"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.
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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.

Initial assessment of seriously ill patient

Hello again,thank you for visiting my blog, forgive me for not writing the topics nicely or the way it should be. I prefer those topic to be discussed in such manner.I am busy and still nothing is done in order. I am worried, nothing is done according to timeline and I am very desperate to reach my goals for this year.

I have started a new interest since I am the coordinator of the advance skill center in my department. I observed that the gap in between knowledge and practical is so real. Previously, the students are given a scenario that is not in the orderly way and results in chaotic debriefing sessions. I am glad to share one of the scenario here. I teach very basic stuff, that include patient safety. My students enjoyed the simulation class but I understand that it is not easy to immerse in the scenario and treat the manikin as a 'real patient'. I noticed, the students lack of adrenaline and always 'asking for some gadgets to drop down from the sky'.

SIMULATION BASED LEARNING: WORKSHOP FOR YEAR 4, SPECIALIZED POSTINGThere are two components of the workshop.
1. Introduction to human patient simulator
2. Airway workshop

1. Introduction to human patient simulator-bridging the gap between theory and practice.
General objectives: Week 1
1. Understand the principles of assessment of seriously ill patient
2. Introduction to patient safety
a. I.V. cannulation
b. Preparation of intravenous drip
c. Breaking ampoules and dilution of drugs
d. Patient monitor3. Handling of defibrillator machine
Venue: ECS room, Advance Clinical Skill Centre, Kulliyyah of Medicine, IMC
Equipments: METI Emergency care simulator, fully equipped emergency room, emergency trolley, I.V. cannulation tray, IV drip and solution, drugs, syringes, defibrillation machine, NIBP, devices for oxygen therapy,
Normal 12 leads ECG, ABG, CXR with pneumonic changes/pneumothorax
Week 2: Assessment of patient in emergency situation:
Scenario 1:25 year old male patient is presenting with a sudden onset of shortness of breath. He has a history of asthma and occasionally uses an inhaler. This asthma attack had a sudden onset. He is very anxious and unable to speak in complete sentences. He appears exhausted.
Allergies: Penicillin
Medications: Occasional albuterol inhaler
Social History: Smoker
Secondary assessment: 70kg, 5’8”, sitting up with obvious difficulty breathing, appears to be leaning over in an effort to catch his breath. He is sweating and in obvious distress.
Objectives:
1. Able to apply the principle of assessment of unstable patient
• Targeted history
• Focused physical examination
• Order Investigations
• Identify abnormal physiology
• Treatment of abnormal physiology
• Differential diagnosis and ‘Best guess’ diagnosis
2. CVS and Respiratory examination
• Recognize abnormal breath sounds
3. Immediate Management of acute exacerbation of bronchial asthma
• Salbutamol nebulizer
• IV hydrocortisone
• Consider antibiotics
4. Recognize easy ABG abnormalities
5. Application of monitors and ECG
6. IV cannulation and IV fluid therapy
7. Initial investigations
N.B. Patient is not allowed to die. The scenario is terminated after all objectives are achieved or they have reached a point whereby it is too dangerous to continue.

Notes for the lecturers:

ASSESSMENT OF UNSTABLE PATIENT
• It is recommended to use a systemic approach to assessment to ensure that all immediately life threatening problems are recognized and the correct treatment is started immediately.
• Critically ill patients often have multiple problems and the use of systemic approach reduces the risk of missed diagnoses and provides a framework for treatment when working under stressful conditions.
• You are interested in all patients’ problems and their responses to the treatments instigated.
The aim of assessment of seriously ill patient is to:1• Identify the life-threatening pathophysiological abnormalities
2• Identify the most appropriate way to correct those abnormalities
3• Diagnose the underlying problem
In emergency, tasks that are typically carried out sequentially often have to be carried out in parallel with history taking (targeted history), examination (focused examination) and initial resuscitation often occurring simultaneously. Treatment is initiated on a “best guess” basis rarely enough time to be certain of cause prior to starting resuscitation. Important to realize that response to treatment needs to be made every few minutes not every few hours. The working diagnosis needs to be repeatedly reassessed as more information becomes available and on the basis of response to treatment.
The focus of subsequent examination is to determine the underlying cause, in order to determine the appropriate definitive therapy.
The first step in assessing a seriously ill patient is to estimate how ill the patient is and how much time is available for assessment and investigation before initiating treatment.
• Assessing the compensatory response to the primary abnormality. This involves activation of the sympathetic nervous system and magnitude of such response. In the pre-terminal patient, this compensatory response id exhausted
• The intensity of supportive therapy e.g. the degree of oxygen therapy and oxygen saturation.

Immediate assessment
A Airway (patency) assessment and treatment if needed
B Breathing assessment and treatment if needed
C Circulation assessment and treatment if needed
D Dysfunction of the central nervous system
E Exposure sufficient to allow complete examination
Process of ABC assessment in an acutely ill patient is predominantly clinical and follows the simple clinical pattern of Look, listen and feel.
In dire emergencies (true emergencies) , e.g. airway obstruction, tension pneumothorax, ventricular dysrhythmias, pericardial tamponade, exsanguination and hypoglycaemia you have to own the airway, breathing (thorax) and circulation (heart, blood vessels).

