"don't pour oil into fire"

I am not going to tell everything about what has happened to me recently. It is about a friend of mine, who I used to label him as my 'best friend forever' but unluckily he is also my colleague. There was a turning point where I have to make a radical changes for the betterment of the department. To cut the story short, because of misunderstanding the whole story was twisted and changed. From his view, I am the bad boy and he is always the good man who is being victimized. Anyway, I requested for not pouring oil into fire.If I bring myself down to his level the situation would turn from bad to worse. I don't think I could find someone who is capable of pouring oil on troubled water. I choose to mum the words, since that is the best solution to protect my self in term of psychological 'safety'.

I've found this article and I would like to share the points here. The title is "How to Not Let Criticism Affect your Self-Confidence".


There are two types of criticism:
(i). the kind that is meant to be constructive
(ii). the kind that is meant to be destructive.

Of course when someone gives you constructive criticism, you should listen to what they’re saying, determine whether or not what they’re saying is the truth and find ways to change it.

Constructive criticism is helpful because it helps you look at yourself as other people perceive you. It can help you change your direction in life to a path more beneficial.

Sometimes, however, we’re faced with criticism that is destructive. This type of criticism serves no other purpose but to tear you down and make you look worse than you really are.

Destructive criticism usually comes in these forms:

1. Derogatory names

2. Subtle put-downs in front of groups of people

3. Attacks against your character

4. Insults concerning your intelligence


The six reasons why people degrade you:

It can be a bewildering experience to be condemned by someone when you can’t think of a good reason why they’re acting that way. You probably never did anything to that person yet they’re saying such awful things about you all the sudden. There are a multitude of reasons why they act the way they do and none of them make sense. They include:

1. Bigotry – The people who condemn you probably think that all beliefs and cultures which differ from theirs are inferior. Many even have intense anger and hatred for people who are different enough from them. Though they may not admit it publicly, they will give you subtle hints every now and then that would make most people feel uncomfortable.

2. "Us vs. Them” Attitude – Since the dawn of time, people united together in groups simply because they shared a common enemy. Sometimes the hatred they felt served no logical purpose and what started off as small erupted into mindless sensationalism. This is an example of bigotry in a group setting.

3. Lack of Empathy – These people often have zero empathy for people who are different from them. This gives them the false impression that they can treat certain groups of people as cruelly and callously as they determine without consequences.

4. Grandiose Self-Worth – People who look down on others tend to think irrationally high of themselves. Self-confidence is an admirable quality but arrogance can be very dangerous to an individual. Arrogance, when left unchecked, will allow someone to become so blind to their own weaknesses that those flaws grow into something that not only hurts themselves but the people that they care about.

5. Failure to Accept Responsibility for Own Actions – Sometimes people hold themselves back from the finer things in life because of their own actions. But they refuse to admit this to themselves. Instead they think that everyone who goes far in life must have something morally wrong with them while they themselves are somehow “better people” because they never “sold out.” But if they were given a chance to switch places, they’d do it in a heart beat.

6. Envy – Some of these people love to be the center of attention. And they view other people’s success as an attack on their own self-esteem. When they see someone outshining them (who they don’t approve of) they’ll find any way possible to disparage that person. But if they’re not careful, that envy could grow into hate, and that hate could grow into insanity.

Don’t bring yourself down to their level

When you meet people who want to tear you down, do not give them attention.
If you respond in kind, you’re only playing into their hands.
They want you to play their games so that they’ll have more reasons to make you look like a bad person to others.

“Never argue with a fool, onlookers may not be able to tell the difference.” – Mark Twain

When someone acts like a fool, don’t bring yourself down to their level. Instead, try to lift them up to your level—as respectfully and sincerely as you can. If they don’t accept, at least you know that you tried to be a person of class and decency.

Stay focused on your goals

The best thing you can do when faced with unreasonable people is to stay focused on your goals and keep moving forward. Every second you spend wrestling in the mud with pigs holds you back from excellence–remember that. If you can take criticism without losing faith in yourself, it is you who has class.

