Monitoring of peripheral nerves and muscle function in patients with multiple organ dysfunction syndrome.
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Biomedical subjects
Publications and source records attributed to N Latronico.
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OBJECTIVE: To evaluate, in a prospective, observational study, whether bilateral monitoring of jugular bulb oxyhemoglobin saturation (SjO2), in addition to standard monitoring, results in modification of the management of severe head trauma. METHODS: The patients underwent bilateral jugular bulb cannulation and observation at 8-hour intervals, during which SjO2 was measured and the neurological condition and physiological variables were assessed. The study group was responsible for evaluating whether the physician's decision-making process was influenced by the detection of SjO2 abnormalities. The SjO2 discrepancy in simultaneous bilateral samples was also evaluated to determine whether it interfered with the interpretation of data and with clinical decision-making. The SjO2-related complications were monitored. RESULTS: Thirty patients underwent 319 observations. In 96% of patients, SjO2 was normal or high and had no influence on the diagnostic or therapeutic strategies. Treatment decisions were dictated by changes in clinical status and in intracranial and cerebral perfusion pressure. When these parameters were abnormal, treatment was administered, even if SjO2 was normal (101 observations). Conversely, when SjO2 was the only detected abnormality (34 observations), no treatment was administered. Abnormally low SjO2 values, caused by hypovolemia and hypocapnia, were detected in 3.4% of observations and actually modified the management. The discrepancies in simultaneous bilateral samples were substantial and gave rise to relevant interpretation problems. Fifteen percent of jugular catheters showed evidence of bacterial colonization. CONCLUSION: Intermittent SjO2 monitoring did not substantially influence the management of severe head trauma. Therefore, recommendation for its routine use in all patients seems inadvisable, and indications for this invasive method should no longer be defined on the basis of experts' opinions, but rather on randomized, prospective studies.
Coma is the condition in which both components of consciousness, wakefulness and awareness, are lost. Therefore, the comatose patient neither opens the eyes, nor utters comprehensible words or follows commands. In the vegetative state (VS), awareness (including all cognitive function and emotion) is lost, while the vegetative functions, including breathing and sleep-wake cycles (the wakefulness), persist. Usually VS follows a state of coma caused by traumatic or anoxic brain damage. Pathologic brain examination demonstrates extensive subcortical, white matter, bilateral thalamic, and brainstem lesions in various combinations. Bilateral cerebral cortical lesions are rare, and therefore cortex can be "out of action" despite unaltered structure. More rarely, VS is caused by brain developmental malformations in children, or metabolic or degenerative diseases in children and adults. These are the only cases in which patients are not comatose before VS becomes apparent. After 6-8 weeks of coma, patients regain the eye opening. In such a condition, the term coma is no longer appropriate. If awareness is absent, the patient can be defined as in VS. Finally, the VS is defined as persistent (PVS) when it has continued for at least 1 month. The diagnosis of VS and PVS are clinical and require assessment over an adequate period of time and the skills of a multidisciplinary experienced team. Diagnosis is very complex in infants younger than 3 months, and is not applicable to preterm neonates, with the unique exception of infants with anencephaly. Among ancillary diagnostic tools, dynamic PET studies show promise.
A prerequisite to the diagnosis of vegetative state is the exclusion of apparently similar syndromes, in which the patient retains the consciousness partially or even completely. Some syndromes are not separate nosological entities and should be abandoned: the apallic state, the neocortical death, the decerebrate and decorticate state, the alpha-coma, the vigil or prolonged or irreversible coma are among them. Three conditions deserve special consideration. The term locked-in syndrome describes a patient completely paralysed and mute, but fully conscious, and is usually caused by ischemic lesions of the pons. Several variants do exist, either in the causes and site of lesion. Some patients may become paralysed and mute, but conscious because of polyneuropathies, that is in the absence of any lesions of the central nervous system. The akinetic mutism is a rare condition characterised by loss of speech and nearly absent bodily movements. Painful stimulation may cause appropriate withdrawing, and wakefulness and self-awareness may be preserved, but cognitive impairment is usually present. It must be emphasised that this condition can be due to potentially treatable lesions, such as hydrocephalus and craniopharyngioma. The term "minimally responsive" or "minimally conscious" describes severely disabled patients in whom meaningful responses can be demonstrated, although inconstantly. This condition, the true diagnostic challenge, often represents a transition phase of vegetative patients recovering consciousness. Physicians, physiotherapists and patient's relatives should work all together to reach a correct diagnosis, by using current available methods to monitorize the recovery of consciousness.