A-AIRWAYTalk to patient, a patient who is able to respond appropriately must at that moment have control of their airway and have adequate oxygenation, ventilation and cerebral circulation to be able to reply coherently.
• LOOK – for the presence of
cyanosis,
obstructed pattern of respiration or abdominal breathing,
Use of accessory muscles of respiration
Tracheal tug
Alteration in level of consciousness
Any obvious obstruction by foreign body or vomit
• LISTEN
For abnormal sounds such as grunting, snoring, gurgling, hoarseness or stridor
• FEEL
For airflow on inspiration and expiration
If an obstruction is present then the immediate goal must be to obtain and secure the airway to allow oxygenation and ventilation. As soon as airway is patent, high concentration of oxygen should be administered.
-Chin lift or jaw thrust
-Suction to remove secretions
-Oral airway is inserted in obtunded patients.
-Patients can be oxygenated by using bag and mask ventilation.
If simple method fails, definitive airway is indicated. If patient is at extremis, intubation may be accomplished without the use of drugs. If patient is responsive, intubation is done with anaesthetic drugs. Attempts at intubation without first preoxygenating the patient are futile and dangerous
If above steps unsuccessful, surgical airway should be performed with cricothyroidotomy being the method of choice.
B- BREATHINGA respiratory rate of less than 12 or more than 30 breath/min, inability to speak in complete sentences because of breathlessness or breathlessness at rest, are all sinister signs of impending respiratory failure. Marked tachypnea is a useful marker of a severely ill patient, regardless of whether the patient has respiratory failure.
• LOOK for:
Central cyanosis
Use of accessory muscles of respiration
High or low respiratory rate
Equality and depth of respiration,
Sweating
Raised JVP
Patency of chest drains
Presence of any paradoxical abdominal or chest wall movement.
Abdominal distension
Note the inspired oxygenation and saturation if pulse oximetry is in use, but remember that pulse oximetry does not detect hypercarbia.
• LISTEN for:
Noisy breathing, audible wheeze, clearance of secretions by coughing
Ability of patient to talk in complete sentences (evidence of confusion or decreased level of consciousness may indicate hypoxia or hypercarbia, respectively)
Change in percussion note
Auscultate for abnormal breath sounds, heart sounds and rhythm
• FEEL for
Equality of chest movement,
Position of trachea
Presence of surgical emphysema or crepitus
Paradoxical respiration
Tactile vocal fremitus if indicated
The best treatment will be determined by the cause and severity of the respiratory failure.

You should look for the signs of immediately life-threatening conditions of tension pneumothorax, massive hemothorax, flail chest and cardiac tamponade and provide immediate appropriate treatment.
Remember that the chest drains may become dislodged or blocked and that their presence does not exclude recurrent pneumothorax. Simple maneuvers such as sitting the patient up can help, but if the patient is tiring to the point of respiratory arrest then assisted ventilation by bagging may be necessary until help arrives.

C-CIRCULATIONAll shocked surgical patients should be assumed to be hypovolemic until proved otherwise
• LOOK for
Reduce peripheral perfusion (pallor, coolness, collapsed or under-filled veins) – remember blood pressure may be normal in the shocked patient. As a result of compensatory mechanisms hypotension is a late feature of cardiovascular dysfunction.
Obvious external haemorrhage from either wound or drains
Evidence of concealed haemorrhage into the abdomen, pelvis, soft tissues or thorax. An empty drain does not exclude the presence of concealed bleeding.
• LISTEN to
Heart sounds: gallop, rhythm, quiet heart sounds or a new murmur may indicate a primary cardiac problem.
• FEEL for
Peripheral and central pulses, assessing volume equality and rhythm.
Unless there are obvious signs of cardiogenic shock (e.g. raised JVP and gallop rythm ) venous access with a 16G cannula should be obtained, blood sent for cross-matching and other routine tests, including clotting screen, and appropriate fluid replacement started: rapid fluid challenge of 10ml/kg or 20ml/kg if patient is hypotensive. Patient with heart failure should receive an initial bolus of 5 ml/kg and closer monitoring may be needed.
If patient is actively bleeding from a non-compressible source, then the correct treatment is surgical control. Fluid resuscitation should be maintained at levels to maintain organ perfusion while surgery is being arranged.

D-DYSFUNCTION OF THE CNSA rapid assessment may obtained by using mnemonic AVPU
A-Alert and orientated
V-vocalizing
P-responding only to pain
U-unconscious

• If time permits, a full Glasgow Coma Scale should be performed as this is a more repeatable and objective measurement of consciousness.
• Alteration of conscious level may be due to intracranial and extracranial causes. Hypoxia, hypercarbia, cerebral hypoperfusion, sedatives or opioid drugs may be responsible. Metabolic or endocrine causes should be considered, notably hypoglycaemia (DEFG=don’t ever forget glucose), uraemia or hypothyroidism. If the diagnosis is not obvious, review the ABCs.
• A marked reduction in conscious level indicates either that compensatory homeostatic mechanisms have been overwhelmed or severe neurological disease. Urgent supportive therapy is advocated. The pupillary response should be checked frequently.

E-EXPOSURE• The patient must be exposed to allow full examination, and the environment should be warm to prevent hypothermia.
• There should be adequate light, and preserving the patient’s privacy by the use of screens is essential. If intimate examinations are planned then a chaperone is required.

At the end of initial assessment the patient should hopefully have a secure airway, with adequate oxygenation, ventilation and circulation.
Commence monitoring of vital signs, including pulse, blood pressure, temperature, urine output and pulse oximetry. At this stage consider the need for specialist help and advice, the requirement for additional investigations and the level of care the patient needs. Do not leave the patient until he/she is stable.
Initial investigations:
ABGs, glucose, ECG, electrolytes, full blood count, CXRIn subsequent assessment, other investigations should be ordered on the basis of the history and clinical findings.
Summary
Beware of patients who demonstrate any of the following features, especially if they are acute in onset or severe. Patients with a greater number of these features are likely to be sicker.
1. Altered level of conscious state
2. Hypotension
3. Tachycardia
4. Tachypnea
5. Cyanosis/hypoxia
6. Oliguria
7. Acidosis

Debriefing:
Debriefing is done at two levels, during the scenario (pause and discuss technique) and at the end of scenario (with or without videotaping). The lecturers must understand the goals of debriefing, the importance of it, various techniques and process of debriefing.
The process of debriefing:
1. Introduction
2. Personal reaction
3. Discussion of events
4. Summary

antifungal agents

Antifungals: Triazole, Polyene and echinocandin
1. Triazole
-inhibits ergosterol synthesis in the fungal cell wall by inhibiting lanosterol demethylase
-examples: fluconazole, itraconazole, voraconazole
-all azoles can cause hepatotoxicity, anaemia, thrombocytopenia, leukopenia, stevens-johnson syndrome, multiple drug interactions - increase levels of phenytoin, warfarin, cyclosporin

