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I completed my medical school and background EM training from India (Christian Medical College, Vellore and Apollo Hospitals, Hyderabad) where I worked for 4 years. Following this, I devoted (with all my heart) about 1.5 years to do US Medical Licensing Exams. My stint towards an EM Residency in States did not work but it took me to places and it has been quite a journey. I then relocated to London, England to work as a Registrar (Non-Trainee) in A&E. This gave me an opportunity to better understand NHS, EM training pathways and more importantly the EM Mindsets in the United Kingdom. 

Currently, I am pursuing Higher Specialist Training in Emergency Medicine at South East Scotland Deanery where I have the honour and privilege of training under some of the most innovative brains in the field of Emergency Medicine. Over the past few years, I have realised that LEARNING and UNLEARNING (which can be challenging!) is equally important to deliver cutting edge care to our patients.And through this blog, I aspire to disseminate knowledge, assist trainees with exams and stay up to date with contemporary EM literature. I have always been an avid FOAMed supporter because FOAMed has always played an indispensable role during my training. 

Lakshay Chanana
ST4 EM Trainee 
Edinburgh, Scotland

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.


  1. many doubts bout mannitol in these pts. What to do?

    1. Thanks for bringing this up Federico,

      Our goal here is to control the ICP. I would make sure that:
      Head end is elevated
      Adequate sedation is given
      Normocapnia (35-38mmHg PCO2)
      No cervical collars, No IJV catheters

      Mannitol/Hypertonic saline
      Mannitol reduces the brain volume by drawing free water out of the tissue into the circulation, thus dehydrating the brain parenchyma and decreasing the ICP. It can be given as a bolus of 1 g/kg (20 percent solution) and can be repeated at 0.25 to 0.5 g/kg q6-8h. It has a quick onset of action. I would probably go ahead and give it when there is clear evidence of raised ICP.

      Possible concerns with Mannitol could be hypovolumia, renal failure, hypernatremia.

      Hypertonic saline bolus is another way to bring down the ICP (preferred in patients with hypotension and raised ICP)

      Hope this helps.