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I have completed bits of my EM training from India. Currently I am boarded with credentials from Christian Medical College, Vellore and also from the prestigious Royal College of Emergency Medicine, UK.  I am currently working in London as an A&E doctor, trying to appreciate the differences in the practise and culture of Emergency Medicine across different healthcare systems. I have always been an avid FOAMed supporter because FOAMed played an indispensable role during the days of my initial training. Through this blog, I aspire to disseminate knowledge and stay up to date with the EM literature. 

Monday, January 25, 2016

The Intracerebral Bleeder

Intracerebral haemorrhage (ICH) is a subtype of stroke AKA Haemorrhagic stroke. Often the outcome turns out to be dismal and unfortunately we cannot do much about it. But luckily ICH makes up only about 10-15% of the total strokes and it is a neurosurgical emergency where we need to act fast and do the best to at least prevent the secondary brain injury. There are two schools of thought about this depending on the circumstances in which you are working. Some physicians go all out and do everything possible for these patients while others have a pretty nihilistic attitude about this. 

Regardless of these, there are some things that we must do in the initial few hours of intracranial haemorrhage that can possibly change the outcome of these patients. Let us go through each one of them.

Rapid and accurate diagnosis using neuroimaging
First and foremost, we should always suspect ICH in anyone presenting with acute CNS symptoms. Some patients might walk into the ED if they have a small bleed but usually they have other worrisome symptoms like acute onset weakness, headache, vomiting, seizures, altered mental status. It is not reliable to distinguish between an Acute Ischemic Stroke (AIS) and Intracerebral Haemorrhage (ICH) based on the history and clinical examination alone and this is the sole reason why a Non-Contrast head CT is ordered for these symptoms. 

If CT shows blood --> ICH
CT Normal --> Probable AIS 

Other information that a CT can give us:
  • Based on the location of blood
Classical hypertensive ICH - seen at basal ganglia, thalamus, pons, cerebellum 
Amyloid Antipathy bleeds/ AVM bleeds - Lobar bleed

Common causes that lead to ICH are chronic hypertension leading to charcot bouchard aneurysms, cerebral amyloid angiopathy, AV malformations, Berry Aneurysms (SAH).

Concise clinical assessment regarding ICH characteristics and patient condition

We will one again start with the mantra of emergency medicine and start off with ABCs. These patients are often comatose and require RSI. 

Avoid ketamine here if they already have a high blood pressure. I prefer using rocorunium with a sedative. This eases the process of intubation and also brings down the blood pressure a bit. Remember with succinyl choline (sux), there is a concern for transient rise in ICP. Though some physicians are of the opinion that this transient bump in ICP with sux in insignificant, I don't recommend using sux here. 

A full neuro exam is hard to perform in these patients but we can do a ICH score to assess the mortality. Each point increase in the ICH score is associated with an increased risk of mortality and a decreased likelihood of good functional outcome. 

Targeted assessment for potential early interventions including:
  1. Control of elevated blood pressure
    The exact number to which the blood pressure should be reduced remains unclear. But a reduction SBP of 140mmHg appress safe. There has been a concern that acutely lowering blood pressure could lead to ischemic brain injury in the peri-hematoma region, but this risk has not been supported by recent studies. 

    American Heart Association/American Stroke Association Guidelines for the Management of Intracerebral Hemorrhage suggest reducing the blood pressure to <160/90 mmHg or a mean arterial pressure (MAP) <110 mmHg. In patients with potential for elevated ICP, a cerebral perfusion pressure (CPP) of >60 mmHg should be maintained.

    Go for quick acting and titratable agents like IV calcium channel blocker infusions (nicardipine or clevidipine) or Labetalol. The worst thing that you can do for these patients is to start them on a nitroprusside or nitroglycerine drip. These dugs cause cerebral vasodilation and can further increase the ICP. 

  2. Correction of coagulopathy
    For some reason, we tend to forget this. But reversing blood thinners and anticoagulants is one of the most crucial steps while managing these patients. A quick guide on reversing these medication is mentioned in the table below:

  3. Need for early surgical intervention and hematoma evacuation

Current AHA ICH guidelines recommend surgical intervention if:
  • Patients with cerebellar hemorrhage who are deteriorating neurologically 
  • Brainstem compression  
  • Lobar ICH with hematoma volume >30 cc and within 1 cm of the cortical surface 
  • Significant life-threatening mass effect
Always correct coagulopathy in patients undergoing surgical hematoma evacuation.  

