Pulmonary Hypertension

Introduction

Pulmonary vascular system is a high-flow, low-resistance circuit. Normal pulmonary arterial systolic pressures range from 15 to 30 mm Hg, whereas diastolic pulmonary arterial pressures range from 4 to 12 mm Hg and Pulmonary hypertension is defined as a mean pulmonary arterial pressure >25 mm Hg at rest or >30 mm Hg during exertion.

Although echocardiography can estimate pulmonary arterial pressure in a patient with suspected pulmonary hypertension, definitive diagnosis requires right heart catheterization. The World Health Organization classifies pulmonary hypertension into five categories based on cause and response to treatment:

Accurate classification of pulmonary hypertension is key to directing treatments. Regardless of the cause, patients with pulmonary hypertension have high morbidity and mortality rates.

Pathophysiology

Endothelial dysfunction results in an imbalance between endogenous vasodilators and vasoconstrictors with net effect leading to vasoconstriction and formation of in situ thrombi. Other pathologic processes include alterations in microvascular permeability, abnormal hypoxic vasoconstriction, microvascular thrombosis, and the formation of plexiform lesions, leading to vascular remodeling. 

Ultimately, these abnormalities result in sustained elevations of pulmonary vascular resistance and impairment of pulmonary blood flow leading to RV dilatation and poor contractility. With progressive RV dilation, the intraventricular septum is displaced toward the left ventricle. This displacement inhibits left ventricular filling and ultimately impairs cardiac output and systemic perfusion.

Clinical Presentation 

• Symptoms can be non-specific which often leads to delayed diagnosis
• Dyspnea, fatigue, chest pain, near syncope, syncope, exertional lightheadedness
• Orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema

The physical examination is often normal in the early stages of pulmonary hypertension.

Late signs include a holosystolic tricuspid regurgitation murmur, jugular venous distention, hepatomegaly, ascites, and lower extremity edema

Diagnosis 

ECG: The most common ECG abnormality seen in pulmonary hypertension patients is right axis deviation. Additional findings associated with pulmonary hypertension include an R/S ratio >1 in lead V1, an R/S ratio<1 in leads V5 and V6, a qR complex in lead V1, an S1Q3T3, right atrial enlargement in the inferior leads, and an incomplete or complete right bundle branch block. The most common dysrhythmias in patients with pulmonary hypertension are atrial fibrillation, atrial flutter, and atrioventricular nodal reentrant tachycardia.

B-type natriuretic peptide and N-terminal B-type natriuretic peptide are often elevated  Elevations in troponin from myocardial ischemia or a strain-induced leak can be seen.

CXR: Common abnormalities associated with pulmonary hypertension include enlargement of the right atrium, RV, and hilar pulmonary arteries. 

TTE: Transthoracic echocardiography is the best initial diagnostic test to assess pulmonary hypertension in the ED. It allows estimation of the pulmonary artery systolic pressure and detection of decreased RV function, right atrial hypertrophy right ventricular hypertrophy and leftward deviation of the intraventricular septum.

Treatment 

No consensus guidelines exist for the management of critically ill patients with pulmonary hypertension in the ED. The mainstays of ED therapy include:

1. Supplemental oxygen (Target SpO2 >90%)

2. Optimizing intravascular volume, augmenting right ventricular function, maintaining coronary artery perfusion, and decreasing right ventricular afterload 

Treatments caveats:

• Intubation: In patients with severe pulmonary hypertension, intubation and venti- lation can cause rapid cardiovascular collapse due to increased intrathoracic pressure from positive-pressure ventilation and effects of sedative medications on right ventricular function and systemic vascular resistance. Adjust the respiratory rate to avoid hypercapnia, which can increase pulmonary vascular resistance, pulmonary artery pres- sure, and RV strain.
• Fluids in RV Failure: Volume overload can cause RV dilation, displacing the intraventricular septum, impairing left ventricular output, and ultimately compromising tissue perfusion.3 For patients who are hypovolemic, give serial boluses of an isotonic crystalloid solution in 250- to 500-mL aliquots with close monitoring.
• RV Dysfunction: Dobutamine is preferred inotrope of choice. Avoid doses>10 micrograms/kg/min, because large doses can increase pulmonary vascular resistance and cause tachydysrhythmias and hypotension. For patients unable to tolerate dobutamine, milrinone is an alternative. Higher doses of milrinone can cause hypotension.
• RCA Perfusion: For the hypotensive pulmonary hypertension patient, use a vasopressor to increase aortic root pressure and maintain RCA perfusion. Norepinephrine is recommended for this purpose. Avoid high doses of nor- epinephrine because it can increase pulmonary vascular resistance and impair right ventricular output.
• RV Afterload reduction: These medications are rarely used in ED setting. Reducing right ventricular afterload with pulmonary vasodilators is a critical component in the management of stable patients with pulmo- nary hypertension. The most commonly used pulmonary vasodilators are prostanoids, endothelin receptor antagonists, and phosphodiesterase-5 (PDE-5) inhibitors. These medications are used primarily in the treatment of patients with pulmonary arterial hypertension. 