2. Polyene
-combines with sterols in fungal membrane to create a channel with leakage of cytosol
-e.g. Amphotericin, nystatin

3. Echinocandin
-inhibit synthesis of D-glucan, a key fungal cell wall component
-e.g. caspofungin, micafungin

what is right is always seen as wrong

Hi again,
thank you guys for visiting my site, it is not great but at least there are some important facts are discussed here.
The world that we live in is a mystery. It is very disheartening when people maybe talk and support about certain values, but on the other hand are fighting against the same facts and ideas.
I am trying to educate people at my work place based on my knowledge, expertise and experience, but people are uncomfortable and prefer to live in ignorance. Recently, I was asked to lower my expectation and quality of practice to their extremely dangerous level instead of striving to improve themselves. The irony is they wanted to be treated like adults but on the other hand required to be told all the instructions step-by-step.
My reminder to them is, alright...you can live in that situation but I won't because I want to live with the Physician's Oath that I had taken upon graduation 21 years ago. I keep wondering why they make it customary for us to read that oath out aloud if it is something that is not going to be lived by.

High frequency ventilation

Currently HFOV is used as salvage therapy for patients failing conventional mechanical ventilation. It should restricted to centres with training and experience in this mode of ventilation. HFOV provides tidal volume below the anatomic dead space at frequencies greater than 60 breaths per second.

Benefits include reduce barotrauma, improve V/Q matching and less respiratory compromise. Complications include dessication and inspissation of mucus, airway damage due to high gas velocities, air trapping and high shear forces at interfaces between areas of the lung at different impedences.

Gas exxchange during HFOV:

• 
  
  direct bulk flow


• 
  
  longitudinal (taylor) dispersion


• 
  
  pendeluft


• 
  
  asymmetric velocity profile


• 
  
  cardiogenic mixing


• 
  
  molecular diffusion

1. Two observational studies, adults who failed to respond to conventional ventilation were managed with HFOV at 5 Hz. Improvement in oxygenation were noted within 8 hours in both studies. (Fort CCM 1997, Mehta CCM 2001).

2. HFOV for ARDS in adults: a RCT. Derdak AJRCCM 2002.

Multicentre Oscillatory Ventilation for ARDS Trial (MOAT)

148 adults were randomised to HFOV or conventional ventilation. The HFOV group had significant improvement in oxygenation within 16 hours,compared to conventional ventilation. However the improvement did not persist and oxygenation was the same in both groups by 24 hours. The survival trend favour HFOV over CV but is underpowered (would need n=199 to evaluate mortality)

The difference in survival rate did not reach significance at 30 or 90 days.

3. High frequency oscillatory ventilation in adults: the Toronto experience. Mehta Chest 2004 Canadian experience, Retrospective chart review of 156 patients treated with HFOV. The authors suggested that HFOV might be an effective rescue therapy for patients with severe oxygenation failure. Because mortality was associated with a greater number of days receiving conventional ventilation prior to HFOV, the authors also suggested that earlier institution of HFOV could be beneficial.

4. High Frequency Oscillatory Ventilation Compared to Conventional Ventilation in ARDS: a RCT. Bollen et al. Crit Care 2005

ICU in London, Cardiff, Paris, Mainz. n = 61

Study stopped prematurely because of la ow inclusion rate and the completion of similar MOAT trial.

No difference in 30 day mortality. Post hoc analysis- better treatment effect of HFOV in patients with higer baseline oxygen index (OI).

Critics: Small number of patients, lack of explicit ventilation protocol and underpowered to show differences in efficacy or safety.

Conclusions:

1. HFOV as safe and efficacious as lung protective controlled ventilation in RCTs.

2. There is a trend of improved mortality with HFOV but this needs to be repeated in a fully powered, properly controlled RCT.

3. HVOV may be more effective in patients with high baseline OI, but this should be studied directly.

Thrombocytopenia in critically ill patients

 

 

 

 

Definition:

1. Plt count less than 150, 000/micL, generally not significant until less than 100,000.
2. Relative  thrombocytopenia - acute drop from a higher platelet count may be pathologic.

Pathophysiology:

1. Decreased production
 a) Isolated thrombocytopenia
 b) Multiple cytopenias

2. Increased destruction and consumption

 a) Immune or alloimmune: primary (idiopathic) or secondary -associated with other autoimmune disease (e.g. SLE), associated with malignancy, maybe complication of infection and drug associated thrombocytopenia

b) Nonimmune -isolated or combined platelet consumption

3. Increased sequestration in enlarge spleen

a) portal hypertension
b) myloproliferative disease
c) lymphoma
d) storage and infiltrative deseases of spleen
e) chronic hemolysis
f) granulomatoses -eg tuberculosis, sarcoidosis

4. Dilutional - effect of massive transfusion and fluid resuscitation

5. States with multiple causes of thrombocytopenia:

a) cirrhosis with portal hypertension
b) hepatitis
c) HIV
d) other viral illnesses
e) patients with multiple medical problems on multiple drugs

Diagnosis

1. FBP with peripheral smear: -Review of rbc abnormalities e.g. schistocytes, teardrops, nucleated RBC. Rule out pseudothrombocytopenia due to platelet clumping.
2. Coagulation testing: Identify associated coagulation abnormalities
3. Additional blood tests, if required:  

• viral titres and antibodies
• autoimmune disorders (e.g. collagen vascular disease)
• other disorders

     4. Radiologic

• abdominal US -evaluation of spleen size
• CT scan -evaluation for lymphoproliferative disease

    5. Indication for bone marrow examination

• unclear pathology
• multiple cytopenias
• suspected infiltrative process

Therapy

1. Transfusion therapy indications:

• bleeding or necessary invasive procedures
• prophylactic - for very severe (less than 10,000) thrombocytopenia
• other blood components as indicated to correct coagulation abnormalities