People who enjoy disparaging people who mean no harm to anyone are small thinkers. But if you think big and focus on the great things you’ll be doing in the future, you’ll be the real winner of any confrontation you come across.

Hypothermia in Traumatic Brain Injury

An increased in temperature increased cerebral metabolism, oxygen requirements, CBF and ICP. Fever has been demonstrated to increase brain injury in animal models. In patients with raised ICP, a raised temperature should therefore treated aggressively (using cooling blankets, cool water, cool intravenous fluids, fans and antipyretic medications) and any evidence of infection identified early and treated with appropriate antibiotics. Fever can make an existing neurological dysfunction more apparent and may worsen an ongoing dysfunction.

It is postulated that fever may worsen ischaemia by following mechanisms:
1. Neurotransmitter and oxygen free radical production.
2. BBB failure.
3. Damaging depolarizations in the ischaemic penumbra.
4. Impaired recovery energy metabolism
5. Cytoskeletal proteolysis

Hypothermia has been known to offer protection for years. First reported as a treatment for brain injury in the 1950s. Currently therapeutic hypothermia is used in post cardiac arrest in particular VF/VT arrest and is supported by two randomized clinical trials  (in Europe and Australia).

In traumatic brain injury, the mechanism of ICP reduction in hypothermia is unknown but may be due to reduction in intracranial blood volume secondary in cerebral vasoconstriction or to alteration in metabolism. Induced hypothermia has been a proposed treatment fo TBI based upon its potential to reduce ICP as well as to provide neuroprotection and prevent secondary brain injury.

At present, there is no evidence that hypothermia  therapy should be used as primary neuroprotective strategy  in patients with severe traumatic brain injury.

1. A systemic review of 12 randomized controlled trials of mild to moderate hypothermia (32-33C) following TBI noted a small but significant decrease in the risk of death or poor neurologic outcome among more than 500 patients treated with hypothermia. Outcomes were influenced however by depth and duration of hypothermia as well as rate of rewarming after discontinuation of hypothermia. Nonetheless, the evidence is not yet sufficient to recommend routine use of therapeutic hypothermia for TBI outside of research settings.
JAMA 2003.

2. Lack of effect of induction of hypothermia after acute brain injury. NEJM 2001. Clifton GL et al. This study which evaluated the efficacy of hypothermia in head injuries was halted after the enrolment of 392 patients because the treatment was ineffective. Cooling patients to 33C within 8 hours after injury and maintaining hypothermia for 48h were not effective in improving the clinical outcome at 6 months and patients older than 45 years of age had a poorer outcome.

3. NABIS H II Trial - Very early hypothermia induction in patients with sever brain injury (the National Acute Brain Injury Study Hypothermia II): a randomized trial.
Prof Guy L Clifton et al. The Lancet Neurology, Volume 10, issue 2, February 2011.

Background: The inconsistent effect of hypothermia treatment on severe brain injury trials might be because hypothermia was induced too late after injury. We aimed to assess whether very early induction of hypothermia improves outcome in patients with severe brain injury.

Methods: It was a randomized multicentre clinical trial of patients with severe brain injury who were enrolled within 2-5 hours of injury at 6 sites in US and Canada. Patients with non-penetrating brain injury who were 16-45 years old and were not responsive to instructions were randomized to hypothermia (cooled to 35C) or normothermia. After trauma assessment was completed, the hypothermia group were cooled to 33C for 48h and then gradually rewarmed. Primary outcome was the Glasgow outcome scale score at 6 months.

