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Time-level relationship between indicators of oxidative stress and Glasgow Coma Scale scores of severe head injury patients.

BACKGROUND: Oxidative stress is said to strongly influence the neurological recovery of patients following a severe head injury. Estimation of the markers of oxidative stress in the blood of such patients can hence aid in predicting the prognosis of head injury. METHODS: Erythrocyte thiobarbituric acid-reactive substances (TBARS) and plasma ceruloplasmin (CP) levels were estimated in 24 severe head-injury patients on days 1, 7 and 21 of the post-traumatic period and compared with levels in 25 healthy age- and sex-matched controls. These parameters reflecting oxidative stress status were related to the Glasgow Coma Scale (GCS) scores of patients noted at the same time points of the study period. RESULTS: Lipid peroxidation as indicated by increased levels of erythrocyte TBARS remained significantly elevated in severe head injury patients compared to controls on day 1 (p<0.001), day 7 (p<0.001) and 21 (p<0.001) of the post-traumatic period. Plasma CP levels remained significantly elevated (p<0.001) at these three time points compared to controls. The significant decrease in lipid peroxidation products (p<0.01) and significant increase in CP levels (p<0.001) on day 21 compared to day 1 in head injury patients correlated well with the significant improvement in GCS scores of patients on day 21 compared to day 1 (p<0.05). CONCLUSION: The above results could account for the adaptation of the study patients to severe oxidative stress, as evidenced by their clinical recovery trend during the study period.

Adult↗

Prevention of methionine and ammonia-induced coma by intravenous infusion of a branched chain amino acid solution to rats with liver injury.

The prevention of hepatic encephalopathy by the intravenous infusion of a branched chain amino acid (BCAA)-enriched solution was investigated in methionine and ammonium acetate-treated rats whose liver was already injured with carbon tetrachloride. A BCAA-enriched solution protected the rats from entering a coma. The brain BCAA contents became higher, and the brain methionine and tyrosine levels and the ratio of glutamine to glutamic acid in the brain diminished after administering the BCAA-enriched solution.

Acetates↗

[Hyponatremic coma as a manifestation of Addisońs disease]

OBJECTIVE: To show the importance of severe hydroelectrolytic disorder as a consequence of previously undiagnosed chronic disease. DESCRIPTION: Case report of hyponatremic coma caused by adrenal crisis in a child with previously undiagnosed Addisońs disease despite suggestive clinical findings of this disease in the last four years. After correction of severe hyponatremia, mild hypovolemia, hypernatriuria and hyperkalemia, the differential diagnosis of this hydroelectrolytic disorder revealed an adrenal crisis resulting from a primary chronic adrenal insufficiency. Oral treatment with hydrocortisone was efficient in correcting the metabolic disorder and the patient was then discharged. COMMENTS: It is very important to highly suspect of Addisońs disease in order to avoid the dangerous consequences of late diagnosis such as severe hydroelectrolytic disorders and retarded growth and development.

Journal Article↗

Presumed apoptosis and reduced arcuate nucleus neuropeptide Y and pro-opiomelanocortin mRNA in non-coma hypoglycemia.

Hypoglycemia reduces sympathoadrenal responses to subsequent hypoglycemic bouts by an unknown mechanism. To assess whether such hypoglycemia-associated autonomic failure is due to actual brain damage, male Sprague-Dawley rats underwent 1-h bouts of insulin-induced (5 U/kg i.v.) hypoglycemia (1.6-2.8 mmol/l) 1 or 3 times on alternate days. Rats remained alert and were rescued with intravenous glucose at 60-80 min. Plasma epinephrine and corticosterone responses were significantly reduced during the second and third bouts. Brains from these rats were processed by the terminal transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) procedure as an index of apoptotic cell death at 24, 48, or 96 h after their first bout. At 48 h, but not 24 h, TUNEL+ cells were consistently seen only in the arcuate nucleus (arcuate hypothalamic nucleus [ARC]). Hypoglycemic rats had 188% more apoptotic ARC cells (1 bout 39+/-5; 3 bouts 37+/-4) than euglycemic controls (13+/-3;P = 0.001). In situ hybridization for neuropeptide Y (NPY) and proopiomelanocortin (POMC) mRNA was performed in sections of ARC containing maximal numbers of apoptotic cells as well as in other fresh frozen brains. After 1 bout, NPY (0.041+/-0.003) and POMC (0.119+/-0.022) mRNA were decreased, respectively, by 52 and 55% vs. controls (NPY 0.076+/-0.007; POMC 0.222+/-0.020; P = 0.01). NPY (0.029+/-0.002) but not POMC (0.093+/-0.013) fell 29% further after a third bout. NPY (r = -0.721; P = 0.001) and POMC (r = -0.756; P = 0.001) mRNA levels correlated negatively with the number of apoptotic ARC cells in the same sections. Thus, non-coma hypoglycemia produces apparent apoptotic cell death with reduced NPY and POMC expression selectively in the ARC. This may contribute to the reduced counterregulatory response following repeated bouts of hypoglycemia.

