Intracranial Hemorrhage

by Nur-Ain Nadir and Matthew Smetana

Case Presentation

As you start your 3rd night shift in a row, paramedics bring in a 70-year-old female with altered mental status. Patient has a history of hypertension and diabetes mellitus. She is on Coumadin for atrial fibrillation. She was last seen normal three hours ago when she went to sleep. Her husband called emergency medical services (EMS) because she was difficult to arouse. Her blood pressure in the emergency department (ED) is 240/120 mmHg, heart rate 45 bpm, respiratory rate 22 bpm, pulse oxygen saturation 96% and temperature 99°F.1 rectally. On physical examination, she is diaphoretic and unresponsive to any commands. She has dilated fixed pupils. During your assessment, she begins to vomit. What should be your next step in management?

Critical Bedside Actions and General Approach

General Assessment: Is the patient Stable or Unstable or in Acute distress?

Primary Survey

Obtain brief chief complaint and history of present illness from EMS providers or bystanders. Include time of onset and preceding symptoms, i.e., a headache, nausea, vertigo, syncope, chest pain, trauma.
Obtain Vital Signs. Don’t forget temperature and blood glucose.
Airway – Is the patient protecting the airway? If not – intubate.
Breathing – Is the patient breathing spontaneously? If not – intubate.
- If the patient is breathing spontaneously but is hypoxic, provide supplemental oxygen.
Circulation – Place two large-bore intravenous lines and check;
- Pulses?
- Blood pressure?
- Skin temperature/quality/moisture/color?
Disability – Check;
- The patient consciousness – Is the patient awake, alert and oriented?
- The patient’s score on the Glasgow Coma Scale (GCS)?
- For lateralizing neurological deficits?
- For gaze preference?
- For posturing? – Is decerebrate or decorticate posture present?
Exposure – Completely expose patient.

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response

BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response

BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response

Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

Secondary Survey

Perform secondary survey which includes complete examination, history taking following the primary survey and initial stabilization.

History and Physical Examination Hints

Obtain a more detailed medical history including surgical, travel, social and medication history. Pay specific attention to risk factors for cerebral hemorrhage.

Modifiable Risk Factors

Hypertension- Results in small vessel damage to deeper structures such as basal ganglia and thalamus
Alcohol- Impairs platelet function and damages endothelial cell wall
Coagulopathy- Warfarin increases ICH risk up to 2x-4x. Inherent coagulopathic situations such as liver failure increase ICH risk
Tobacco Use- promotes vascular damage.

Non-modifiable Risk Factors

Cerebral Amyloid Angiopathy- Risk increases with age. Amyloid protein deposition weakens vessels’ structural integrity
Age- Directly proportional to ICH risk.
Structural Abnormalities- aneurysms, connective tissue diseases, congenital arterio-venous malformations (AVMs) and family history of subarachnoid hemorrhage (SAH) increases ICH risk.

Physical Exam

HEENT exam – Pupils equal round and reactive? Papilledema/Venous pulsations present on fundoscopic examination? Bruising? Raccoon’s eyes? Battle sign? Hemotympanum? Ottorhea? Rhinorrhea?
Neck Exam – C Spine tendernes? deformity? Bruising?
Cardiovascular Exam – Bradycardia? Hypertension? Chest Trauma?
Respiratory – Spontaneously breathing? Crackles/Rales? – pattern?
Abdomen – Signs of trauma? Hepatomegaly? Ascites? Signs of cirrhosis?
Skin – Signs of trauma? Needle tracks? medication patches? rashes?
Neurological – complete full neurexam.

Differential Diagnoses

Hemorrhagic stroke
Ischemic stroke
Infectious – abscess/meningitis
Medications – overdose
Metabolic- HONK, hypoglycemia, electrolyte abnormalities

Emergency Diagnostic Tests and Interpretation

A non-contrast head CT is typically the first neuro-imaging performed in the ED due to availability, low cost, and high speed. Acute bleeding appears hyperdense in a pre-contrast CT scan. Then the blood starts to appear isodense and hypodense in weeks, respectively. Radiologic signs of elevated intracranial pressure (ICP) include loss of compressible spaces (basal cisterns, ventricles, cortical sulci), midline shift, herniation, and loss of grey-white matter junction.
Magnetic Resonance Imaging is equally effective for the detection of acute ICH. However, scanning typically takes longer to perform. It may show the underlying cause of ICH such as a tumor or a vascular aneurysm.
Blood tests should include a comprehensive chemistry panel, complete blood count, coagulation profile, urinalysis. A chest X-ray should be ordered.

