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"The Knowledge we take into our shifts does matter"
The case has been adapted from a case report(1) for teaching.
This is the case of a patient in his 50's brought in by ambulance, with a feeling of generalised weakness and inability to walk. The patient had presented to the emergency department earlier that day, but at this time was able to walk, although with some difficulty. He had also presented to the emergency department for each of the last two days, initially with complaints of numbness in the mouth, loss of taste, back stiffness and diplopia. This was on the background of an original illness of a sore throat, cough and a runny nose 3 days prior. He then developed weakness in the arms which progressed to the legs and then a generalised weakness and some generalised discomfort.
He had no past medical history of note, was on no medications and had no allergies.
What is your differential diagnosis at this point?
Could this be a stroke or something else?
On examination he was alert and oriented, but with some slurring of his speech.
Heart sounds were dual, chest was clear and abdomen was soft.
A neurological examination demonstrated a pronator drift with an abnormal cerebellar examination including past pointing and dysdiadochokinesea. The lower limb examination showed normal tone and sensation, with decreased power of 4/5 and loss of reflexes. Gait could not be examined.
His cranial nerve examination demonstrated a lateral rectus-like palsy, nystagmus on lateral gaze, with bilateral ptosis. The Facial nerve was intact.
Has your differential changed at all?
Could this be cerebellar ischaemia, thyroid disease, myasthenia Gravis, Wernicke's or something else?
Investigations were performed.
He had normal labs ie., all of FBC, EUC, LFT, TSH, ECR, CRP, Cardiac markers and HIV screening were all normal.
A chest x-ray and CT Brain with contrast was also normal.
It was decided to lumbar puncture the patient. The results showed a mildly elevated protein with cytoalbuminologic dissociation (raised protein and low cell count).
Serum antibodies to GQ1b return, confirming a diagnosis of Miller-Fisher Syndrome (A Guillain-Barré syndrome variant). The patient is commenced on IV immune globulin. He improves.
What is Miller-Fisher Syndrome?
It is one of the variants of Guillain-Barré syndrome.
It is characterised by:
TheGQ1b ganglioside complex is positive in > 90% of patients with this syndrome.
Watch the 4 minute video below of Dr Adam Michael presenting this variant of Guillain-Barré syndrome at EMCORE.
Ilya V et al Miller Fisher Syndrome: A Case Report Highlighting Heterogeneity of Clinical Features and Focused Differential Diagnosis. Hawaii Journal of Medicine and Public Health. July 2016, Vol 75, No 7 pp 196-199.
This review first appeared on Resus.com.au and is based on a great journal article just published (1)
The most common hip dislocation is a Posterior Dislocation
The most common Cause of a posterior hip dislocation is:
The affected leg is shortened and internally rotated. It may be held in adduction
There are many reduction techniques, shown in the feature article and in the literature. Some of the techniques require flexibility, dare I say even contortion ability, by the clinician. They may be too difficult to use. My aim here is to choose the easiest techniques to apply.
The keys to reduction:
Here are three of my favourite techniques:
THE WHISTLER TECHNIQUE (4)
I sometimes call this the under-over technique. It's my favourite technique.
THE ROCKET LAUNCHER (5)
The first version of this that I saw, appeared quite dangerous for the patient. In that version, the clinical was at the end of the bed and the patient's unaffected limb, hung off the end , with the other limb on the doctors shoulder.
A better form is the following:
THE MODIFIED ALLIS (6)
This was the original technique I used, when I worked in a single doctor emergency department. I stood on the bed and the patient's hip and knee were flexed at 90 degrees. I used to then pull upward on the leg, applying traction. It worked, but was potentially quite dangerous for me. I nearly came off the bed on several occasions.
This is a much better and safer version.
Below is a case with 8 MCQ questions that address the anticoagulation management of atrial fibrillation/flutter. Try them. (Originally published on the RESUS Blog)
A 60 yo male presents to the Emergency Department with palpitations. He has had palpitations in the past. On a recent presentation to the emergency department, with the same complaint, the patient was found to be in atrial fibrillation, which self reverted within 9 hours of commencement.