2. Platelet transfusion relatively contraindicated:

• TTP unless bleeding present
• ITP unless bleeding present
• HIT without bleeding - unknown

3. Primary thrombocytopenia - depends on specific disorder

4. Secondary thrombocytopenia -direct therapy at underlying causes

Propofol Infusion Syndrome

Propofol is an intravenous anesthetic that is commonly used for sedation in ICU. the elimination of propofol is not impaired by hepatic or renal dysfunction. Propofol has a large volume of distribution and is highly protein bound. During administration serum triglycerides should be monitored in all patients who receive propofol in doses > 50 mcg/kg/min for more than 2 days. If hypertriglyceride is detected, alternative should be considered. Unusual and potentially serious complications are associated with continous infusion of propofol for longer tnan 24 to 48 hours. These include progressive hyperglyceridaemia, pancreatitis, increased carbon dioxide production and excessive caloric load (the emulsion contains approcimately 1.1 kcal/ml, most of which derived from lipids).

Propofol Infusion Syndrome (PRIS): PRIS is a rare complication of propofol for longer than 24 to 48 hours. It is associated with high doses ( more than 4 mg/kg/hour of mone than 67 mcg/kg/min) and prolonged use (more than 48 hr). Characteristic of the syndrome include acute refractory bradycardia, severe metabolic acidosis, CVS collapse, rhabdomyolysis, hyperlipidaemia, renal failure and hepatomegaly. Mortality is high, more than 60% in a study. Risk factors:

• large doses and duration more than 48hrs


• younger age


• acute neurological injury


• low carbohydrate intake


• catecholamine and corticosteroid infusion

Clinical and lab findings:

• unexplained lactic acidosis


• increasing inotropic support


• Brugada like ECG abnormalities


• Green urine


• CVS collapse


• rhabdomyolysis, high CK, hyperkalaemia


• arrythmia/ heart block


• renal failure

Management:

1. high index of suspicion


2. discontinue infusion immediately


3. monitor for early warning signs: lactate, CK, urine myoglobin, ECG


4. standard cardiorespiratory support


5. consider pacing for bradycardia ( often resistant to high dose of CA )


6. adequate carbohydrate intake


7. ECMO: 2 case reports


8. haemoperfusion and haemodialysis are used with uproven benefit


9. carnitine supplementation: theoretical benefit

Extracorporeal membrane oxygenation (ECMO)

1. Extracorporeal membrane oxygenation for 2009 Influenza (H1N1) ARDS - ANZ ECMO influenza investigators. Journal: JAMA, Oct 19, 2009 A descriptive analysis of all adult and paediatric (neonates excluded) patients treated with ECMO, 1st june - 31 August 2009 in Australia, NZ ICU's during 2009 H1N1 epidemic. In 200 ICUs, 15 supplied ECMO for 61 (32%) of 194 H1N1/ Influenza A ventilated patients with 21% mortality. All these patients met inclusion criteria for the CESAR trial. to be continued..

MRI pearls

1. FLAIR - fluid attenuated inversion recovery sequence eliminates the signal from CSF. it is sensitive to oedema and inflammation. Axial T2 FLAIR: nulls the normally bright T2 signal of CSF (becomes black), while other parenchymal fluid appears bright (as in oedema or tumour).


2. Diffusion Weighted Imaging (DWI) DWI assesses the movement of protons due to diffusion over a short time. If there is restricted diffusion the signal is of high intensity. If there is unrestricted diffusion (e.g. CSF), there is low intensity signal. Unfortunately the signal on DWI is not just produced by the diffusion characteristics but also changes in parallel with the T2 and PD of the tissue. To eliminate these cofounders an apparent diffusion coefficient (ADC) map is generated. The ADC signal is low with true restricted diffusion. Using a combination of these sequences vasogenic oedema (intensity high on T2, high on DWI and high on ADC map) may be distinguished from cytotoxic oedema (intensity high on T2, high on DWI and reduced on ADC map).


3. Gadolinium contrast: Gd is a paramagnetic substance that acts as a contrast agent by markedly shortening T1 when it is present. Gd based contrast distributes throughout the extracellular fluid, and does not cross the normal BBB. In pathological conditions in which the BBB breaks down, there is marked hyper-intensity (enhancement) of affected areas on T1 weithted images.

Radiology pearls 3 --> subaxial cervical spine and thoracolumbar spine

subaxial cervical spine - C3 to C7

The classification of injury is based on the mechanism of injury. The patterns are distraction, compression, flexion and extension. Then there are distractive flexion, distractive extension, compressive flexion and compressive extension injuries.

A. On sagittal reconstructions, check for the following:

• anterior and posterior vertebral body lines and spinolaminar line are uninterrupted
• vertebral body height is the same anteriorly and posteriorly
• no prevertebral swelling
• no widening of distances between spinous process
• facet joints aligned, appearing as stacked parallelograms
• disc spaces intact

B. On coronal images check the following:

• height on each side of the vertebral body is the same
• disc spaces are intact
• facet joints are aligned

C. On axial images check the following:

• no soft tissue swelling
• facet joints aligned
• no significant rotation

i. compressive extension injury:

there is damage to the vertebral arch but the body remains intact. The vertebral arch fractures may be unilateral or bilateral, involving the pedicle, articular process, the lamina or a combination of these. In more severe injuries, the affected vertebra may be displaced anteriorly relative to the subjacent vertebra. The antero superior aspect of the subjacent vertebra may be sheared off.

ii. compressive flexion injury:

• stage 1 - there is blunting of the anterior-superior vertebral margin.
• stage 2 - there is a beak like appearance to the anterioe vertebral body with loss of anterior vertebral height and oblique contour.
• stage 3 -there is fracture extending from anterior surface of the vertebral body into the disc space.
• stage 4 - there is posterior displacement of the inferoposterior aspect of the vertebral body less than 3 mm.
• stage 5 -displacement relative to the vertebra below is more than 3 mm

iii. distractive extension injury

• stage 1 -abnormal widening of the disc space, representing disruption of the anterior longitudinal ligament and disc
• stage 2 - posterior ligaments are disrupted and the cephalad vertebtrae are displaced into the spinal canal

iv. distractive flexion injury:

range from facet subluxation, through unilateral facet fracture or dislocation to bilateral facet joint fracture or dislocation.

v. vertical compression

• stage 1: there is central fracture of either the superior or inferior endplate with a cupping deformity of the endplate.
• stage 2: bothe endplates are involved.
• stage 3: the vertebral body is fragmented with fragments displaced in multiple directions. The vertebral arch may not be involved.