Findings: Enrolment occurred over 4 years and the trial was terminated early due to suggestion of futility. Follow-up was from June 2006 to December 2009. 232 patients were intially randomized a mean of 1.6h after injury: 119 to hypothermia and 113 to normothermia. 97 patients (52 in the hypothermia froup and 45 in the normothermia group) did not meet any of the second set of exclusion criteria. The mean time to 35C for the 52 patients in the hypothermia group was 2.6h and to 33C was 4.4h. Outcome was poor (severe disability, vegetative state or death) in 31 of 52 patients in the hypothermia group and 25 of 56 in the normothermia group (RR 1.08, 95% CI 0.76-1.53; p=0.67). 12 patients in the hypothermia group died compared with eight in the normothermia group (RR 1.30, 95% CI 0.58-2.52; p=0.52).

Interpretation
This trial did not confirm the utility of hypothermia as a primary neuroprotective strategy in patients with severe traumatic brain injury.
Given the uncertainties surrounding its appropriate use, therapeutic hypothermia treatment should be limited to clinical trials or to patients with elevated ICP refractory to other therapies.

Decompressive Craniectomy in Diffuse Traumatic Brain Injury - DECRA trial

A must read paper published in New England Journal of Medicine, April 21, 2011.
The study was led by Prof DJ Cooper MD.
Funded by the National Health and Medical Research Council of Australia and others: DECRA Australian Clinical Trials.
DECRA - decompressive craniectomy for refractory intracranial hypertension in TBI.

Background: It is unclear whether decompressive craniectomy improves the functional outcome in patients with severe  TBI and refractory raised ICP.

Methods: In between December 2002 and April 2010, 155 adults with severe diffuse  TBI and intracranial hypertension that was refractory to first tier therapies were randomly assigned to undergo either bifrontotemporalparietal decompressive craniectomy or standard care.

The original primary outcome was unfavourable outcome (composite of death, vegetative state or severe disability) as evaluated on the GOS-E at 6 months after the injury.

The final primary outcome was the score on the GOS-E at 6 months.


Results:

Patients in the craniectomy group had less time with ICPs above the treatment threshold (p<0.001), fewer intervention for raised ICP and fewer days in ICU.

However patients undergoing craniectomy had worse scores on the GOS-E than those receiving standard care and greater risk of an unfavourable outcome.


Rates of death at 6 monts were similar in the craniectomy group (19%) and the standard care group (18%).


Conclusions:

In adults with severe diffuse TBI and refractory intracranial hypertension, early bifrontotemporoparietal decompressive craniectomy decreased intracranial pressure and length of stay in the ICU but was associated with more unfavourable outcomes.

+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++

For many years Neurosurgeons and intensivists have speculated that decompressive craniectomy in patients with severe TBI and refractory intracranial hypertension my improve clinical outcomes eventhough there have been no well conducted randomised controlled trials in its favour. DECRA was conducted by ANZICS CTG and studied  155 patients over 7 years. 
This randomized trial revealed unexpected results that  showed early decompressive craniectomy reduced ICP and the length of stay in the ICU but it was also associated with a greater risk for unfavourable outcome at 6 months compared with standard care. Rates of death didn't differ between groups, but scores on the GOS-E were lower in the surgical group  and there was a significant increase in risk, more than double for an unfavourable outcome on that same scale.

The findings differ from those of most nonrandomized studies and are contrary to the hypothesis. This surgical strategy is increasingly used at neurotrauma centres internationally.

The original primary outcome was unfavourable outcome on the GOS-E, a composite of death, vegetative state or severe disability. However, after the interim analysis in 2007, the primary outcome was revised to be the functional outcome at 6 months after injury on the basis of proportional odds analysis  of the GOS-E.

The editorial points out that most neurosurgeons wouldn't consider this aggressive strategy in patients who have increased ICP  for such a short time, in this study ICP more than 20mmHg for 15 minutes. In addition,  in screening of 3478 patients, only 155 patients enrolled in the trial suggests a selected population excluding both patients with mass lesions  and those whose intracranial pressure was successfully brought under control. 

For reasons that are not clear decompressive craniectomy appeared to convert survivors from a favorable outcome to an unfavorable outcome. Among many possible explanations are variations in surgical technique and unintended changes in brain physiology - swollen brain expansion outside the skull causing axonal stretch and injury of changes in cerebral blood flow. Other issues that may explain the results include heavy enrolment from a single centre or baseline imbalances  between groups. Even considering these effects, craniectomy was not shown to be beneficial.

