Demographic profile and extent of healthcare resource utilisation of patients with severe traumatic brain injury: still a major public health problem.

INTRODUCTION: Trauma is the fifth principal cause of death in Singapore, with traumatic brain injury (TBI) being the leading specific subordinate cause. METHODS: This study was an eight-year retrospective review of the demographic profiles of patients with severe TBI who were admitted to the neurointensive care unit (NICU) of the National Neuroscience Institute at Tan Tock Seng Hospital, Singapore, between 2004 and 2011. RESULTS: A total of 780 TBI patients were admitted during the study period; 365 (46.8%) patients sustained severe TBI (i.e. Glasgow Coma Scale score ≤ 8), with the majority (75.3%) being male. The ages of patients with severe TBI ranged from 14-93 years, with a bimodal preponderance in young adults (i.e. 21-40 years) and elderly persons (i.e. > 60 years). Motor vehicle accidents (48.8%) and falls (42.5%) were the main mechanisms of injury. Invasive line monitoring was frequently employed; invasive arterial blood pressure monitoring and central venous pressure monitoring were used in 81.6% and 60.0% of the patients, respectively, while intracranial pressure (ICP) measurement was required in 47.4% of the patients. The use of tiered therapy to control ICP (e.g. sedation, osmotherapy, cerebrospinal fluid drainage, moderate hyperventilation and barbiturate-induced coma) converged with international practices. CONCLUSION: The high-risk groups for severe TBI were young adults and elderly persons involved in motor vehicle accidents and falls, respectively. In the NICU, the care of patients with severe TBI requires heavy utilisation of resources. The healthcare burden of these patients extends beyond the acute critical care phase.

Postoperative permanent pressure alopecia.

A 49-year-old Chinese female underwent elective laparoscopic assisted Whipple's surgery lasting 12 h. This was complicated by postoperative pressure alopecia at the occipital area of the scalp. Pressure-induced hair loss after general anaesthesia is uncommon and typically temporary, but may be disconcerting to the patient. We report this case of postoperative permanent pressure alopecia due to its rarity in the anaesthesia/local literature, and review the risk factors for its development.

Direct comparison of the effect of desflurane and sevoflurane on intraoperative motor-evoked potentials monitoring.

BACKGROUND: During spinal surgery, intraoperative monitoring of motor-evoked potentials (MEPs) is a useful means of assessing the intraoperative integrity of corticospinal pathways. However, MEPs are known to be particularly sensitive to the suppressive effects of inhalational halogenated anesthetic agents. OBJECTIVE: To investigate the effects of increasing end-tidal concentrations of desflurane and sevoflurane anesthesia in a background of propofol and remifentanil with multipulse cortical stimulation on intraoperative monitoring of MEPs. METHODS: In this randomized crossover trial, 14 consecutive patients (7 in each arm) undergoing major spine surgery, under a background anesthetic of propofol (75 to 125 mcg/kg/min) and remifentanil (0.1 to 0.2 mcg/kg/min), were randomly assigned to receive the sequence of inhalational agents studied: either DES-SEVO (desflurane followed by sevoflurane); or SEVO-DES (sevoflurane followed by desflurane). Multiples (0.3, 0.5, and 0.7) of minimum alveolar concentration (MAC) of desflurane and sevoflurane were administered. After a washout period of 15 minutes using high fresh oxygen/air flows, each of the patients then received the other gas as the second agent. Cortical stimulation was achieved with a train of 5 equivalent square pulses, each 0.05 ms in duration, delivered at 2 ms intervals. MEP recordings were made in the upper limb (UL) from first dorsal interosseus and lower limb (LL) from tibialis anterior with subdermal needle electrodes. RESULTS: At 0.3 MAC desflurane, there was no statistical significant difference in transcranial-evoked MEP amplitudes from the baseline in both UL and LL stimulation. However, this was not the case for sevoflurane for which even a low concentration at 0.3 MAC significantly depressed MEP amplitudes of LL (but not UL) from baseline value. Desflurane at 0.5 and 0.7 MAC depresses LL MEP to 58.4% and 59.9% of baseline, respectively (P<0.05), whereas sevoflurane at 0.3, 0.5, and 0.7 MAC depresses LL MEP to 66.2%, 41.3%, and 25.3% of baseline, respectively (P<0.05). There was no difference in latency of the responses at any MAC. CONCLUSIONS: Inhalational anesthetic agents (sevoflurane >desflurane) suppress MEP amplitudes in a dose-dependent manner. The use of 0.3 MAC of desflurane (but not sevoflurane) provided good MEP recordings acceptable for clinical interpretation for both upper and LLs. The LL appears to be more sensitive to anesthetic-induced depression compared with the UL. All patients studied had normal neurological examination hence, these results may not be applicable to those with preexisting deficits.

Cerebral ischaemia in pituitary disorders--more common than previously thought: two case reports and literature review.

Vasospasm and consequent cerebral ischaemia in aneurysmal subarachnoid haemorrhage are well-described. The development of cerebral ischaemia following pituitary tumour surgery is under-appreciated, and can be attributed to mainly cerebral vasospasm or internal carotid artery compression. We report on two patients with pituitary tumours who developed delayed cerebral ischaemia after transsphenoidal and transcranial pituitary macroadenoma decompression. The patients had vasospasm of intracranial vessels demonstrable on magnetic resonance angiogram. One recovered neurologically following nimodipine and hypertensive-hypervolaemia therapy while the other developed fulminant cerebral infarction. We discuss the complex multi-factorial mechanisms of cerebral ischaemia in pituitary disorders, as well as the management strategies and their limitations.