Prostanoids (epoprostenol, treprostinil, and iloprost) are potent vasodilators and are the initial treatment of choice in patients with pulmonary arterial hypertension and right ventricular failure. These medications have antiplatelet and antiproliferative properties.

Endothelin receptor antagonists (Currently not used for critically ill ED patients) are administered orally and increase exercise capacity, improve hemodynamics, and can delay the time to clinical worsening in pulmonary hypertension patients. Drugs: bosentan and ambrisentan. 

PDE-5 inhibitors (Currently not used for critically ill ED patients) sildenafil and tadalafil are approved for use in patients with pulmonary hypertension. They are administered orally, seeking to improve hemodynamics and exercise capacity in patients with pulmonary arterial hypertension.

Pulmonary HTN patients presenting to ED are often critically ill and require HDU/ICU level care. Therefore, almost all of them require admission with expert input. 

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh
     Department of Emergency Medicine

     Edinburgh
     Scotland

     @EMDidactic

Acute Aortic Syndromes

Background

Acute aortic dissection is part of a spectrum of diseases referred to as Acute Aortic Syndromes which basically encompasses 3 related conditions: 

(1) Aortic dissection
(2) Intramural hematoma (lacks blood flow in the false lumen or its lack of an intimal flap or entry point. Believed to originate from a rupture of the vasa vasorum within the medial layer; or from microscopic intimal tears )
(3) Penetrating atherosclerotic ulcer (typically seen in older population and often found incidentally, may progress to intramural hematoma)

The pathology, diagnosis, and treatment of these three entities are similar

Presentation
While aortic dissection usually presents with severe pain, its presentation can be more subtle and should be considered in anyone with chest pain, back pain or abdominal pain and pain with either syncope or focal neurological deficits.  Aortic dissection can also present as an acute stroke. There are 2 main anatomic classification systems: 

Stanford type B dissections are further classified as:
1. Complicated - Radiographic evidence of thoracic aortic rupture (eg, blood outside the aortic wall); ischemia involving the viscera, kidneys, spinal cord, or lower extremities; persistent pain; or rapid expansion in the distal arch or proximal descending aorta to a total aortic diameter of > 4.5 cm. These findings require immediate intervention due to the threat to life and limb.
2. Uncomplicated


The dissection creates a new false lumen, which separates the media from the adventitia and can extend either anterograde or retrograde involving the aortic root, arch, or any of the main aortic branches. The false lumen may compress the true lumen and compromise blood flow to distal arteries and causing ischemic complications such as renal failure, stroke, spinal infarction, limb ischemia, and myocardial events.

Classically, aortic dissection will present with abrupt chest or back pain, but about  5% of patients with an acute aortic dissection will have no pain. 

Aortic dissection should always be considered in the differential diagnosis of patients with suspected acute coronary syndromes or pulmonary embolism. 

Atypical presentations can also occur. 

• Syncope has been reported in up to about 20% of patients
• Acute neurological deficits or coma occur in 30% of patients presenting with an acute type A dissection. Neurological findings can be associated with aortic dissections secondary to the extension of the dissection into the aortic branches. These branches can be occluded by either expansion of the false lumen occluding the true lumen or by emboli from an expanding thrombus. Deficits may occur from insults to the brain or spinal cord.

• Patients may be hypertensive (49%), normo- tensive (35%) orhypotensive (8%), or in shock (8%). The presence of hypotension or shock is an ominous finding. 
• Blood pressure discrepancy can occur when a dissection extends into a branch of the aorta occluding the subclavian artery. A difference of 20 mm Hg between arms is considered positive and can be suggestive of an aortic dissection (this finding cannot be used to rule out dissection); however, 20% of the population will have a blood pressure differential without an aortic dissection.
• A pulse deficit is defined as having weak or no pulse on the affected side. However, data from the IRAD database of 2538 patients founda pulse de cit or blood pressure differential in only 20% of patients.
• An aortic dissection may extend retrograde and involve the aortic valve or coronary arteries. A diastolic murmur can be heard in about 1/3rd of patients with an aortic dissection and may represent severe aortic regurgitation but the presence of a diastolic murmur is neither sensi- tive nor specific for aortic dissection.
• 2-5% of patients with aortic dissections will have concurrent myocardial ischemia. Proximal aortic dissections can dissect into the right coronary artery, causing occlusion, and can present with a STEMI. If clinical suspicion for aortic dissection is present, other diagnostic modalities should be used to evaluate for proximal aortic dissection prior to anticoagulation or thrombolytics. 