His only past medical history is hypertension.
His ECG is shown below.
Q1. What does the ECG show?
(a) Sinus Tachycardia
(b) Atrial Fibrillation
(c) Atrial Flutter
(d) AV Nodal Re-entry Tachycardia
Q2. You send the ECG to the Cardiologist on call. Cardiology recommend that you perform a Lewis Lead/ECG. What does a Lewis Lead ECG do?
(a) It allows differentiation between AVNRT and AVRT
(b) It detects atrial activity
(c) It allows the diagnosis of long QT to be made
(d) All of the above
b. The Lewis Lead detects atrial activity. It is used when P wave may not be readily seen.
It is especially useful in:
Q3. You diagnose Atrial Flutter. What is the best option from those shown below to treat this arrhythmia?
(a) Vagal Manoeuvres
(d) DC Cardioversion
d. DC Cardioversion, usually at 100J will be adequate to cardiovert. A lower energy level is required to revert atrial fibrillation, which is the most resistant arrhythmia and usually requires 200J.
Vagal Manoeuvres do not usually revert atrial flutter, even though they may be effective against SVT.
Adenosine will block the AV node and thus block ventricular response, uncovering the P waves.
Q4. The atrial flutter is treated. Given the patient's history of atrial fibrillation, should the patient be anticoagulated?
(a) No as the episode of atrial fibrillation lasted less than 24 hours
(b) No as the atrial flutter is reverted and he has no stroke risk.
(c) Yes as the patient's CHAD2DS2VASc score is > 1
(d) Yes but only if the patient has diabetes
c. The patient has hypertension and thus scores 1 on CHAD2DS2VASc, so will probably need anticoagulation for life.
Q5. The patient represents to the Emergency Department 3 weeks later, at 2pm, for an unrelated reason. Following the previous presentation, he was cardioverted and commenced on Apixaban. He has forgotten to take his morning 7am dose of Apixaban. It is now 5 hours, since he was due to take his dose. He asks what he should do?
(a) Do not take the NOAC, but take a bridging dose of enoxaparin
(b) Do not take the dose, but double the next dose.
(c) Take the missed dose immediately.
(d) Change the NOAC to a single daily dose medication
c. As per the 2021 European Heart Rhythm Practical guide on Non-Vitamin K management of ainticoagulated patients Europe (2021) 23, 1612-1675
Q6. In general, which of those shown below is a definite contraindication to a NOAC?
(a) Mild Aortic Stenosis
(b) Moderate to Severe mitral regurgitation
(c) A bio prosthetic valve
(d) A transcatheter aortic valve implantation
Q7. The same patient presents to the emergency department 1 month later, still on Apixaban. His complaint is a toothache with a swollen jawline. You diagnose a tooth abscess and commence antibiotics. You refer him back to his dentist for a tooth extraction. In which of the following cases should NOACs be withheld?
(a) Simple Tooth Extraction
(c) Liver Biopsy
(d) All of the above
Minor risk interventions include:
Q8. The same patient presents to the emergency department 3 months later, still on Apixaban. He has a severe headache. A CT reveals an intracranial haemorrhage. Whish of the following is correct?
(a) Immediate reversal with Idarucizumab 5mg IV is needed which can be given as two consecutive infusions of 2.5mgIV over 5 minutes( or as bolus)
(b) Fresh Frozen Plasma
(c) Andexanet Alpha at 400mg (at 30mg/min) bolus, followed by an infusion
(d) Coagulation factors VII IX, X, must be given
Idarucizumab is for Dabigatran reversal.
FFP does not work as well and Coagulation factors don't need to be given.
Steffel J et al. 2021 European Heart Rhythm Association Practical Guide on the Use of Non-Vitamin K Antagonist Oral Anticoagulants in Patients with Atrial Fibrillation. Europe (2021) 23, 1612-1676.
In a recent paper by Driver et al (1) there was a comparison of Ketamine-Only intubation with topical anaesthetic and traditional RSI. The primary outcome was 1st attempt intubation success and it was found that Ketamine only intubation had the worst success rate of all the techniques and it also had the greatest incidence of adverse events, which included cardiac arrest, airway injury, hypotension and hypoxia. This is an excerpt from a review on the RESUS Blog
What they did
ConclusionKetamine only intubation had a lower first pass success rate and a higher rate of adverse events.