Animals↗

Successful treatment of hepatic coma probably caused by acute infectious hepatitis with balanced solution of amino acids.

Therapy with balanced amino acid solution enriched in branched amino acids has been reported to favourably influence hepatic encephalopathy due to liver cirrhosis. We here report the same favourable effect in 3 patients aged 29, 30 and 41 yr with hepatic coma at least in part induced by acute viral hepatitis. The patients regained consciousness within 8, 12 and 12 h, respectively. The treatment was continued for 9, 6 and 5 days, respectively.

Adult↗

Failure of prophylactic barbiturate coma in the treatment of severe head injury.

In certain subgroups of severely head-injured patients, the mortality rate remains unacceptably high. The authors describe a randomized, controlled trial of prophylactic pentobarbital therapy in a group of these patients. Pentobarbital was started as soon as possible after the head injury, regardless of the intracranial pressure (ICP), and was continued for a prescribed period of time. The study included 53 consecutive head-injured patients over the age of 12 years, who had either an acute intradural hematoma (subdural and/or intracerebral, large enough to warrant surgical decompression), or no mass lesion but whose best motor response was abnormal flexion or extension. All patients in the study were randomly assigned to a control group (26 cases) or a pentobarbital-treated group (27 cases) once the diagnosis had been made and informed consent obtained. All patients were treated with the same protocol of aggressive resuscitation, prompt diagnosis and treatment of mass lesions, and intensive care, with close follow-up monitoring. The randomization was effective in producing a close match between the control and treated groups with respect to age, sex distribution, cause of injury, neurological status, intracranial lesions, prevalence of early systemic insults, midline shift, and initial ICP. Outcome was essentially the same in each group. There was no difference between groups in the incidence of elevated ICP, the duration of ICP elevation, or the response of ICP elevations to treatment. Arterial hypotension occurred in 14 patients (54%) in the treated group and only two patients (7%) in the untreated group. Based on these data the authors cannot recommend the prophylactic use of pentobarbital coma in the treatment of patients with severe head injury. They also believe that its use is accompanied by significant side effects which can potentially worsen the condition of a patient with severe head injury.

Adolescent↗

[Polyarticular heterotopic ossification complicating drug induced coma].

The Authors describe a case of generalised heterotopic ossification (HO) complicating the course of a 31 years old male patient, with a history of Hodgkin's lymphoma and a of long staying in an intensive care unit, where he had been placed on artificial coma. The clinical features, as well as radiological findings and therapy, are discussed.

Adult↗

[New research and considerations in managing minimally conscious coma patients].

The "Wachkoma", minimally conscious state (synonyms in use: "apallic syndrome", "vegetative state"), is a severe, complex condition arising from brain damage of diverse etiologies, for which definitional consensus does not exist internationally; it gives rise to frequent misdiagnosis and carries substantial insecurities concerning treatment outcomes. In the framework of expanding early rehabilitation, however, recent years have seen a distinct shift away from a defect-oriented, reductionist view towards a relational-medicine based understanding of patients with severe brain damage, seeking to gain a comprehensive perception of the patient's altered physical existence and taking a multidisciplinary--nursing, medical, therapeutic and neuropsychological--perspective which includes the patient's relatives and family. Historically, a transition is under way away from the classical brain-pathology focus toward a neuropsychologically grounded, differentiated perspective. Along with in-depth differential diagnostics and assessment of rehab potentials (early intervention diagnostics), comprehensive intervention measures are initiated as early as possible by an interdisciplinary team. These include "coma stimulation" measures, body language forms of interaction ("dialogue management"), and technical communication devices. By building long-term care assistance in ambulatory and residential service delivery systems ("small social network"), social reintegration of these very severely affected patients is attempted, involving the familial and social resources available. Recurrently raised within the bioethical discourse, demands to consider doctor-assisted dying or food withdrawal are to be rejected from a clinical, medical and social-ethical perspective.

