests the high level of inhalation in agonic process of any cause: 1/4 of autopsy findings. In our department, 200 cases of inhalation pneumonia, during comatose intoxications have been registered between 1972-1982, with a frequency of 1/28 patients. All the patients were under assisted ventilation. 4 deaths occurred in this serie. This 2% mortality suggests the curability of gastric juice inhalation during comatose intoxications in not specifically respiratory-orientated intensive Care Units. These relatively good results are probably party related to the patients' recruitment: young population without underlying organic disease, with a rapid turnover and little hazards of nosocomial superinfections.
Alteration of the early component of the blink reflex (delayed latency or abolished reflex) is considered to be relatively specific for pontine lesions (multiple sclerosis, vacular lesions of the brain-stem, neoplasms, syringes); provided, the trigeminal and facial nerve are unaffected. In comatose patients the electrically, by stimulation of the supraorbital nerve elicited blink reflex was super-imposed (50 or 100 responses) with the LAB 8/e-computer (off-line). It was found that the R1 component was abolished even in cases with supratentorial lesions and secondary brain-stem alterations, while no specific pontine lesions were demonstrated by neuropathological examination. Therefore it is suggested that delayed or abolished blink reflexes in coma due to supratentorial mass lesions are not concluslive for pontine lesions: they rather may reflect an unspecific secondary brain-stem alteration. Recording of the EEG reveals that in some cases the extinction of the early blink reflex precedes corresponding EEG alterations; this may be a matter of prognostic value.
In three cases of severe hypophosphatemia profound coma was associated. Although the occurrence of hypophosphatemia appeared to coincide with a high rate of intravenous administration of glucose and water, two of the three patients had liver disease and the other had hypothermia. In two instances the neurologic status improved with intravenous phosphate therapy. These case reports emphasize the importance of early recognition and treatment of profound hypophosphatemia in critically ill patients.
Artificial barbiturate coma was induced in 13 patients with disorders of consciousness from traumatic or spontaneous diseases. Early respiratory complications consisting with Adult Respiratory Distress Syndrome (ARDS) were found in 10 out of these 13 patients; on the contrary, only 2 out of 13 patients, treated with routine intensive care therapy without barbiturate, showed analogous respiratory complications. The literature on the subject and the possible pathophysiological mechanism of respiratory distress are discussed.