Other issues:

Prophylactic AEDs

Current guidelines do not recommend routine use of prophylactic anticonvulsants though some practitioners still use a short course in patients with lobar ICH and those undergoing hematoma evacuation. Clinical seizures should be treated.  

Need for intracranial pressure (ICP) or other neuromonitoring
ICP monitoring is recommended in patients with GCS < 9, large hematomas with mass effect suggestive of elevated ICP, or hydrocephalus. As a goal, an ICP <20 mmHg and a CPP> 60 should be maintained.
Patient disposition from emergency department (ED):

‘I have a 62 year man with known DM/HTN/A fib who was on warfarin. He was found at home this morning at 7 AM by his wife who last saw him normal at 5 AM. He had left-sided weakness, pre hospital GCS was 12, and BP was 190/100.’’
‘‘On arrival to the ED, he was the same, so we took labs and sent him for a head CT.’’
‘‘CT completed at 10 AM showed a 20-mL right thalamic ICH with mild IVH, but no hydrocephalus. There is about 4 mm of right-to-left midline shift. CTA/CTP showed no AVM or aneurysm."
‘‘When he returned to the ED, he was comatose with a GCS of 10, and his left-sided weakness was worse. So he has an ICH Score of 2. His labs came back with an INR of 2.8.’’
‘‘We intubated him using rocuronium and etomidate and transfused PCC. He also had 10 mg of IV vitamin K.’’
‘‘Neurosurgery has been called, and they are on their way to see him. He is in ED, intubated and sedated now on propofol drip. His BP is 150/85 with no other treatment.’’
‘‘They are ready to take him in Bed 2 in the ICU in 5 min.

The first 24 h are critical for blood pressure management, identification of seizures, ICP management, and maintaining a secure airway. Avoidance of fever, hyperglycemia/hypoglycemia, and hypoxia are also important, as these may affect outcomes. In addition, patients with ICH are at increased risk for the development of deep venous thrombosis (DVT); current guidelines recommend use of compression stockings and pneumatic compression devices at hospital admission, as well as initiation of prophylaxis-dose UFH/LMWH within 1–4 days following onset (assuming cessation of bleeding).

Take Home
  • DNR is a self fulfilling prophecy. Give them the best chance.
  • Do the ABCs, reverse blood thinners/anticoags and control BP (140 SBP is acceptable)
  • Get neurosurgery involved ASAP
  • When you handover, make sure to convey the volume, location, medication reversal.

  1. www.neurocriticalcare.org
  2. Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2010;41: 2108–29. 
  3. Kothari RU, Brott T, Broderick JP, et al. The ABCs of measuring intracerebral hemorrhage volumes. Stroke. 1996;27:1304–5.
  4. Hemphill JC 3rd, Newman J, Zhao S, Johnston SC. Hospital usage of early do-not-resuscitate orders and outcome after intracerebral hemorrhage. Stroke. 2004;35:1130–4.
  5. Hemphill JC 3rd, White DB. Clinical nihilism in neuroemer- gencies. Emerg Med Clin North Am. 2009;27:27–37. vii-viii. Qureshi AI, Wilson DA, Hanley DF, Traystman RJ. No evidence for an ischemic penumbra in massive experimental intracerebral hemorrhage. Neurology. 1999;52:266–72.
  6. Zazulia AR, Diringer MN, Videen TO, et al. Hypoperfusion without ischemia surrounding acute intracerebral hemorrhage. J Cereb Blood Flow Metab. 2001;21:804–10.
  7. Antihypertensive Treatment of Acute Cerebral Hemorrhage Investigators. Antihypertensive treatment of acute cerebral hemorrhage. Crit Care Med. 2010;38:637–48.
  8. Anderson CS, Huang Y, Wang JG, et al. Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurol. 2008;7:391–9.
  9. Kirollos RW, Tyagi AK, Ross SA, van Hille PT, Marks PV.Management of spontaneous cerebellar hematomas: a prospective treatment protocol. Neurosurgery. 2001;49:1378–86. Discussion: 86–7. 
  10. Frontera, Jennifer A., et al. "Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage." Neurocritical care (2015): 1-41.

Monday, January 18, 2016

The value of a stress test

This was a talk that I got to see about 2 years ago. I am sure you will take home a few great points from this one which might sound trivial but can actually be life saving right from your next shift in the ED. Listen to Amal Mattu and get ready to be mesmerised.

Monday, January 11, 2016

The "tunnel vision" of ACS!

This week, I have a case to share. It was a couple of years back when I came across this one.