Brain Damage, Chronic↗

Drug-related Coma in the Adolescent.

The poisoned and comatose adolescent presents numerous diagnostic and management problems. Often interventions must be performed before a specific diagnosis is made. A history may be impossible to obtain, thus forcing the physician to rely on physical findings, rapid diagnostic testing, and expectant supportive care. The first stage of treatment is stabilization, which involves basic and advanced life support, rapid assessment, presumptive substrate and antidotal therapy, and gastrointestinal decontamination. The second stage, definitive care, requires a careful history, detailed physical examination, and diagnostic studies tailored to narrow the possible etiologies. The authors describe each stage in detail, including evaluation and treatment, as well as discuss common toxic causes of coma in adolescents.

Journal Article↗

[Plasmapheresis in the treatment of hepatic coma].

Fourteen patients, including 6 with viral hepatitis B and 8 with liver cirrhosis were treated with plasmapheresis for hepatic coma. Altogether 29 plasmaphereses were carried out. Complete recovery was achieved in one patient with viral hepatitis B and in 3 patients with liver cirrhosis. Plasmapheresis should be performed in patients with severe lesions to the liver. Classification of patients to the treatment should include clinical examination, biochemical and enzymatic tests, and evaluation of liver reserve with isotope hepatography. In case of the acute poisoning with hepatotoxic agents indications to plasmapheresis should be evaluated from the toxicologic point of view.

Adolescent↗

Convulsions and Coma Associated with Iatrogenically Elevated CSF Calcium Levels Post Spinal Surgery: A Case Report.

Following elective revision of lumbar decompression and non-instrumented fusion, a 69 year old woman developed confusion, convulsions and coma associated with greatly elevated cerebrospinal fluid (CSF) calcium levels. It is presumed that the elevated calcium was secondary to the use of OsteoSet, a calcium sulfate pellet preparation used to augment autologous bone graft growth.

Journal Article↗

[Prolonged coma due to fat embolism syndrome after fracture of the femur].

A 24-year-old male came to the emergency department with a diaphyseal fracture of the femur resulting from a motorcycle accident. Neurological deterioration was progressive, although a computed tomography scan was normal. Endotracheal intubation for mechanical ventilation was necessary. His condition progressed to sepsis and multiorgan failure before resolving. Magnetic resonance images of the brain suggested a fat embolism. The presence of a patent foramen ovale was investigated. The patient remained in a state of coma vigil for 3 months after the accident. After ruling out other more likely causes of neurological deterioration after trauma with fractures, fat embolism should be suspected. The prognosis for the neurological manifestations of fat embolism syndrome are generally good. Severe cases suggest massive (paradoxical) embolization of the brain and are associated with a patent foramen ovale. Early diagnosis will identify the patient at high surgical risk. A favorable course and outcome have been reported with preoperative closure of the foramen ovale.

Accidents, Traffic↗

Early and aggressive treatment of medically intractable cerebral vasospasm with pentobarbital coma, cerebral angioplasty and ICP reduction.

The authors present the unique experience of one neurovascular service under the direct supervision of the senior author, for which surgical, endovascular, and intensive care treatments were conducted in a select group of 32 patients with aneurysmal subarachnoid hemorrhage who had medically intractable symptomatic vasospasm. A protocol of early and aggressive treatment was instituted using pentobarbital coma, cerebral angioplasty, and intracranial pressure (ICP) reduction. The patient population consisted of 25 women and seven men, whose ages ranged from 34 to 60 years (average 47 years). The patients' Hunt and Hess grades on presentation were as follows: Grade 0 (one); Grade I (three); Grade II (two); Grade III (nine); Grade IV (10); Grade V (seven). Microsurgical clipping alone was performed in 15 of 32 patients, endosaccular occlusion was performed in 17 of 20 patients, and two patients underwent combined treatment. Subsequent angioplasty was performed in 26 of 32 patients. Additionally, all 32 patients underwent treatment of increased ICP with ventriculostomy placement, removal of the bone flap (11), evacuation of associated intracranial hematoma (five), and decompressive obectomy (four). Twenty-one patients survived and 11 died. Of the 21 survivors, seven have returned to work, live independently, and have no neurological deficits; eight require minimal assistance at home; four are in rehabilitation with moderate deficits at 3 months; and two remain in a persistent vegetative state. In this group of aggressively treated patients who received pentobarbital cerebral protection, successful treatment of medically intractable cerebral vasospasm was related to time of treatment (< 2 hours), expeditious reduction of elevated ICP, and angioplasty.

