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Kevin Holly
Kevin Holly

Comatose REPACK

In 2015, Jon Taylor of the Anthesis Group in partnership with Jonathan Koomey Research Fellow at Stanford University, published a report revealing that 30% of enterprise servers in the five facility, 4000 server sample were comatose, performing no useful computing over a 6 month period in 2014.


Finding and eliminating comatose servers would also save many enterprises money, but more importantly, taking that action would eliminate an unappreciated security risk. Zombie servers are unlikely to have the latest security patches, which makes them an open door to many enterprise data centres. If the monetary incentives are not enough to ensure prompt action, concern over cybersecurity should.

In previous work, we showed that about thirty percent of the enterprise servers were comatose in a 4000 server sample across five data centre environments, performing no useful computing over a six month period in 2014. This finding mirrored earlier work by the Uptime Institute and McKinsey and Company, which showed very low server utilisation and significant percentages of zombie servers in enterprise data centres.

In comatose cardiac arrest survivors, clinical, biomarker, electrophysiology, and imaging studies identified patients destined to a good neurological outcome with high specificity within the first week after cardiac arrest (CA).

About 80% of patients who are successfully resuscitated from cardiac arrest are comatose on arrival at hospital [1] because of post-cardiac arrest brain injury (PCABI) [2], and their prognosis is uncertain. An accurate prediction of poor neurological outcome in these patients is important to avoid pursuing futile treatments in patients with irreversible PCABI.

Based on the PICOST template, the review question was formulated as follows: in adult patients who are comatose following resuscitation from cardiac arrest in all settings (P), does the use of predictors based on clinical examination, electrophysiology, serum biomarkers or neuroimaging (I) recorded within 1 week after cardiac arrest (T), allow accurate prediction of good outcome (O)? We selected prognostic accuracy studies (S), i.e., those in which sensitivity and specificity of the index test was reported. The accuracy of the index test was assessed by comparing the predicted outcome with the final outcome, which represented the comparator (C).

Predicting good neurological outcome has a potential to reduce uncertainty in the prognostication process, which is currently almost entirely focused on poor outcome prediction. In one study [88] on 486 comatose resuscitated patients, 330 (68%) had an indeterminate outcome after the application of the 2015 ERC-ESICM prognostication algorithm at 72 h. Of these, 250 (74%) had a favourable EEG (continuous or nearly continuous, normal voltage background without seizures or abundant discharges), which was associated with neurological recovery in 184 (74%) patients. Future prospective studies are needed to assess the potential of good outcome prediction to reduce uncertainty in patients assessed using the 2021 prognostication algorithm. Although the 2021 guidelines for post-resuscitation care [5] do not recommend any specific strategy for predicting good outcome, they mention low NSE or NFL blood values and normal MRI as signs suggesting a potential good outcome and recommend caution when these signs coexist with others predicting poor outcome. This cautionary recommendation, based on expert opinion, is confirmed by the present review. However, direct evidence on the prognosis of patients showing discordant signals from neurological predictors is lacking. Investigation in this field is warranted to validate current recommendations.

Ophthalmologists and neurologists are often required to evaluate patients in varying degrees of consciousness. This article focuses on the ocular findings present in comatose patients that can be used to localize deficits, diagnose pathology, and prognosticate for possible recovery.

Coma is a state of prolonged unconsciousness during which a person is alive but unresponsive to all external stimuli, noxious or otherwise.[1] Coma is typically caused by significant injury to the brain. The many etiologies of a comatose state include trauma, stroke, brain tumors, severe hyper- or hypoglycemia, prolonged cerebral hypoxia, seizure, and toxins.[2] While individuals in such a state have lost their ability to think and their awareness of their surroundings, they retain non-cognitive functions and a normal sleep pattern.[3] Many people gradually recover after coma but others may enter a persistent vegetative state or die. The outcome largely depends on the cause, severity, and site of the neurological damage. Those who survive may emerge with lasting physical, intellectual, and physiological deficits that require special care.