The main lesson from this study is that surgical reduction of ICP by the technique that was used by the investigators does not necessarily result in better outcomes for patients and indeed appears to worsen them in at least some circumstances. The procedures should not be abandoned on the basis of these results. Rather, the risks and benefits of the decompressive craniectomy must be weight carefully and must work to define appropriate clinical settings for this procedure. Caution should be applied in the routine use of this strategy.
xoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxoxox

Further comments:
1. 3478 patients were screened over 7 years to enrol 155 patients. Shouldn't this trial have been stopped for futility?
2. Median ICP at randomization was 20 mmHg, did these patients even have intracranial hypertension?
3. ICP was managed for 15 minutes before surgery, is this clinical equipoise?
4. In this trial, decompressive craniectomy was performed at an average ICP of 22 mmHg for 30 minutes
5. There were 2.5x as many patients with bilateral fixed pupils in the surgical group. This between group difference was statistically significant (p=0.04).
6. After post-hoc adjustment for pupil reactivity at baseline, the between group differences were no longer significant for the score on the GOSE and for the risk of an unfavourable outcome.
7. the conclusion that decompressive craniectomy is associated with more unfavourable outcomes is highly misleading and not supported by the data.





 

Disorders of consciousness

-A normal level of consciousness depends on the interaction between the cerebral hemispheres and the rostral reticular activating system.
-Anatomical bilateral hemispheric lesions or brainstem lesions may result in an altered level of consciousness.
-Large unilateral hemispheric lesions may produce impairment of consciousness by compression of the upper brainstem.
-Metabolic processes may result in coma from interuption of energy substrate delivery or alteration of neuronal excitability.

Disorder of consciousness are characterized by an alteration of either the level or content of consciousness.

1. Consciousness - an awake individual demonstrates full awareness of self and environment.
2. Confusion - Inability to think with customary speed and clarity, associated with inattentiveness, reduced awareness and disorientation.
3. Delirium - Confusion with agitation and hallucination.
4. Stupor - Unresponsiveness with arousal only by deep and repeated stimuli.
5. Coma - unarousable unresponsiveness.
6. Locked in syndrome - total paralysis below third cranial nerve nuclei; normal or impaired mental function.
7. Persistant vegetative state - Prolonged coma > 1 month, some preservation of brainstem and motor reflexes.
8. Akinetic mutism - Prolonged coma with apparent alertness and flaccid motor tone.
9. Minimally conscious state - Preserved wakefulness, awareness and brainstem reflexes but poorly responsive.

Coma -like syndromes and related states:

1. Locked in syndrome
Features: alert and aware, vertical eye movements present, and able to blink. Quadriplegic, lower cranial nerve palsies (below CNIII nerve nuclei). No speech, facial or pharyngeal movements.
Site of lesion: bilateral anterior pontine lesion which transects all descending motor pathways bu spares ascending sensory and RAS.
Normal EEG. 90-100% of normal metabolism.
Similar state seen with severe polyneuropathies, MG and NMB.

2. PVS (apallic syndrome, neocortical death)
Features: Previously comatose, who now appear to be awake. Spontaneous limb movements, eye movements and yawning seen. However patient is inattentive, no speech, no awareness of environment and total inability to respond to commands.
Site of lesion: Extensive damage to both cerebral hemispheres with relative preservation of the brainstem.
EEG: polymorphic delta or theta waves, sometimes alpha. 40-60% of normal metabolism.
When vegetative state lasts longer than 4 weeks, it is termed persistent. PVS lasting for longer than 2 weeks implies a poor prognosis.

3. Akinetic mutism (coma vigile)
Features: Partially of fully awake patient, immobile and silent.
Site of lesion: Lesion is bilateral frontal lobes or hydrocephalus or third ventricular masses.
EEG: diffuse slowing. $0-80%  normal metabolism.
'Abulia' is the tern applied to milder forms of akinetic mutism.