My take on this
Perhaps the most important part of this is to understand why you might use this and to be knowledgeable as to how to use it. What we need to do, is define a group of patients where this might be used.
Read about Ketamine-only breathing intubation.
This is a review of a recent paper in JAMA Cardiology:
Hauw-Berlemont C et al. Emergency vs Delayed Coronary Angiography in Survivors of Out of Hospital Cardiac Arrest. Results of the Randomised, Multicentric EMERGE Trial. JAMA Cardiol. 2022;7(7):700-707. (1)
Our assumption would be that most patients would benefit from coronary angio post survival from cardiac arrest. Let's put it into context. Our goal is to have neurologically intact survivors.
This authors of this research wanted to determine, if there was any benefit (and which patients might benefit the most) in early coronary angiography in patients with output following out of hospital cardiac arrest if there were no ECG changes consistent with acute infarction.
Previous randomised trials have shown no difference in survival between immediate vs delayed coronary angiography. However registry studies have suggested benefit form early intervention.
A 72 yo patient normally otherwise well, collapses at home. It is not witnessed, however the patient's wife is in the next room. She calls the ambulance and commences CPR.
On ambulance arrival, the patient is in PEA, that progresses to Asystole, then PEA again and then a sinus rhythm. He has been treated with 3 doses of Adrenaline.
On arrival to the Emergency Department, he is intubated and has output. His pupils are non reactive and his initial VBG has a pH or 7.12.
What would you rate the chance of good neurological outcome here; low, intermediate or high?
Let's look at the results of this paper.
What they Did
Patients were randomised following out of hospital cardiac arrest, with no obvious cause such as trauma, to receive either emergency vs delayed coronary angiography.
The Primary Endpoint was 180 day survival with good neurological outcome.
Secondary endpoints included shock, VT/VF, Survival, length of hospital stay.
There was no difference in overall survival rate with good neurological outcome at 180 days between the two groups (36.2 vs 33.3%)
The study was underpowered.
Why do the registry studies results differ so much?
Firstly, we have seen discrepancies between randomised trials and registry studies in the past.
The selection process in the registry studies may differ, as these patients will undergo selection at the Paramedic and the Emergency level. Decisions about their survival or otherwise are made at those points.
The registry studies found that those with less benefit where those with a higher risk of poor neurological outcome. This might be expected.
Let's go back to our case
There are several scoring systems that we can use to determine potential neurological outcome.
One of those is the MIRACLE2 score(2).
The score has some limitations. It was derived from a restrospective chart review. However it determines 7 variables as being important in making predictions on neurological outcome. See below:
If we don’t enter a discussion about the utility of pupillary reflex following adrenaline, or acidosis secondary to adrenaline and simply apply the score to our 72 yo patient above.
The score would be a 7/10 ie., a high risk of poor neurological outcome.
At high scores, the positive predictive value of MIRACLE2 is about 92%.
At present we should watch this space. There appears to be no benefit in sending patients to the Cath lab for out of hospital cardiac arrest, if there are no ECG findings of an acute infarction. However younger patients with early CPR and defibrillation, should perhaps still go for early coronary angiography, until we have a better answer.
The diagnosis of pulmonary embolism(PE) is an almost common occurrence in the emergency department. The question of which patients to thrombolyse can be a difficult one to answer. Certainly there is consensus over patients with massive PEs needing thrombolysis. The same cannot be said for those patients with a submissive PE, because our greatest fear is the complication of intra-cranial haemorrhage.
CASEA 78 yo male presents with shortness of breath. He has a past medical history of hypertension. His vitals are HR 114, BP 128/80,RR 28, Sats 91% on room air. He has no chest pain and is sitting up feeling very comfortable with supplementary oxygen.
Should this patient be offered thrombolysis? Would you give thrombolysis?
Let’s begin by defining the different sizes of PE.