Management plan to reduce risks in perioperative care of patients with obstructive sleep apnoea averts the need for presurgical polysomnography.

INTRODUCTION: Obstructive sleep apnoea (OSA) is associated with increased perioperative morbidity and mortality. Patients at risk of OSA as determined by pre-anaesthesia screening based on the American Society of Anesthesiologists checklist were divided into 2 groups for comparison: (i) those who proceeded to elective surgery under a risk management protocol without undergoing formal polysomnography preoperatively and; (ii) those who underwent polysomnography and any subsequent OSA treatment as required before elective surgery. We hypothesised that it is clinically safe and acceptable for patients identified on screening as OSA at-risk to proceed for elective surgery without delay for polysomnography, with no increase in postoperative complications if managed on a perioperative risk reduction protocol. MATERIALS AND METHODS: A retrospective review of patients presenting to the preanaesthesia clinic over an 18-month period and identified to be OSA at-risk on screening checklist was conducted (n = 463). The incidence of postoperative complications for each category of OSA severity (mild-moderate and severe) in the 2 study groups was compared. RESULTS: There was no statistically significant difference in the incidence of cardiac (3.3% vs 2.3%), respiratory (14.3% vs 12.5%), and neurologic complications (0.6% vs 0%) between the screening-only and polysomnography-confirmed OSA groups respectively (P >0.05). There was good agreement of the OSA risk that is identified by screening checklist with OSA severity as determined on formal polysomnography (kappa coefficient = 0.953). CONCLUSION: Previously undiagnosed OSA is common in the presurgical population. In our study, there was no significant increase in postoperative complications in patients managed on the OSA risk management protocol. With this protocol, it is clinically safe to proceed with elective surgery without delay for formal polysomnography confirmation.

Anesthesia for cerebral revascularization for adult moyamoya syndrome associated with sickle cell disease.

We report the anesthetic management of an adult patient undergoing cerebral revascularization surgery for moyamoya syndrome complicating sickle-cell disease (SCD). We present a 25 year-old male of African ethnicity with homozygous SCD who was experiencing worsening ischemic neurologic symptoms culminating in intraventricular hemorrhage from rupture of moyamoya vessels. Despite an extracranial-intracranial superficial temporal artery-middle cerebral artery bypass that was angiographically patent postoperatively, he subsequently required an intracranial omental transplant to improve cerebral blood flow to the anterior cerebral artery territory. Prior to both cerebral revascularization procedures, the patient had continued with his regularly scheduled red blood cell exchange transfusion. The importance of normothermia, normocarbia, normotension, and normovolemia is emphasized in the neuroanesthetic management. We conclude that the safe and efficacious operative treatment of moyamoya disease, using both direct and indirect revascularization procedures, is being increasingly described, and therefore anesthesiologists are likely to encounter similar cases in the future and need to be aware of the surgical procedures and perioperative implications. The overall principles of safe anesthesia (normotension, normocarbia, good oxygenation, normothermia, normovolemia) for patients with SCD also applies to patients with moyamoya. During a craniotomy, certain deviations from these are needed (hyperventilation and mannitol diuresis for brain volume reduction, induced hypothermia or manipulations of arterial blood pressures) but they can be safely used with careful monitoring of the patient.

Case series: monocular visual loss associated with subarachnoid hemorrhage secondary to ruptured intracranial aneurysms.

PURPOSE: To describe variations in the presentation of monocular visual loss associated with intracranial aneurysm rupture. The clinical course, possible etiologies and management of visual loss in three patients are described. CLINICAL FEATURES: The first patient developed Terson's syndrome (vitreal hemorrhage associated with raised intracranial pressure secondary to subarachnoid hemorrhage). Following aneursymal clipping, her postoperative management was conservative and there was no improvement in visual acuity. The second patient underwent surgical clipping of internal carotid aneursysms and sustained visual loss subsequent to surgical dissection and temporary clipping around the optic nerve and anterior choroidal artery. The vessel subsequently thrombosed. Potential contributing factors to visual loss in this case included intraoperative hypotension and anemia. This patient received anti-platelet medications, and experienced subsequent improvement in visual acuity to 6/9. A third patient underwent a right orbito-frontal keyhole craniotomy with the cranial flap retracted across the orbit. Elevated intraocular pressure secondary to external orbital compression may have compromised retinal and choroidal perfusion. This patient also developed vasospasm of both anterior cerebral arteries which resolved partially with papaverine therapy. Hypertension-hypervolemia therapy was instituted, with subsequent partial recovery of visual acuity in her right eye. CONCLUSION: Perioperative monocular visual loss associated with intracranial aneurysm repair is an infrequent occurrence, and clinical presentations may be quite variable. The primary pathophysiological mechanisms are intraocular hemorrhage and ischemia of ocular structures, including the optic nerve. Early detection, via regular fundoscopic examination and treatment aimed at decreasing intraocular pressure and augmenting ocular perfusion may improve outcomes.