4. Catatonia
Features: awake patients, sometimes a fixed posture, muteness with decreased motor activity.
Site: usually of psychiatric origin.
EEG: non specific EEG patterns associated with associated medical conditions. Variable metabolic changes in prefrontal cortex.
May be mimicked by frontal lobe disease and drugs.

5. Minimally conscious state
Features: Globally imparied responsiveness, limited but discernible evidence of self and environment.
Site: Global neuronal damage.
EEG: theta and alpha waves. 40-60%  normal metabolism.
Differs from PVS in that patients diagnosed with minimally conscious state have some level of awareness.

Jugular bulb oximetry in Traumatic Brain injury

There is insufficient data to provide evidence based indications for the routine use of jugular bulb oximetry.
Measurement of oxygen saturation in th jugular bulb by the retrograde placement of a fibreoptic catheter provides an indirect assessment of cerebral perfusion by measurement of oxygen saturation in the blood exiting the brain. Normal SJO2 is about 60%.
1. Low saturation < 55% may be indicative of cerebral hypoperfusion due to systmemic hypotension or hypocapnia.
2. High saturation > 85% may be indicative of cerebral hyperaemia or inadequate neuronal metabolism, such as occurs during the hyperaemic phase or during the evolution of brain death.

Its use is limited to experience units when an index of CBF is required during adjunctive therapies in patients with intracranial hypertension e.g. CPP augmentation with catecholamines, barbiturate coma, hyperventilation or hypothermia.

CT scan in Traumatic Brain injury

The following patients should undergo CT head scan following TBI:
1. All patients with a history of LOC or traumatic coma
2. Combative patients where clinical assessment is masked by associated alcohol, drugs or extracranial injuries. These patients may require endotracheal intubation , sedation and ventilation to facilitate completion of CT scanning.
The most important role of CT scanning is prompt detection of mass lesion such as extradural or subdural hematomas. Therafter, the degree of brain injury may be quantified by radiological criteria.
Marshal classification of CT scan appearance following traumatic brain injury.
1. Diffuse injury (DI) I - no visible intracranial pathology seen
2. DI II (diffuse injury) - cisterns are present with midline shift 0-5mm, lesion densities present, no high or mixed density more 25mm, may include bony fragments and foreign bodies.
3. DI III (swelling) - cisterns are compressed or absent with ML shift 0-5mm, no high or mixed density > 25mm.
4. DI IV (shift) - ML shift > 5 mm, no high or mixed density > 25mm.
5. Evacuated mass lesion -any lesion surgically evacuated.
6. Non-evacuated mass lesion - High or mixed density lesion > 25 mm, not surgically evacuated.

The criteria are important for:
1. providing an index of injury severity
2. providing criteria for intracranial pressure monitoring
3. comparing the progression of injuries with subsequent scans
4. providing an index for prognosis

the presence of traumatic SAH should be recorded since it is an important index of severity of injury and is relevant for prognostication.

Severe head injury 1-Cerebral blood flow and autoregulation

Cerebral blood flow is normally maintained at a constant rate by myogenic and metabolic autoregulation. These homeostatic mechanisms are impaired following head injury. Distinct patterns of CBF have been described following head injury that have direct clinical relevance with regard to management of TBI. (Martin et al. J neurosurg 1997).

1. Hypoperfusion phase

CBF is reduced in the first 72 hours following injury with resultant global and regional ischaemia. Myogenic autoregulation is severely impaired and CBF is directly dependent of systemic BP. Resultant cerebral ischaemia may result in cytotoxic cerebral edema and increased ICP. In this phase systemic BP must be maintained to achieve CPP in between 60-70 mmHg (BTF guideline).

Management: defend ICP, restore MAP, reduce ICP.