Risk Factors

• Poorly controlled hypertension
• Connective tissue disorders (eg, Marfan syndrome, Ehlers-Danlos syndrome)
• Congenital valvular disorders (eg, bicuspid aortic valve)
• Aortic coarctation
• Homocystinuria
• Previous cardiac surgery
• Familial aortic dissections, aortic aneurysms
• Pheochromocytoma
• inflammatory vasculitis
• Sympathomimetics (eg, cocaine)
• Cardiac surgery (eg, aortic valve replacement, coronary artery bypass grafting) or percutaneous catheter placement (eg, cardiac catheterisation),

Diagnosis

D-Dimer
More and more evidence is accumulating in support of the use of D-dimer as a screening tool for aortic dissection but currently, only a few small studies have looked at the sensitivity of D-dimer in ruling out aortic dissection (need further validation). Also, Intramural hematoma or aortic dissections with a thrombosed false lumen can have a false negative D-dimer. If there is sufficient clinical suspicion for an acute aortic dissection, advanced imaging is indicated. 

A Negative D-dimer cannot rule out Aortic Dissection

Imaging Modalities for Acute Aortic Syndrome

CXR
Chest radiography can suggest an aortic dissection. Abnormalities are seen in approxi- lately about 88% of patients. A widened mediastinum is commonly associated with aortic dissection and is seen in approximately 60% of patients. 

A normal CXR cannot rule out an aortic dissection.

Treatment

• ABCs
• Adequate Pain Relief (Morphine or Fentanyl)
• Target HR< 60 beats/min and Target SBP  between 100-120 mm Hg. Always start with Beta Blockers first (not vasodilators)
• In case of cocaine toxicity, use benzodiazepines to decrease the sympathetic drive.
• Type and Screen
• If hypotensive with poor perfusion then use inotropes (can potentially worsen dissection due to increase in shearing forces) or consider pericardicentesis in cases of tamponade (poor prognosis)

• Emergent Vascular Surgery Consultation - Type A acute aortic dissections require prompt surgical treatment. Definitive treatment of type B acute aortic dissections is unclear. Uncomplicated distal dissections have traditionally been treated with blood pressure control. Surgery has been reserved for patients who have persistent pain, uncontrolled hypertension, occlusion of a major arterial trunk, frank aortic leaking or rupture, or development of a localized aneurysm. 

Rationale for Beta-Blockers First: Aortic wall stress is directly affected by the velocity of ventricular contraction over time (dP/dt). Initiation of treatment to decrease these shear forces should occur as soon as the diagnosis is made or suspected.intravenous narcotics should also be given and titrated to pain control.  Beta-blocker therapy should be given prior to initiating intravenous vasodilators to prevent reflex tachycardia. However, in cases of severe aortic regurgitation, use of intravenous beta blockers or calcium-channel blockers with caution.  

Chronic Dissection
Patients who present with chronic aortic dissection have already survived their period of greatest mortality risk and are usually treated by blood pressure control and close monitoring unless complications mandate surgery. All patients who have sustained and survived an aortic dissection, regardless of the type of definitive therapy used, require careful long-term surveillance and treatment. 


Documentation:

• Document HPI with pertinent negative findings
• Presence of Absence of risk factors
• Listen for bruits
• Pulsate Mass, BP difference in lies or any pulse deficits
• Neuro Exam and CXR, ECHO findings

Take Home

• Use your gestalt to work up dissections. Read more here on ADvISED Trial.   Currently, no validated clinical decision rule exists to rule out an acute aortic dissection. Historical and physical exam can be used to increase or decrease probability, but atypical presentations are common. 
• Aortic dissection should always be in the differential for patients with chest pain, back pain, or abdominal pain.
  
• Once the diagnosis is made or strongly suspected, ED Management is limited to pain relief, HTN and BP control and urgent Vascular surgery consulnation.
  
• D-dimer and CXR alone should not be used to “rule out” aortic dissection. POCUS can be helpful in unstable patients but it should not be relied upon to rule out an aortic dissection. 
  