Thoracolumbar spine

Classification of injury is based on three column concept. Columns of thoracic spine are anterior, middle and posterior. common injury patterns are compression fractures, burst fractures, flexion distraction (seat belt type), and fracture dislocations.

The anterior column:is formed by the anterior longitudinal ligament, the anterior half of the vertebral body and the anterior annulus fibrosus.

Middle column: posterior longitudinal ligament, the posterior half of the vertebral body and posterior annulus fibrosus.

Posterior column: posterior osseous arch, supraspinous and interspinous ligaments, the ligamentum flavum and the facet joint capsule.

The features sought on sagittal, coronal and axial images of the T-L spine are similar to those described for lower cervical spine injuries.

i. compression fracture:

the anterior column fails under compression. The middle column remains intact and acts as a hinge. The posterior column is usually intact but with severe injuriew it may partially fail in distraction. This injury may be anterior or lateral.

ii. burst fractures:

there is failure of compression of the anterior and middle columns, but no posterior column. Failure in compression of the anterior column is shown by fracture of the cortex of the anterior vertebral body, which loses height. Failure in compression of the middle column is shown by similar findings in the posterior vertebral body. Characteristically the pedicles are spread apart by the posterior vertebral body fracture. There is commonly a vertical fracture of the lamina, and splaying of the facet joints, without which there could not be significant widening of the interpedicular distance.

iii. flexion distraction "seat-belt type" injury:

there is failure in distraction of the middle and posterior columns with either no injury to the anterior column or minor compression. The injury may be through bone, through the ligaments or a combination of the two. When injury is through the bone at one level, it is known as "chance" fracture. There is a high incidence (around 60%) of intra-abdominal injury in association with flexion-distraction injuries.

iv. fracture dislocation:

failure of all three columns leading to translational deformity (sublaxation or dislocation) which may be in the sagittal or coronal plane. Fracture dislocation of thoracic spine occur with high energy trauma.

Fracture dislocations involve all three column making them extremely unstable injuries, commonly associated with neurological damage.

======================================================================================

Clearing the C-spine

The best approach to clearing the cervical spine with multiple trauma remains controversial. In this group of patients, plain XRay miss a significant proportion of bony cervical injuries. A single cross table lateral view missed 37% of significant injuries. A three view series missed 10% while cervical spine CT missed none. Ligamentous injuries are not well imaged with CT scan. When multiple trauma patients are imaged with CT scan, 6% have discoligamentous injuries that are not detected.

CT is the imaging modality of choice in this group of patients with supplementary MRI when spinal cord of ligamentous injury is suspected.

Radiology pearls 2 -craniocervical junction

Craniocervical junction: the skull base, atlas and axis form the craniocervical junction that in conjunction with associated ligaments acts as a single functional unit.
A. On sagittal CT images check for the following:

1. atlanto dental space should be less than 3 mm in adult and less than 5 mm in child
2. anterior cortex of the odontoid peg and posterior cortex of anterior arch of C1 are parallel
3. anterior aspects of the laminae of C1-C3 are in alignment, the spinolaminar line
4. bodies of C2 and C3 are in alignment with a normal disc space
5. no sublaxation or widening of the atlanto occipital joints
6. facet joints between C1/C2 and C2/C3 are aligned

B. On axial images check the following:

1. space between anterior arch of C1 and the odontoid peg should be less than 3 mm
2. C1 is symmetrically aligned around the odontoid peg
3. no significant rotation of C0/C1 or C1/C2
4. absence of soft tissue swelling

C. On coronal images, check the following:

1. space between odontoid peg and lateral mass of C1 is the same on both sides
2. there is no sublaxation or widening of the atlanto-occipital joints
3. the facet joints between C1/C2 and C2/C3 are aligned
4. the edge of the lateral mass of C1 does not over hang C2 at the facet joint

The major ligaments of the craniojunction are:

1. the paired alar ligaments that extend from the odontoid peg to the medial aspect of the occipital condyles
2. the posterior longitudinal ligament that runs posterior to the vertebral bodies and extends as the tectorial membrane to insert into basion
3. the anterior longitudinal ligament that runs anterior to the vertebral bodies and extends as anterior atlanto occipital membrane to insert into the basion
4. the transverse atlantal ligament that extends between the lateral masses of C1, passing posterior to the odontoid peg.

Occipitocervical dissociation

occipitocervical dissociation which is also known as atlanto-occipital sublaxation is easily missed on plain radiography, and is potentially fatal!

It maybe

• type 1 - anterior sublaxation
• type 2 -vertical distraction of atlanto-occipital joint more than 2 mm, or
• type 3 - posterior dislocation

CT Brain pearls -1

CT features suggesting elevated ICP include:

• effacement of basal cisterns
• loss of grey-white differentiation
• loss of sulci
• midline shift
• herniation of cerebellar tonsils into the foramen magnum
• uncal herniation

The features of uncal herniation are:

• shift of the brainstem and distortion of adjacent cisterns
• dilatation of contralateral temporal horn
• compression of the posterior cerebral artery as it crosses the tentorium, causing a posterior cerebral artery territory infarct

PATTERN OF BRAIN HERNIATION

• Uncal transtentorial herniation: the uncinate process of the temporal lobe herniates into the anterior part of the opening of the tentorium cerebelli.
• Central tentorial herniation: there is symmetrical downward movement of the thalamic region through the opening of the tentorium cerebelli
• Subfalcine herniation: there is displacement of the cingulate gyrus under the falx and across the midline
• Foraminal herniation: there is downward herniation of the cerebellar tonsils into the foramen magnum

The level of foramen magnum is measured on the saggital T1 image. It is defined as a line between the front (basion) and the back (opisthion) of the foramen magnum. The signal of cortical bone, not marrow must be used to define these landmarks.