Massive PETraditionally this has been defined by the angiographic burden, however a more appropriate definition may be related to what we see clinically. I prefer the American Heart Association(AHA)(1) definition:
“Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).”
Submassive PESubmassive PE is defined by the AHA(1) as:
“Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis.”
1 RV dysfunction means the presence of at least RV dilation or RV systolic dysfunction on echocardiography, RV dilation on CT, Elevation of BNP (>90 pg/mL), Elevation of N-terminal pro-BNP (>500 pg/mL); or
2 Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)
3 Myocardial necrosis is defined as either of Elevation of troponin I (>0.4 ng/mL) or Elevation of troponin T (>0.1 ng/mL)
Who Gets Thrombolysis?It’s generally accepted that massive pulmonary embolism gets thrombolysed, although there may be some contraindications. What do we do with submassive PE’s? Are some of them deserving of lysis? Until now it has been accepted that those patients with haemodynamic stability and RV dysfunction and myocardial necrosis should be candidates for thrombolysis.
There is no doubt that the use of thrombolytic significantly reduces clot size. This may have the direct result of decreasing pulmonary pressures, which may themselves lead to future complications. However, there is no significant effect on patient mortality(2). In fact, in normotensive patients thrombolytics are associated with increased mortality(3), with the primary complication being intracranial haemorrhage, in up to 6.4% of patients(4).
There are several trials, however two are considered major trials, the MOPETT and the PEITHO trials. Even with these, the question still hasn’t really been answered. The two trials use a different type of lytic agent and different endpoints.
The MOPETT Trial(5)This trial wanted to address the concerns of full dose thrombolysis and potential intracranial bleeding, by proposing a ‘safe dose’ of 0.5mg/kg to a maximum of 50mg (50%) of the regular dose of tPA. It was given as 10mg over one minute and the rest within a 2 hour period.
This was a single centre, small numbered study, that really didn’t find any statistically significant results in reduction of pulmonary hypertension. It is questionable as to whether the patients chosen, were all appropriate, as not all met the criteria of submissive PE. What did come out of it was that there were no cases of intra-cerebral bleed with half dose tPA. This is a very important finding.
The PEITHO Trial (6)This was a trial of 1006 patients treated with Tenecteplase. Although the results didn’t for the most reach statistical significance, the trend towards haemodynamic compromise was much higher in the placebo group than the Tenecteplase group. The rate of major bleeding was 6.3% in the thrombolytic group and the rate of intra-cranial bleeding was 2% with tenecteplace versus 0.2% with placebo. Those at greater risk appeared to be those patients older than 75 years.
Pulmonary Embolism Severity IndexThe Pulmonary Embolism Severity Index is a validated score that provides independent predictors of 30 day mortality and can be used to determine those patients at higher risk(6). This may help us in determining those patients that will have a worst outcome if not treated.
The scoring system is shown below:
How does this apply to our patient?
The patient in the case above, would fall into the HIGH RISK group in terms of poor outcome. He would score a 78(age) + 10(male) + 20(HR) =108. Thrombolysis should be considered in him, however I would consider half dose if tPA were being given and would get advice on Tenecteplase.
My Overall Approach
Given the risk of intra-cerebral bleeding I would thrombolyse only massive PE’s. In those that are haemodynamically stable I would look for RV strain or cardiac necrosis, I would still probably only anticoagulant that submissive PE group, and use thrombolytics if their haemodynamic status began to be compromised.
The alternative is to calculate a PE Index and decide and then probably give half dose thrombolytic to the high risk group. Further, I would consult with a pulmonary hypertension expert……yes you heard right. They are at the large tertiary centres and give advice on this very matter.
What about special cases?
Recent SurgeryThe risk of bleeding if patient have had recent surgery is significant in the first 2 weeks after surgery. That risk falls two weeks following surgery.
Is all surgery the same? No, brain or spinal surgery does not carry the same risks.
Please consult with the surgeons prior to giving.
What about PE in pregnancy?
Massive PE should be treated with thrombolysis.
Submassive PE should be treated with LMWH (warfarin has teratogenic effects)
If there is a high risk of bleeding then consider IVC filter.