To define a vegetative state (VS) as permanent is to declare its irreversibility. In 1994 a North-American multidisciplinary task force, by extensively analysing the literature, concluded that the recovery of consciousness from a post-traumatic or non-traumatic VS is unlikely after 12 and 3 months respectively. These conclusions did not obtain unanimous consent. The term permanent was in fact inappropriately used to define either the loss of consciousness or of function. Furthermore, patients with traumatic brain injury have been shown to recover the consciousness in a substantial greater percentage (6-7%) than previously appreciated (1.6%). This is hardly compatible with the peremptoriness of the term permanent, which should be used only in case of certainty. Ancillary tests are important in defining the prognosis. Patients in deep coma after an anoxic brain injury can be predicted as having a poor prognosis (death or permanent VS) with 100% specificity within one week of the insult. Magnetic resonance of the brain can predict patients at high risk of permanent VS within 6-8 weeks of a traumatic brain injury. In conclusion, the available evidence does not permit to define with certainty the patients who have irremediably lost their consciousness after a devasting brain insult. However, it seems possible to reliably define the risk of severe disability. Whether or not this knowledge might or should be used to titrate the intensity of therapeutic approach is to be defined. In this respect, it is central the definition of what an "acceptable outcome" is, certainly not an exclusive medical attribution.
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OBJECTIVE: To describe a syndrome of acute neuromuscular respiratory failure (NM-ARF) caused by ICU-acquired acute myopathy and neuropathy. DESIGN: Case series. SETTING: General Regional University Hospital in Brescia, Italy. PATIENTS: Five adult patients with NM-ARF after prolonged ICU stay and successful weaning from the ventilator and ICU discharge. INTERVENTIONS: None. MEASUREMENTS: Clinical signs of NM-ARF, electroneurography and electromyography (ENMG) of peripheral nerves and muscles, and functional assessment of respiratory muscles. RESULTS: NM-ARF was diagnosed at the time of (one case), or 1-3 days after, ICU discharge. Limb weakness alarmed the physicians, while the signs of the NM-ARF were initially undetected. In the first observed case the acute respiratory failure was near fatal, and necessitated ICU readmission, while in the other cases 2 weeks of aggressive chest physiotherapy permitted resolution of the respiratory failure. History, clinical course and ENMG indicated the diagnosis of critical illness myopathy and neuropathy (CRIMYNE). Three patients recovered fully, while two had persisting evidence of axonal polyneuropathy several months after the onset. CONCLUSIONS: Critically ill patients with prolonged ICU stay, sepsis and MOF are at great risk of developing CRIMYNE, which in turn may be responsible for NM-ARF. This latter complication may arise after resolution of the respiratory and cardiac dysfunctions and successful weaning from the ventilator. As NM-ARF may cause unplanned ICU readmission or even unexpected death, strict clinical surveillance and monitoring of respiratory muscle function is recommended after discharge to the general ward of patients with proven NM-ARF. Early intensive chest physiotherapy can resolve the condition.
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OBJECTIVE AND IMPORTANCE: Cerebral venous and dural sinus thrombosis is a rare cause of stroke. Although morbidity and mortality have greatly decreased in recent years as a result of early diagnosis and timely medical treatment, when coma occurs the prognosis remains poor. We evaluated whether emergent decompressive craniectomy has a role in the treatment of patients with brain herniation from dural sinus thrombosis and hemorrhagic infarct. CLINICAL PRESENTATION: Three patients developed large hemorrhagic infarct with coma and bilaterally fixed and dilated pupils resulting from aseptic dural sinus thrombosis. INTERVENTION: Two patients underwent emergent surgical decompression as soon as brain herniation developed, and these patients had complete functional recovery. One underwent delayed surgical decompression and remained severely disabled. CONCLUSION: Our results provide preliminary evidence that emergent decompressive craniectomy is effective in patients with brain herniation from dural sinus thrombosis, provided that the clinical onset is recent. We therefore recommend consideration of this aggressive surgical technique for such patients, who may survive with good outcomes.
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The authors describe a patient with severe head injury and sepsis who became acutely quadriplegic 3 days postinjury because of a critical illness polyneuropathy (CIP) and critical illness myopathy (CIM), which resolved rapidly after treatment of the underlying infection. In only 3 days the patient developed septic shock together with flaccid quadriplegia and absent deep tendon reflexes with no clinical or radiological evidence of central nervous system deterioration. Neurophysiological studies showed an acute axonal sensorimotor polyneuropathy, whereas the clinical course strongly suggested a concurrent myopathy. A severe Staphylococcus epidermidis infection accompanied by bacteremia was treated and the patient recovered fully within a few days. Although the case described here is unique because of its very early onset and rapid resolution, CIP and CIM are frequent complications of sepsis and multiple organ failure. The authors suggest that severely head injured patients with sepsis should be evaluated for CIP and CIM when presenting with unexplained muscle weakness or paralysis.