Brain herniation

There are two type of cerebral oedema:

1. Cytotoxic: intracellular oedema caused by cell swelling with an intact blood brain barrier. Cytotoxic oedema affects predominantly grey matter, with subsequent loss in grey-white matter differentiation. It generally accompanies stroke and hypoxia and gives a pattern of "restricted diffusion" on MRI sequences

2. Vasogenic: extracellular oedema caused by loss of integrity of the BBB. Vasogenic odema predominantly affects white matter and spreads along white matter tracts, accentuating the grey-white matter differentiation. It generally accompanies inflammatory disease and brain tumors. It does not give a pattern of "restricted diffusion" on MRI sequences.

http://en.wikipedia.org/wiki/Brain_herniation

Radiological signs suggesting aortic disruption

Hi again,
This week I am studying radiology. Certain essential knowledge must be remembered by heart. There is a classic constellation of signs on the chest X-Ray associated with aortic injury. (Clarke 1977):

1. Displacement of trachea and NG tube to the right
2. Wide upper mediastinum
3. Left pleural cap
4. Loss of aorto-pulmonary window, the space on the left mediastinal border between the aortic knuckle and the pulmonary artery.
5. Indistinct outline of aortic knuckle
6. Depression of left main bronchus
7. Fracture of first or second rib
8. Left haemothorax
9. Loss of paratracheal stripe

CT angiography, TEE or DSA would be acceptable for investigation of a possible traumatic rupture of the aorta. MRA may be used, but the requirement for prolonged investigation in a suboptimally monitored environment limits its usefullness.

Differential diagnosis of weakness in ICU

Weakness in ICU is another common case during the clinical exam. I have found this in one of my books and I thought that it might be useful in helping me to organise my thought in synthesising the diagnosis during that time. Critically ill patient frequently have ICU myopathies and polyneuropathy. Weakness is common with SIRS and organ transplantation. Steroids, muscle relaxants and prolonged ventilation increase risk. MRI or CT scan, EMG and muscle biopsy may guide diagnosis.

1. Critical illness: - Clinical illness neuropathy, Myopathy of Intensive Care
2. Autoimmune: -Guillain-Barre syndrome, Myasthenia gravis, Dermatomyositis, Polymyositis
3. Nutritional: -Increased catabolism and wasting, undernutrition
4. Electrolyte disorders: -Phosphate, -Mg, K, Na
5. Endocrine disorders:-Hyper and hypo-thyroidism
6. Infection: -Botulism, poliomyelitis, tetanus, diphtheria, HIV, West Nile, Creutzfekdt-Jacob
7. Toxins: -Organophosphates, lead, tick paralysis, beliadonna
8. Drugs: -Muscle relaxants, steroids, magnesium, aminoglycosides, dapsone
9. CNS injury: -Stroke, spinal cord injury
10. Congenital: -Muscular dystrophy, periodic paralysis, motor neuron disease, spinal muscular atrophy, Tay-Sachs, Lower motor neurone syndromes, myotonia, acute intermittent porphyria
11. Metabolic: -alkalaemia
12. Paraneoplastic: Eaton Lambert syndrome, proximal myopathy

Causes of generallised muscle weakness, hyporeflexia and no sensory signs:

• Guillain Barre Syndrome
• Myasthenia Gravis
• Botulism
• Toxic Neuropathy : thallium, arsenic, hexane
• Acute intermittent porphyria
• Tick paralysis
• Lyme disease
• Poliomyelitis

Q: How would you differentiate a myopathy from a neuropathy clinically?

A: Distinguishing features:

1. Neuropathy

• site of weakness: distal
• sensory: may have concomintant sensory and signs
• reflexes: reflexes lost early
• fasciculations: may be present
• contractures: not a feature
• myocardial dysfunction: not a typical feature

2. Myopathy

• site of weakness: usually proximal
• sensory: usually pure motor
• reflexes: preserved until late
• fasciculations: not typical
• myocardial dysfunction: may have accompanying cardiac dysfunction witn the dystrophies

A young lady presents with a short history of progressive difficulty in walking, and now has shortness of breath. She was brought to DEM with RR 32 b/min, oxygen saturation of 90% on room air. Neurological examination reveals normal higher mental function, reduce power in all four limbs, left sided ptosis, absent DTRs, bilateral plantar responses and no sensory loss.

Q: How would you asses her clinically at this stage?

A: ability to protect, bulbar weakness, pooling of salive and ability to cough

B: evidence of shallow breathing, bilateral chest expansion, focal lung signs

C: evidence of autonomic dysfunction

D: neurological examination

Baseline bloods, ABG

get the past history, examination

In this case the most likely diagnosis is GBS

Q: What conditions may precede or trigger GBS?

A:

i. often preceded by URTI or diarrheal illness caused by various pathogens such as -CMV, EBV, HSV, mycoplasma, chlamydia, campylobacter jejuni.

ii. vaccines - rabies, swine flu

iii. pregnancy

iv. surgery

v. cancer (Hodgkin's disease)

Q: What are the indications for ICU admission?

A:

-rapid progression of symptoms

-aspiration

-bulbar dysfunction

-bilateral facial weakness

-neck weakness with inability to raise head against gravity

-significant dysautonomia

-evidence of respiratory failure

Q: what are the various monitoring parameters you would use to make a decision to intubate this lady?