There is some concern with giving thrombolysis within 3-6 months of ischaemic stroke, in an increased rate of intracranial haemorrhage(7), although the evidence does not appear to be consistent. Specialist advise should be sought.
Space Occupying Lesions
There appears to be an increased risk of haemorrhage in all except meningiomas(8). Expert advice should be sought.
Once you've read the summary below, come back and watch this lecture from 2017.
10% of strokes are due to intracerebral haemorrhages (ICH). This type of stroke has a mortality of 30-40%. It increases with age and with anticoagulation. Approximately 73% of ICH is attributable to uncontrolled hypertension.
Two cerebral small vessel pathologies that account for the majority of ICH are; arteriosclerosis and cerebral amyloid angiopathy.
How do Bleeds cause brain injury?
Brain tissue is injured by:
CT is the most widely used modality to rule out ICH. It also provides useful information on haematoma volume. Haematoma expansion usually occurs within the first 24 hours and is an independent predictor of increased mortality.
Repeat CT to evaluate haematoma expansion and oedema, is helpful especially if the patients neurological status deteriorates.
Investigation of the cause of the ICH is important as it may affect acute treatment and prognosis.
Patients who are <70yo and who have not had a hypertensive deep territory ICH, have a 1 in 4 to 1 in 7(depending on age) chance of an underlying vascular cause such as:
Catheter intra-arterial DSA is the gold standard for determining the macrovascular cause with highest yield being for:
Blood Pressure Control
Patients with acute ICH present with increased BP, which is associated with haematoma expansion, neurological deterioration and mortality.
Should we treat raised Blood Pressure? The results from major trials have been equivocal.
There are 2 major trials:
Studies have also shown that large reductions ie >60mmHg in the first hour was associated with worst outcomes. Therefore lowering the SBP too quickly should be avoided.
Smooth continuous lowering of blood pressure to a systolic blood pressure of 130-140mm Hg in acute ICH and SBP of 150-220mm Hg, is safe and may improve functional outcome.
Avoid lowering the SBP to < 130 mm Hg as it could be potentially harmful.
The BP lowering drug used should have a:
The RIGHT-2 (Rapid Intervention With Glyceryl Trinitrate in Hypertensive Stroke Trial), used transdermal nitroglycerine in ambulance, had worst outcomes with larger haematoma and oedema volumes. Venous vasodilators may be harmful due to unopposed venodilatation and its effects on haemostasis and ICP.
Haemostasis and Coagulopathy
Haemorrhage expansion and poor outcome is increased in patient with ICH on anticoagulation. Rapid reversal is required.
If the patient is on Warfarin (Vitamin K antagonist)
Antiplatelet therapy at time of haemorrhage has been associated with increased mortality and an unfavourable functional outcome.
There is no evidence that platelet transfusions, Desmopressin and TXA result in benefit to patients with ICH on antiplatelets.
One group which might benefit are those that are receiving an emergency craniotomy for haematoma removal. Platelet transfusion may reduce postoperative haemorrhage volume.
30% chance of developing a significant arrhythmia.
Older patient with large bleed ie >5cm had a higher likelihood of developing an arrhythmia. Most are in the first 24-72 hours.
Fever in ICH is associated with increased clinical severity and worst outcomes. There is not great evidence that treating fever results in better outcomes.
Therapeutic hypothermia and other means of reducing temperature are a means of reducing perihaematoma oedema, however no clinical benefit has been demonstrated.
Seizures and Antiseizure Medications
New onset seizures in ICH occur in about 28% of patients and tend to occur in the first 24 hours.
The benefit of prophylactic use of anti-seizure medication is unclear.
Small studies initially showed some benefit with Sodium Valproate and worst outcomes with Phenytoin
Recent studies have not shown consistent harm or benefit.
Neuroinvasive Monitoring, ICP and Oedema Management.
Ventricular drainage should be performed in intraventricular haemorrhage.
Hyperosmolar therapy can be used to transiently reduce intracranial pressure, however the use of prophylactic hyperosmolar agents is uncertain.
Corticosteroids should not be administered for treatment of elevated ICP in ICH.
ICH score has been used for severity, but its use in clinical practice has not been clarified.