Emergency Treatment Options

Medications and Procedures

Intubation
- Airway protection is the priority. Assess the patient neurologic status briefly before sedation/paralysis. Prefer short-acting sedative and paralytic agents so that frequent neurological examination can be performed. Protect the patient from hypoxia during the procedure.
Impending Herniation
- Clinical signs of elevated ICP may be subtle due to the brain’s intrinsic autoregulatory mechanisms or more severe including Cushing’s triad (Hypertension, Bradycardia, Irregular respirations), altered mental status, headache, vomiting or focal neurological deficit.
- When elevated ICP is suspected rapid treatment must be performed to decrease the risk of herniation and secondary ischemia.
- Steps to prevent pending herniation:
  - Head elevation to 30 degrees
  - Ensure midline head position to maximize venous drainage.
  - Titrate sedation to reduce agitation
  - Osmotic Agents- Mannitol
    - Mannitol (1 g/kg) and hypertonic saline reduce cerebral edema by producing an osmotic gradient that prevents water from moving into the cells during membrane pump failure and drawing tissue water into the vascular space.
Hyperventilation to produce vasoconstriction.
- Hyperventilation should be closely monitored. The goal PCO2 is between 30-35 mmHg. Extreme vasoconstriction secondary to PCO2 less than 20 mmHg may cause brain ischemia. This should be a temporizing step as injured cerebral blood vessels lose their responsiveness to hyperventilation-induced hypocarbia within 12 hours. Surgical management of the elevated ICP should be the definitive measure.
Neurosurgical Consultation
- ICH dictates immediate neurosurgical consultation. If hydrocephalus is present, a ventricular drain will allow both measurement of ICP and drainage of cerebrospinal fluid (CSF). Additional hematoma evacuation or decompressive craniotomy may be performed.
Hypertension
- Blood pressure should be closely monitored. An invasive arterial catheter may be needed. The blood pressure targets in ICH is controversial and depends on the specific type of ICH. Recommended guidelines from the AHA/ASA are illustrated below.
- Recommended Guidelines from the AHA/ASA for Treating HTN in ICH
  1. SBP >200 mm Hg or MAP >150 mm Hg, consider aggressive reduction of BP with a continuous intravenous infusion
  2. SBP >180 mm Hg or MAP >130 mm Hg and the possibility of elevated ICP, consider monitoring ICP and reducing BP while maintaining a cerebral perfusion pressure ≥60 mm Hg.
  3. SBP >180 mm Hg or MAP >130 mm Hg and no evidence of elevated ICP, then consider reduction of BP (e.g., a MAP of 110 mm Hg or target BP of 160/90 mm Hg).
- While the decrease in blood pressure may reduce the hematoma formation and risk of re-bleeding, it may also reduce cerebral perfusion. One should avoid over-lowering blood pressure as significant drops may minimize perfusion to the ischemic penumbra. Rapidly titratable antihypertensive drugs are recommended. Hypotension may be managed by crystalloid fluid, blood or vasopressors to maintain a systolic blood pressure of >90 mmHg.
Seizures
- Patients with ICH are at an increased risk of developing seizures. This risk increases with lobar hematoma location, hemorrhage size, depressed mental status, history of epilepsy, history of cirrhosis and penetrating trauma.
- The current guideline recommends against the routine administration of antiepileptic medication. However, in case of seizure, antiepileptics such as fosphenytoin (20mg/kg loading dose) should be initiated.
Anti-coagulation
- Coagulopathy should be reversed. Common anti-coagulants and their reversal agents are illustrated in Table.