  

   References and Further Reading:

1. Friado FJ. Aortic dissection: a 250-year perspective. Tex Heart Inst J. 2011;38(6):694-700. (Review)
2. Hagan PG, Nienaber CA, Isselbacher EM, et al. The Inter- national Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903. (Retrospective; 464 patients)
3. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/ STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the Ameri- can College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American As- sociation for Thoracic Surgery, American College of Radiol- ogy, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Soci- ety of Thoracic Surgeons, and Society for Vascular Medicine. Circulation. 2010;121(13):1544-1579. (Guideline) 
4. Mancini MC. Aortic dissection. Medscape. Available at: http://emedicine.medscape.com/article/2062452-overview.
5. Accessed June 10, 2013. (Review)
6. Hardie AD, Wineman RW, Nandalur KR. The natural his- tory of acute non-traumatic aortic diseases. Emerg Radiol. 2009;16(2):87-95. (Review) 
7. Collins JS, Evangelista A, Nienaber CA, et al. Differences in clinical presentation, management, and outcomes of acute type A aortic dissection in patients with and without previ- ous cardiac surgery. Circulation. 2004;110(11 suppl 1):II237- II242. (Retrospective; 617 patients) 
8. Bossone E, Rampoldi V, Nienaber CA, et al. Usefulness of pulse de cit to predict inhospital complications and mortal- ity in patients with acute type A aortic dissection. Am J Cardiol. 2002;89(7):851-855. (Retrospective; 513 patients) Rogers AM, Hermann LK, Booher AM, et al. Sensitivity of the aortic dissection detection risk score, a novel guideline- based tool for identi cation of acute aortic dissection at initial presentation: results from the international registry of acute aortic dissection. Circulation. 2011;123(20):2213-2218.
9. Lo BM. An evidence-based approach to acute aortic syndromes. Emergency medicine practice. 2013 Dec 1;15(12):1-23.

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

  

Posterior Reversible Encephalopathy Syndrome (PRES)

Introduction

Posterior Reversible Encephalopathy syndrome PRES (also known as reversible posterior leukoencephalopathy syndrome) is a constellation of clinical and radiological findings which presents with rapid onset headache, seizures, altered consciousness, and visual disturbances. 

It strongly associated with with renal disease, vascular and autoimmune diseases, immunosuppressive medications, and organ transplantation. Nearly 3/4 patients with PRES are hypertensive, but others may have normal or only mildly elevated blood pressure.

Pathophysiology

Failure of Cerebral Autoregualtion, endothelial injury, disruption of blood brain barrier leading to Vasogenic edema is a proposed mechanism. However, the exact pathophysiology remains unclear. 

Diagnosis 

Prompt recognition of PRES is important to prevent permanent damage due to ongoing cerebral ischemia. Having a high index of suspicion is important. PRES must be added to our routine list of differentials of Posterior Circulation Stroke, SAH, Cerebral Venous Thrombosis. Focal neurologic deficits are uncommon in PRES and Seizures are the most common presentation. 

It is reasonable to start with CT Head in the Emergency Department to rule out other CNS Catastrophes. However, MRI is a better tool to diagnose PRES. Magnetic Resonance Imaging recordings showing white matter abnormalities without infarction. Classical MRI findings of vasogenic edema involving bilateral parietal-occipital lobes. 

PRES appears to be a misnomer as the syndrome is not always reversible, and it may not be localised to either the white matter or the posterior regions of the brain. Atypical features— including hemorrhage, asymmetrical changes, isolated involvement of the frontal lobes, and cortical lesions are common.

Management

• Rapid withdrawal of the trigger (Eclampsia, Drugs)
• Prevent Seizures
• Aggressive blood pressure management 

Take Home:

• PRES should be considered in patients who present with seizures, altered consciousness, visual disturbances, or headache, particularly with acute hypertension.
• PRES has been associated with chronic and acute kidney disease, solid organ transplantation, and use of immunosuppressive drugs.
• Typical MRI findings include reversible, symmetrical, posterior subcortical vasogenic edema.
• If recognized and treated promptly, the rapid-onset symptoms and radiologic features usually fully resolve within days to weeks.

References:

• Hinchey J, Chaves C, Appignani B, et al.  A reversible posterior leukoencephalopathy syndrome. N Engl J Med. 1996;334(8):494-500
• Hobson, E. V., Craven, I., & Blank, S. C. (2012). Posterior Reversible Encephalopathy Syndrome: A Truly Treatable Neurologic Illness. Peritoneal Dialysis International : Journal of the International Society for Peritoneal Dialysis, 32(6), 590–594. http://doi.org/10.3747/pdi.2012.00152
• Fugate, J. E., Claassen, D. O., Cloft, H. J., Kallmes, D. F., Kozak, O. S., & Rabinstein, A. A. (2010). Posterior Reversible Encephalopathy Syndrome: Associated Clinical and Radiologic Findings. Mayo Clinic Proceedings, 85(5), 427–432. http://doi.org/10.4065/mcp.2009.0590
• https://radiopaedia.org/articles/posterior-reversible-encephalopathy-syndrome-1

Author:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

                    

HELLP Syndrome - Podcast

HELLP syndrome - Another great masquerader that requires a high suspicion for diagnosis. Check out the show notes and listen to the podcast.


Hellp

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).

• Calculate the ICH Volume

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.

References:

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.