Despite its clinical localizing value, the neuro-ophthalmic exam on comatose patients has certain limitations. Firstly, many patients are given sedatives prior to the time of evaluation, often to facilitate intubation. Sedation can dampen neurological responses and thus lead to exam findings that are misattributed to brain damage. An important exception is the evaluation of pupil size which remains a highly sensitive test despite sedation.[5] Furthermore, early on in emergency situations, healthcare workers may not have a complete medical history of the comatose patient. This can cause abnormalities in the ocular exam to be attributed to acute brain damage when in fact they are due to preexisting neurologic or metabolic disorders or pharmacologic agents such as opioids. This can lead to a misdiagnosis and subsequent inappropriate management of the patient.[5] Additionally, interobserver variability in the ocular evaluation of comatose patients has been observed in multiple studies.[5][6][7] Finally, some of the individual components of the exam have their own limitations. Testing for the oculocephalic reflex requires a stable spine while caloric testing requires an intact eardrum.

Before proceeding with this test, ensure the patient has an intact tympanic membrane. A small amount of fluid (water or air), either 7oC over (warm) or 7oC under (cold) the bodily temperature, is flushed into one of the ear canals. A positive finding will show conjugate horizontal nystagmus; however, the direction of the nystagmus is dependent on the relative temperature of the fluid. Warm fluid will cause the fast phase of nystagmus to be towards the irrigated ear, while cold fluid will cause the fast phase to be away from the irrigated ear.[19] One study showed that a positive finding in a comatose patient is a strong predictor (PPV=0.93) for emergence from a vegetative state.[20] Another study showed that the absence of a vestibulo-ocular reflex predicted 100% of cerebral death.[21] Similar to the oculocephalic reflex, a negative finding indicates a deep metabolic coma, vestibular damage, or brainstem dysfunction from the level of the midbrain to the pons.

Modern high-end power distribution units (PDUs) support the measurement of current and voltage at the infeed and outlet level and sit on the network. These PDUs can serve as a data collection point that provides another aspect of the necessary information for determining whether or not a server is truly comatose. By gathering server power consumption data from the PDU into a database or DCIM tool, simple analytics can show whether or not a server is in a low power or constant current consumption state over time. By integrating this information back into the orchestration layer and running some reports, the data center operator can then easily determine if the server is truly comatose or if it is just underutilized due to lack of workload. This would indicate whether or not turning off the server could be done without undue business interruption.

Providing an accurate assessment of a comatose patient is important as several conditions share similar features with coma but vary in their physiological findings, prognosis, and standards of care. This NeuroBytes video aims to introduce the main features of coma and the key elements in the evaluation of a comatose patient to help guide your clinical skills development.

The BOX (Blood Pressure and OXygenation Targets After OHCA) trial investigators randomly assigned comatose adults with out-of-hospital cardiac arrest in a 1:1 ratio to either a restrictive oxygen target of a partial pressure of arterial oxygen (Pao2) of 9-10 kPa (68-75 mm Hg) or a liberal oxygen target of a Pao2 of 13-14 kPa (98-105 mm Hg) in this randomized trial with a 2-by-2 factorial design. The primary outcome was a composite of death from any cause or hospital discharge with severe disability or coma (Cerebral Performance Category [CPC] of 3 or 4; categories range from 1-5, with higher values indicating more severe disability), whichever occurred first within 90 days after randomization. Secondary outcomes were neuron-specific enolase levels at 48 hours, death from any cause, the score on the Montreal Cognitive Assessment (ranging from 0-30, with higher scores indicating better cognitive ability), the score on the modified Rankin scale (ranging from 0-6, with higher scores indicating greater disability), and the CPC at 90 days. The authors performed Cox proportional-hazards analysis with adjustment for trial site to calculate the hazard ratio and 95% confidence interval (CI) for the primary composite outcome in the oxygenation intervention.

The authors concluded that a restrictive or liberal oxygenation strategy in comatose patients after resuscitation for cardiac arrest resulted in a similar incidence of death or severe disability or coma.

This randomized trial compared a restrictive oxygenation target of 68-75 mm Hg with a liberal oxygenation target of 98-105 mm Hg in comatose patients who had been resuscitated after out-of-hospital cardiac arrest and found no significant difference between liberal and restrictive oxygenation targets in the composite outcome of death or survival with a poor neurologic outcome. Furthermore, the results were consistent in all prespecified subgroups. The potential pathophysiological link between brain injury and oxygenation seems to occur in the early period after cardiac arrest and to be driven by reperfusion injury with mitochondrial dysfunction and tissue inflammation, but no significant between-group difference in the primary outcome was seen in this open-label study. 041b061a72

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