• Inability to protect airway
• significant hypoxia or hypercarbia
• bedside assessment of respiratory muscle weakness, such as increased RR, decreased VT, paradoxic inward movement of abdomen during respiration, use of acessory muscles, ineffective cough
• 20-30-40 rule (Lawn et al.)

-VC <>

Glutamine and Arginine in ICU nutrition

I want to make a note on arginine and glutamine today, just for me to remember some important points if asked during viva.
Glutamine

• serves as an oxidative fuel and nucleotide precursor for enterocytes and immune cells, mainly lymphocytes, neutrophils and macrophages.
• regulates the expression of many genes related to signal transduction and to cellular metabolism and repair.
• During critical illness glutamine is released in large quantities from skeletl muscle in order to supply this need. In these circumstances it may become 'conditionally essential' and is vulnerable to depletion, with potentially adverse effects on gut barrier and immune function which may in turn impair the ability to survive a sustained period of critical illness once glutamine stores are depleted.
• Evidence is debatable. Reductions in infectious complications and length of ICU stay were shown in small early studies of enterally fed trauma and burns patients. A larger study in unselected ICU patients found no effect on any outcome. (Intensive Care Med 2003).
• The evidence for TPN is contradictary. There are suggestions from meta analysis that there is a demonstrable mortality benefit from higher doses of parenteral glutamine (http://www.criticalcarenutrition.com/). This awaits confirmation in a large RCT. It seems that the patients most likely to benefit are those requiring TPN for more 10 days.

Arginine

• a non-essential amino acid acts as a precursor of NO, polyamines (important in lymphocyte maturation) an nucleotides.
• Animal studies suggest enhanced cell mediated immunity and survival when arginine is supplemented.
• Several commercially available enteral feeding solutions combine omega 3 fatty acids, arginine, nucleotides and in one case glutamine to produce imune enhancing diets. They have been assessed in a number of trials. Meta-analysis has suggested reductions in hospital stay and infections but not in mortality.
• Subgroup analysis revealed an increase in mortality when arginine supplementation was given to septic patients (JAMA 2001). Interim safety assessment of a RCT led to its early cessation when this finding was replicated in the subgroup of patients with sepsis (Intensive Care Med 2003). It appears that arginine should not be used septic patients. There are suggestions of benefit in patients undergoing surgery or suffering from a burn injury, there is little basis for their general use in ICU patients unless it is justified by future prospective trials.

Reference: Oh Intensive care manual

Please refer to recent post for the update

Steroid for Acute Traumatic Spinal Cord Injury

This article just to help me in giving my evidence during management of traumatic SCI
Methylprednisolone is the only treatment that has been suggested in clinical trials to improve outcomes in patients with acute traumatic, nonpenetrating SCI. It has been shown that in animal studies, glucocorticoids reduces edema, prevents intracellular potassium depletion, and improves neurologic recovery.

Two blinded randomized controlled trials studied the efficacy of glucocorticoid therapy in patients with acute SCI.
1. The National Acute Spinal Cord Injury Study (NASCIS) II compared methylprednisolone (30mg/kg I.V., followed by 5.4mg/kg/hr over 23hours), Naloxone and placebo in 427 acute SCI patients. (J.Neurosurgery 1992;76(1))
At one year, there was no significant difference in neurologic function among treatment groups. However, within the subset of patients treated within eight hours, those who received methylprednisolone had a modest improvement in motor recovery compared with those who received placebo. Wound infections were somewhat more common in patients who received methylprednisolone.
2. NASCIS III compared three treatment groups: methylprednisolone administered for 48h, methylprednisolone administered for 24h, and tirilizad mesylate (a potent lipid peroxidation inhibitor) administered for 48 hours in patients with acute complete or incomplete TSCI. (J Neurosurg. 1998;89(5)). All 499 patients received an initial IV bolus of 30mg/kg methylprednisolone and were treated within 8 hours of TSCI. For patients treated between three hours, there was no difference in outcomes among treatment groups at one year. For patients treated between 3 to 8 hours, 48 hours of methylprednisolone was associated with a greater motor but no functional recovery, compared to other treatments. Patients who received the longer duration infusion of methylprednisolone had more severe sepsis and severe pneumonia compared with the shorter duration of infusion; mortality was similar in all treatment groups.

Data analysis led to the conclusion that the risk of high dose steroids outweight their benefits, and this therapy has been abandoned by many medical centres. A Consortium for Spinal Cord medicine concluded that no clinical evidence exists to definitely recommend the use of steroid therapy. (www.pva.org paralysed veterans of America)

Community Acquired Pneumonia

This week is another busy week since the third block of undergraduate medical students are starting their new session this coming Monday. I have to ensure the course guideline, log books and rosters are ready by then. I am just helping the department, yes the department (not MY department). I am having problem with someone, let me correct it not just me..at least there are two more members feel the same way......"Please" costs nothing, "Sorry" costs your pride, "I forgive you" liberates you from the shackles of prejudice.

The mortality of CAP patients admitted to ICU is about 35%. About 20% of patients admitted to ICU with CAP are in septic shock, with mortality as high as 60%.
The presence of comorbidities below contribute significantly to mortality and also alter the etiologic organisms underlying the infection.