Common anti-coagulants and their reversal agents

Drug	Mechanism of Action	Reversal Medication
Warfarin	Inhibits Vitamin K clotting factors (2,7,9,10)	Vitamin K FFP Prothrombin Complex Concentrates
Unfractionated Heparin	Binds to antithrombin 3	Protamine
Low Molecular Weight Heparin	Inhibits factor Xa	Protamine incompletely reverses factor Xa inhibition
Aspirin	Irreversibly blocks cyclooygenase	Platelet transfusion to increase normal platelet count by 50,000
Clopidogrel	Inhibits ADP receptor on platelet membrane	Platelet transfusion
Dabigatran	Direct thrombin inhibitor	No specific reversal
Rivaroxaban, apixaban	Inhibit factor Xa	No specific reversal

provided by authors

Pediatric, Geriatric, Pregnant Patient, and Other Considerations

Geriatric patients: The elderly are particularly at risk for spontaneous and traumatic ICH due to higher hypertension and brain atrophy prevalence, and frequent use of anticoagulation.

Pregnant Patients: During pregnancy, ICH risk increases in case of preeclampsia, eclampsia and gestational hypertension.

Pediatric Patients: The majority of childhood ICH is secondary to trauma. The physician must always look for the signs of non-accidental injury in pediatric patients with ICH even if the history suggests otherwise.

Disposition Decisions

Patients are typically admitted to an ICU.

References and Further Reading

Knudsen KARJ, Karluk D, Greenberg SM. Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria. Neurology 2001;56:537–539.
van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ. Incidence, case fatality, and functional outcome of intracerebral hemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010;9(2):167–176.
Feigin VL, Lawes CM, Bennett DA, Barker-Collo SL, Parag V. Worldwide stroke incidence and early case fatality reported in 56 population-based studies: a systematic review. Lancet Neurol. 2009;8(4):355–369. doi: 10.1016/S1474-4422(09)70025-0.
Juvela S, Hillbom M, Palomäki H. Risk factors for spontaneous intracerebral hemorrhage. Stroke. 1995;26: 1558–1564.
Badjatia N, Rosand J. Intracerebral Hemorrhage. Neurologists. 2005: 11,6 311-324
Martin-Schild S, et al. Intracerebral Hemorrhage in Cocaine Users. Stroke. 2010;41(4):680–684.
Levine MN, Raskob G, Landefeld S, et al. Hemorrhagic complications of anticoagulant treatment. Chest. 2001;119:108S–121S.
Ruiz-Sandoval JL, Cantu C, Barinagarrementeria F. Intracerebral hemorrhage in young people: analysis of risk factors, location, causes, and prognosis. Stroke. 1999;30:537–541.
Naidech AM. Intracranial hemorrhage. Am J Respir Crit Care Med. 2011;184:998–1006.
Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011
Caceres J, Goldstein J, Intracranial Hemorrhage. Emerg Med Clin North Am. 2012 August; 30(3): 771–794
Hemphill JC III et al. Guidelines for the management of spontaneous intracerebral hemorrhage: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2015 May 28 – See more at: http://www.jwatch.org/na38140/2015/06/23/updated-guidelines-treating-spontaneous-intracerebral#sthash.fUJQkEkH.dpuf
Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons. Guidelines for the management of severe traumatic brain injury. J Neurotrauma. 2007;24: S1–106
Marx JA, Hockberger RS, Walls RM, et al., eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Mosby/Elsevier; 2010
15) Roberts, James R., Catherine B. Custalow, Todd W. Thomsen, and Jerris R. Hedges. 2014. Roberts and Hedges’ clinical procedures in emergency medicine.
Halle, Jesse B., Schmidt Gregory A., Wood Laurance D.H., Principles of Critical Care 3rd ed. 2014. McGraw-Hill
Antithrombotic therapy and prevention of thrombosis 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. CHEST. 2012;141
Mathew A, Kumar A, Focus on: Reversal of Anticoagulation, ACEP News 6/2010
Siegal DM, Cuker A. Reversal of novel oral anticoagulants in patients with major bleeding. J Thromb Thrombolysis. 2013;35:391–398.
Levine JM, Kumar MA. Traumatic brain injury [white paper]. Neurocritical Care Society Practice Update: Pennsylvania, 2013.
Armin SS, Colohan ART, Zhang JH. Vasospasm in traumatic brain injury. Acta Neurochirurgica, Supplementum. 2008;104(13):421–425.
Blok, B, Cheung D, and Platts-Mills T. First Aid for the Emergency Medicine Boards. McGraw-Hill Medical, 2008.
Van Asch CJJ, et al. Incidence, case fatality and functional outcome of intracerebral haemorrhage over time, according to age, sex and ethnic origin: a systematic review and meta-analysis.