10:45 AM    33 year old guy walked into the ED complaining of chest pain, sudden onset, left sided, continuous, funny sensation, no aggravating or relieving factors, 6-7/10 scale, no nausea/sweats/vomiting, No fever or any other recent illness. No other co morbidities or similar previous episodes. Not on any medications, No Allergies, Non Smoker, Not an alcohol consumer.

10:54 AM    ED ECG: 92/min, NSR, Normal axis, No ST-T changes

10:58 AM    General Exam: Comfortable, No Pallor, Icterus, Cyanosis
VS: PR 96/min, BP 110/80, SpO2 98%, RA, RR 18/min T 98F
Exam was documented as normal

11:05 AM    He got Paracetamol PO

11: 20 AM    ED ECHO - No RWMA
A few more ECGs were done over next 2-3 hours but they all looked normal. Labs sent.

12:00 PM     First Troponin reported - Normal (CBC, ESR, Renal function - All with normal limits)

12:10 PM     Pain was persisting so Cardiology was called in for their EXPERT opinion, because we were not sure about the cause of chest pain and thought its probably a MSK pain or atypical ACS.

12:50 PM     Cardiology Consultant walked in, Everything happened once again (History, Physical) and then what? Yes, one more troponin and one more shot of pain killer.

01:30 PM     He got a NSAID this time and troponin was sent (once again reported back as normal)

02:00 PM     Time for shift change and handover in the ED. This guy got handed over to a new set of residents who fortunately once again examined him and found something different this time.

Breath Sounds: Decreased (not absent) on the left side, his RR interval was fluctuating on the monitor as well as on the ECG, could be sinus arrhythmia or something else. They decided to do a CXR this time that was not done so far. And here is what the CXR looked like!!

Left sided Spontaneous Pneumothorax 
So, this guy who came with a typical Pnemothorax story was getting worked up for ACS. ECGs, cardiac biomarkers, routine labs and Echo were done but a CXR was skipped! He eventually got admitted, did well and got discharged. But we took about 5 hours to reach the diagnosis for a classical presentation in the ED. Lets see what made us pick this one up eventually and what could have been done to avoid this at the first place:

When the new team of residents took over this patient, a quick re examination made pick this finding. After handover, it is always good to tell patients what you have been told about them. Do they have anything else to tell you? You would be surprised to hear new information many times, that can actually make a difference. Make this a habit.

If you go back and look at the respiratory rate on this man, it was 18bpm. Well that is not normal. Normal RR is 12-14 bpm. 18 is definitely above normal. This can be either tachypnea or dyspnea! Make sure you always count and document the RR. We all like "even numbers" but it is not fair to write just another even number here. Count the RR, look at the respiratory effort and document it. This is a VITAL SIGN. Respect it.

When the RR interval shows quite a bit of fluctuation on the monitor, get a ECG STAT. Things that you should think about are A.Fib, A.Flutter, AV blocks, Pneumothorax or sinus arrhythmia. ECG changes in pneumothorax have not been extensively described in literature (like pulmonary embolism) but do remember that any lung pathology can produce ECG changes. So always think beyond ACS for every chest pain when the first ECG looks normal. 

Chest Pain can be due pathology in any of these organs:
Heart, Lungs, Aorta, Oesophagus, Stomach, Pancreas, Ribs, Pleura, Pericardium etc. But when you call in a consult from any speciality, do not expect a thorough review of the patient by them. Most of them focus only on their area of focus and there is nothing wrong with that. In fact, that was the reason why you called them at the first place, to evaluate the heart (in this case). I am pretty sure that a Pulmonologist would have picked this up instantaneously with examination/ CXR or USG because that is how they are trained.
It is only the internists, emergency and critical care personnel that evaluate the patient completely. With no offence to any specialists and sub specialists, as they specialise more and more, they focus on only a few diagnosis related to their pertinent organs or organ systems. You as a emergency physician, do not have that luxury. The brunt of missing a diagnosis always and always falls on the ED no matter how many specialists have evaluated the patient. 

You might also consider having a ED Chest pain USG protocol which scans all chest pain patients for RWMA, Dilated RV, fluid around the heart/lungs and Pnemothorax. USG is undoubtedly an extension of physical examination, it will take a few more minutes at the bedside and give you vital bits of information. 

Take Home
  • Re-examine patients after you take the handover.
  • RR of 18 is not normal. Count the RR, look at the effort and then document that.
  • PTx may have decreased breath sounds not necessarily absent breath sounds.
  • Every chest pain is not ACS - go beyond it and think PE, PTx, Dissection based on History and examination!
  • Have a chest pain ECHO protocol to look at RWMA, Dilated RV, Fluid around the heart/lungs and a pnemothorax!