1. COPD
2. asthma
3. diabetes mellitus
4. renal insufficiency
5. congestive heart failure
6. coronary artery disease
7. malignancy
8. alcoholism
9. age>70years
10. chronic nerological disease
11. chronic liver disease

The most common pathogens are:

1. Strep pneumonia
2. Legionella species
3. Staphylococcus aureus
4. Haemophillus Influenza
5. Gram negative bacilli

Pathogens associated with underlying comorbid condition:
1. S.pneumonia

• Dementia
• congestive heart failure
• COPD
• Cerebrovascular disease
• Institutional crowding
• seizures

2. Penicillin resistant and drug resistant pneumococcus

• age>65
• alcoholism
• immunomodulating illness or therapy (including steroids)
• Previous B lactam therapy within 3 months
• Multiple medical comorbidities
• exposure to child in day care centre

3. Enteric gram negatives

• residence in long term facility
• underlying cardiopulmonary disease
• recent antibiotic therapy
• multiple medical comorbidities

4. Pseudomonas aeruginosa

• broad spectrum antibiotics for > 7 days in the past month
• structural lung disease (bronchiectasis)
• corticosteroid therapy
• malnutrition
• undiagnosed HIV infection
• netropenia

5. Legionnaires' disease

• AIDS
• haematologic malignancy
• end stage renal disease

Non infectious diseaseas masquerading as CAP should be excluded:

1. Cryptogenic organizing pneumonia (COP)
2. Eosinophilic pneumonia
3. Hypersensitivity pneumonia
4. Drug induced pneumonitis: methotrexate, nitrofurantoin, gold, amiodarone etc
5. Pulmonary vasculitis
6. PE/ infarction
7. Pulmonary malignancy
8. Radiation pneumonitis
9. TB

The following are the major reasons for a failure to respond to anti microbial agents:

1. Wrong antibiotic: wrong spectrum or drug resistance. Wrong dosage
2. Viral, fungal, or opportunistic pathogen.
3. Unusual pathogens
4. Superadded complication
5. Complicated pleural effusion/ empyema
6. endocarditis
7. Purulent pericarditis
8. Septic arthritis
9. Meningitis
10. Exclude masquerader
11. Consider CA-MRSA in toxic patients and those with severe disease.

Unusual pathogens

1. Coxiella burnetii - cats, goats, sheep, cattle
2. Tularemia - rabbits, ticks
3. Leptospirosis -rats
4. Hantavirus - rats
5. SARS
6. Psittacosis - birds
7. Nocardia - steroids
8. Aspergillus -steroids
9. Pneumocystis jiroveci -immunosuppression
10. Dimorphic fungi -recent travel
11. Burkhodelria pseudomallei -recent travel
12. TB

Complicated Pleural effusions -
drainage is necessary if the pleural fluid is grossly purulent or if pleural fluid show the following

• pH less than 7.2
• Glucose less than 2.2mmol/l
• WCC > 10,000/ml

Delirium

Delirium is defined in the American Psychiatric Associations Diagnostic and Statistical Manual of Mental Disorders as a disturbance of consciousness and cognition that develops over short period of time (hours to days) and fluctuates over time.
Many different terms have been used to describe the syndrome of cognitive impairment in critically ill patients include:
ICU psychosis, acute confusional state, ICU encephalopathy and acute brain syndrime. However, ICU delirium is the preferred term.
Important of delirium:
ICU delirium has been demonstrated to be an independent predictor of the length of hospital stay as well as ICU and 6-month mortality rates.
As many as 70-80% of ICU patients experience delirium. It is the most common mental disorder among elderly patients in the ICU. Sleep deprivation, sepsis, hypoxaemia, use of physical restrains, fluid and electrolytes imbalances, and metabolic and endocrine derangements have been implicated in the causation of delirium. On average, ICU patients sleep only 2 hours/day and less than 6% of their sleep is REM sleep.
Delirium is characterised by fluctuating disturbance of consciousness, cognition, concentration, memory and attention. Delirium can be categorised into subtypes according to psychomotor behaviour. Hypoactive delirium is characterised by decreased responsiveness, withdrawal and apathy. Whereas, hyperactive delirium is characterised by agitation, restlessness, and emotional liability.
Peterson and coworker observed that in a cohort of ICU patients; pure hyperactive delirium was rare (1.6%). In contrast, 43.5% of patients had purely hyperactive delirium and 54.1% had mixed delirium.

Mneumonics for Clinical Picture
Disordered thinking
Euphoria, fearful, depressed or angry
Language impaired
Illusions/delusions/hallucinations
Reversal of sleep-wake cycle
Inattention
Unaware/disoriented
Memory deficit

Important aetiologies of delirium:

Demented or elderly/Disturbed sleep/Dehydration
Electrolyte disturbance/Emotional stress
Lung or Liver failure
Intubation and ventilation
Renal failure
Infection/Injury
Use of catheters (e.g. venous or bladder) or physical restrains
Metabolic problems (e.g. thyroid)/Medication/Malnutrition

Delirium Assessment:
The Intensive Care Delirium Screening Checklist (ICDSC) being the most validated. It is an eight item delirium checklist (Bergeron, Intensive Care Medicine 2001).
The score of 1 is given if each of the following elements is met:
1. Altered level of consciousness: -non-responsive, poorly responsive, drowsy, or hypervigilant
2. Inattention -difficulty following instruction, cannot focus
3. Disorientation
4. Hallucinations, delusions, or psychosis
5. Psychomotor agitation or rertardation - hypo or hyper activity
6. Inappropriate speech or mood -inappropriate, disorganised or incoherent speech or inappropriate display of emotion
7. Sleep-wake cycle disturbance -sleep less than 4 hours or waking frequently at night
8. Symptom fluctuation
A SCORE OF 4 OR MORE IS CONSIDERED INDICATIVE OF DELIRIUM.
==> All patients should be regularly screened (8 hourly) for the presence of delirium.
The second validated tool is Confusion Assessment Method for the ICU (CAM-ICU) which is easy to use and requires minimal training.

Management:
1. Patient orientation and preservation of the sleep-wake cycle are important to minimise the risk of delirium.
2. Sedation with benzodiazepines should be avoided. Benzodiazepines SHOULD NOT be used for the treatment of delirium.
3. Dexmedotemidine is a promising drug for the prevention and treatment of delirium.
4. Haloperidol is recommended as the drug of choice for the treatment of delirium by the society of critical medicine (SCCM) and the American Psychiatric Association.
5. Melatonin has been suggested to reset the internal circadian rythm and sleep-wake cycle and may have a role in the treatment and prevention of delirium in ICU patients. Bourne and colleagues demonstrated that melatonin given at night increased the duration of sleep. The recommended dose is 2 mg.

interesting website: www.icudelirium.org