Journal Article↗

Neurologic improvement of patients with hepatic failure and coma during sorbent suspension dialysis.

Fifteen patients with acute deterioration of liver function, high serum ammonia, and an average coma level of 3.9 (of 4) were treated for 8-12 hrs daily with a system that uses the membranes of a cellulosic plate dialyzer to pump blood through a single access at 200-225 ml/min, and includes a sorbent suspension as dialysate. Neurologic status of the patients was declining before treatment, but significantly improved during each treatment and over the course of 1-12 (average, 4) treatments. Diastolic blood pressure and pulse rate normalized. For half the patients, treatment with the BioLogic-DT system served as a bridge to liver transplant or liver recovery.

Adult↗

[Barbiturate coma in the treatment of refractory status epilepticus in adults. Usefulness of continuous electroencephalography in intensive care].

Status epilepticus represents one of the most frequent neurological reasons for admission to the intensive care ward. If it resists well-managed treatment, more aggressive measures must be taken. We report 3 such situations in which patients were treated by barbiturate coma under continuous electroencephalographic monitoring. On the basis of this experience we attempt to elaborate guidelines for the use of this technique.

Adult↗

Revised EEG coma scale in diffuse acute head injuries in adults.

The validity of a recently published EEG grading scale applied to patients with acute head injuries has been investigated. This scale is based on 15 individual grades and subdivisions and 3 major groups: 4 patterns are benign regarding survival, 4 are of uncertain significance and 7 patterns are prognostically malignant. The evaluation was performed in 90 adult patients with acute head injuries in whom EEGs obtained during the 36 hours after the injury were evaluated retrospectively without knowing the clinical details or the outcome. By employing previously reported definitions it was possible to allocate EEG abnormalities in all cases. The assumption was made that at the time of the EEG investigation the impact of the head injury on cerebral function was already established. All patients displaying 'benign' patterns survived. 'Uncertain' patterns were the most common ones and in patients with these the reactivity of EEG activity was more important for prognosis than the quality of the background activity. All but 3 of the patients with a 'malignant' pattern died, and the survivors remained in a vegetative state. There was a correlation between the EEG findings and the Glasgow Coma Scale score on admission and also with the results of computerized tomography of the brain. In those patients who died there was no significant relationship between EEG signs and autopsy findings. Repeated EEGs are always desirable with severe head injuries but the results of this study suggest that useful prognostic information can be obtained from an EEG recorded within 36 hours after the head trauma.

Adolescent↗

Hypoglycemic coma in anorexia nervosa. Case report and review of the literature.

Clinically significant hypoglycemia is an unusual complication of anorexia nervosa. We describe a 44-year-old woman with a 5-year history of anorexia nervosa who presented with hypoglycemic coma and eventually experienced sudden death. Biochemical studies showed suppressed levels of insulin, C peptide, and proinsulin during hypoglycemia; appropriate elevations of growth hormone and cortisol levels were observed, suggesting that the hypoglycemia was related to severe malnutrition. Nine previously reported cases of severe hypoglycemia in anorexia nervosa are reviewed (six of the patients involved also died). The presence of severe hypoglycemia in anorexia nervosa implies a grave prognosis and mandates aggressive medical and nutritional therapy to improve the chance of survival.

Adult↗

[Amino acid reserves of the blood in patients with schizophrenia and their correction in insulin coma].

Free amino acid content was measured in the blood serum in patients with permanently progressive paranoid schizophrenia under conventional insulin shock therapy. The influence of several amino acids (methionine, glutamic acid) preinjection on their base levels was also assessed. Metabolic response to the insulin coma was different in preinjected vs. control groups. Glutamine acid-preinjected patients displayed less pronounced shifts in amino acid reserves in the blood serum that smoothed the shock-related metabolic stress in these patients as related to conventional shock.

Amino Acids↗