2. The hyperaemic phaseFollowing hypoperfusion phase, autoregulatory mechanisms may start to recover with improved blood flow. This phase may persist up to 7-10 days post injury and occurs in 25-30% of patients. Intracranial inflammation and effects of medical therapies directed at maintaining adequate cerebral perfusion may result in cerebral hyperaemia and increased ICP. The consequences of hyperaemia, inflammation and altered blood brain permeability result in vasogenic cerebral edema.Since there is restoration of CBF or increased CBF, a range of CPP recommended is 50-70 mmHg.

Management: optimize CPP, normalize MAP, reduce ICP.

3. The vasopastic phase

In about 10-15% of patients, particularly in those with severe primary and secondary injuries or those with significant traumatic SAH, a vasopastic phase may persist up to 14 days. This phase represents a complex of cerebral hypoperfusion due to arterial vasospasm, posttraumatic hypometabolism and impaired autoregulation.

Management: maintain CPP, maintain MAP.

GLASGOW OUTCOME SCALE

GOS is used to assess the general functioning of the patient who sufferred a traumatic brain injury and to categorize their outcome. It is named for Glasgow, Scotland where its use was first described. It is a five-point score given to victims at some point in their recovery and it is often used in research to quantify the level of recovery patients have achieved. Lower scores indicating a poorer functional outcome. More specific and detailed grading, extended GOS (GOS-E) was used in the recent DECRA trial.
In research, common time points to evaluate the GOS include 3 months, 6 months and 12 months after injury.

GOS:1. Dead
2. Vegetative State - patient is unable to interact with environment and unresponsive, but alive; a "vegetable" in lay language.-Patient show no evidence of meaningful responsiveness. Patients who obey even simple commands, or who utter any words are assigned to the better category of severe disability. Vegetative patietns breathe spontaneously, have periods of spontaneous eye-opening when they may follow moving objects with their eyes, show reflex responses in their limbs (to postural or painful stimuli), and they may swallow food placed in their mouths. This state must be distinguished from other wakeful, reduce responsiveness such as the lock-in-syndrome, akinetic mutism and total global aphasia.
3. Severely Disabled - conscious, able to follow commands but the patient requires others for daily support due to disability.-This indicates that a patient is conscious but needs the assistance of another person for some activities of daily living every day. This may range from continuous total dependency (for feeding and washing) to the need for assistance with only one activity such as dressing, getting out of bed or moving about the house, or going outside to a shop. Often dependency is due to combination of physical and mental disability because when physical disability is severe after head injury there is almost always considerable mental deficit. The patient cannot be left overnight because they would be unable to plan their meals or to deal with callers, or any domestic crisis which might arise. The severely disabled are described by the phrase "conscious but dependent".
4. Moderately Disabled - the patient is independent but unable to return to work or school.-These patients may be summarized as "independent but disabled", but it is perhaps the least easily described category of survivor. Such a patient is able to look for himself at home, to get out and about to the shops and to travel by public transport. However, some previous activities either at work or in social life are now no longer possible by reason of either physical or mental deficit. Some patients in this category are able to return to certain kinds of work, even to their own job if this happens not to involve a high level of performance in the area of their major deficit.
5. Good recovery - the patient has resumed most normal activities and able to return to work or school but may have minor residual problems.-This indicates the capacity to resume normal occupational and social activities, although there may be minor physical or mental deficits. However for various reasons the patient may not have resumed all his previous activities and in particular may not be working.

comment: it is rather a coarse scale with only 5 levels, it has been argued that this scale is not ideal for research purposes.

The extended GOS or GOS-E has extended scale to an 8 level score:1. Dead
2. Vegetative State
3. Lower Severe Disability
4. Upper Severe Disability
5. Lower Moderate Disability
6. Upper Moderate Disability
7. Lower Good Recovery
8. Upper Good Recovery

comment: GOS-E was developed to address the limitations of the original GOS. A structured interview has been provided to improve reliability of rating. Good interrater reliability and content validity have been demonstrated for the GOS-E. Compare to GOS, GOS-E has been shown to be more sensitive to change in mild to moderate TBI.