Alexios A. Adamides

CURRENT CONTROVERSIES IN THE MANAGEMENT OF PATIENTS WITH SEVERE TRAUMATIC BRAIN INJURY

Background:  Traumatic brain injury is a major cause of mortality and morbidity, particularly among young men. The efficacy and safety of most of the interventions used in the management of patients with traumatic brain injury remain unproven. Examples include the ‘cerebral perfusion pressure‐targeted’ and ‘volume‐targeted’ management strategies for optimizing cerebrovascular haemodynamics and specific interventions, such as hyperventilation, osmotherapy, cerebrospinal fluid drainage, barbiturates, decompressive craniectomy, therapeutic hypothermia, normobaric hyperoxia and hyperbaric oxygen therapy.

Endogenous melatonin increases in cerebrospinal fluid of patients after severe traumatic brain injury and correlates with oxidative stress and metabolic disarray

Oxidative stress plays a significant role in secondary damage after severe traumatic brain injury (TBI); and melatonin exhibits both direct and indirect antioxidant effects. Melatonin deficiency is deleterious in TBI animal models, and its administration confers neuroprotection, reducing cerebral oedema, and improving neurobehavioural outcome. This study aimed to measure the endogenous cerebrospinal fluid (CSF) and serum melatonin levels post-TBI in humans and to identify relationships with markers of oxidative stress via 8-isoprostaglandin-F2α (isoprostane), brain metabolism and neurologic outcome. Cerebrospinal fluid and serum samples of 39 TBI patients were assessed for melatonin, isoprostane, and various metabolites. Cerebrospinal fluid but not serum melatonin levels were markedly elevated (7.28±0.92 versus 1.47±0.35 pg/mL, P<0.0005). Isoprostane levels also increased in both CSF (127.62±16.85 versus 18.28±4.88 pg/mL, P<0.0005) and serum (562.46±50.78 versus 126.15±40.08 pg/mL (P<0.0005). A strong correlation between CSF melatonin and CSF isoprostane on day 1 after injury (r=0.563, P=0.002) suggests that melatonin production increases in conjunction with lipid peroxidation in TBI. Relationships between CSF melatonin and pyruvate (r=0.369, P=0.049) and glutamate (r=0.373, P=0.046) indicate that melatonin production increases with metabolic disarray. In conclusion, endogenous CSF melatonin levels increase after TBI, whereas serum levels do not. This elevation is likely to represent a response to oxidative stress and metabolic disarray, although further studies are required to elucidate these relationships.

The role of decompressive craniectomy in the management of traumatic brain injury: a critical review

Brain swelling and intracranial hypertension following severe head injury are known to contribute to secondary brain damage, and have been shown to adversely affect patient outcome. The use of unilateral craniectomy following the evacuation of a mass lesion, such as acute subdural haematoma or traumatic intracerebral haematoma, is accepted practice. The following review focuses on a bi-fronto-temporal decompressive craniectomy, used as an isolated operation for the control of intracranial hypertension, secondary to diffuse brain swelling refractory to medical management. Though the operation is being increasingly used, current opinion is still divided regarding its overall effects on outcome. This review examines the experimental and clinical evidence for and against the use of decompressive craniectomy, highlights the lack of class I evidence relevant to this topic and emphasises the necessity for well-designed prospective randomised controlled trials.

A review of the current management of severe traumatic brain injury

Traumatic brain injury accounts for up to half of trauma related fatalities. This review describes current management practices including pre-hospital care, surgical interventions and various treatment modalities for intracranial hypertension. The lack of class I evidence for the majority of interventions is highlighted.

Pneumocephalus from gas-forming Escherichia coli subdural empyema

We present the case of a 91-year-old man with a history of poorly controlled, non-insulin dependent diabetes mellitus who four months previously had burr-hole evacuation of a left-sided chronic subdural haematoma (Fig. 1). Post-operatively he was selfcaring and mobile with a frame. Two days prior to the most recent admission he presented to his local doctor with a one-week history of confusion and reduced mobility. Urine microscopy showed 442 leucocytes and 18 erythrocytes and he was commenced on trimethoprim. Urine cultures confirmed sensitive Escherichia coli. He further deteriorated and presented to emergency. On admission his Glasgow Coma Scale score was 12/15 (E4V2M6) and had right-sided hemiparesis (4/5). His pupils were equal and briskly reacting to light. He was afebrile with stable vital signs. His laboratory investigations were as follows: blood glucose 26 (3.3 – 8.0 mmol/L), white cell count 13.5 (4.6 – 10.5610/ L) with a neutrophilia of 10.9 (1.9 – 8.0610/L), and C-reactive protein 320 (0 – 5 mg/L). His CT brain scan showed a chronic left subdural collection with increased pneumocephalus (Fig. 2) compared to previous imaging. He underwent an emergent left fronto-parietal craniotomy and a purulent collection was evacuated. Samples sent for microbiological analysis showed polymorphs and gram negative rods on gram stain, which grew Escherichia coli on culture. Despite adequate drainage of the collection and appropriate antibiotic therapy (ceftriaxone, 2 grams, IV, BD, and metronidazole, 500 mg, IV, TDS) he deteriorated. He had a peri-operative myocardial infarction and multiple focal seizures. He died twelve days post-operatively. Pneumocephalus following evacuation of a subdural collection is common and usually resolves within days. Increasing pneumocephalus, long after surgery, is unusual and suspicious of ongoing pathology. In this case, we suggest that the significant increase in intracranial air was from contamination of the subdural collection by gas-forming Escherichia coli. Gas-forming bacteria include the following anaerobic species: Clostridia, Escherichia coli, Klebsiella, Peptostreptococcus, Bacteroides, Enterobacter and Pseudomonas. Gas-forming Escherichia coli have been previously reported to cause emphysematous pyelonephritis, intramyocardial and intramuscular air collections. It is believed that relatively insoluble gases such as nitrogen and hydrogen are produced from the anaerobic fermentation of glucose and these accumulate to cause pneumocephalus. In this patient, high blood glucose from poorly controlled FIG. 1. Non-contrast brain CT one week following initial burr-hole evacuation showing a residual subdural collection with a small amount of pneumocephalus.