Intracranial hemorrhage (main)

(Redirected from ICH)

Background

Intracranial Hemorrhage Types

AHA Spontaneous ICH BP Guidelines 2015[1]

  1. If SBP is 150-220mmHg without contraindication to BP lowering, it is safe to acutely lower BP to 140mmHg and can be effective for improving functional outcome. (Class I Level A)
  2. For ICH patients presenting with SBP >220 mm Hg, it may be reasonable to consider aggressive reduction of BP with a continuous intravenous infusion and frequent BP monitoring (Class IIb; Level of Evidence C)

AHA Aneurysmal SAH BP Guidelines[2]

  1. No well-controlled studies exist that answer whether BP control influences rebleeding
  2. BP should be controlled to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure (Class I, Level of Evidence B).
  3. Nicardipine, labetalol, and esmolol are appropriate choices for BP control (Sodium nitroprusside may raise intracranial pressure and cause toxicity with prolonged infusion and should be avoided)

AHA ICH Coagulopathy Guidelines 2015[3]

  1. Patients with a severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate factor replacement therapy or platelets, respectively (Class I; Level of Evidence C). (Unchanged from the previous guideline)
  2. Patients with ICH whose INR is elevated because of VKA should have their VKA withheld, receive therapy to replace vitamin K–dependent factors and correct the INR, and receive intravenous vitamin K (Class I; Level of Evidence C). PCCs may have fewer complications and correct the INR more rapidly than FFP and might be considered over FFP (Class IIb; Level of Evidence B). rFVIIa does not replace all clotting factors, and although the INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is not recommended for VKA reversal in ICH (Class III; Level of Evidence C). (Revised from the previous guideline)
  3. For patients with ICH who are taking dabigatran, rivaroxaban, or apixaban, treatment with FEIBA, other PCCs, or rFVIIa might be considered on an individual basis. Activated charcoal might be used if the most recent dose of dabigatran, apixaban, or riva- roxaban was taken <2 hours earlier. Hemodialysis might be considered for dabigatran (Class IIb; Level of Evidence C). (New recommendation)
  4. Protamine sulfate may be considered to reverse hep- arin in patients with acute ICH (Class IIb; Level of Evidence C). (New recommendation)
  5. The usefulness of platelet transfusions in ICH patients with a history of antiplatelet use is uncer- tain (Class IIb; Level of Evidence C). (Revised from the previous guideline)
  6. Although rFVIIa can limit the extent of hematoma expansion in noncoagulopathic ICH patients, there is an increase in thromboembolic risk with rFVIIa and no clear clinical benefit in unselected patients. Thus, rFVIIa is not recommended (Class III; Level of Evidence A). (Unchanged from the previous guideline)

Clinical Features

A history of hypertension, trauma, illicit drug abuse, or a bleeding diathesis may be elicited.

  • Acute onset, with rapid clinical deterioration (within minutes-hours)
  • Alteration in level of consciousness (approximately 50%)
  • Nausea and vomiting (approximately 40-50%): but rarely at the onset
  • Headache (approximately 40%)
  • Seizures (approximately 6-7%)
  • Anisocoria
  • Focal neurological deficits

With the progression of hematoma, development of intracranial hypertension (See also brain herniation syndromes):

  • Coma
  • Respiratory failure
  • Hypertension, bradicardia, TWI (T Waves inversion)
  • Central hyperthermia

Focal neurological deficits

Related to the area involved

  • Putamen
    • Contralateral hemiplegia
    • Contralateral sensory loss
    • Aphasia
    • Dysphagia
    • Head and gaze deviation towards "healthy limbs"
    • Homolateral mydriasis
    • Homonymous hemianopia
    • Neglect or apraxia
  • Caudate nucleus
    • Contralateral hemiparesis
    • Contralateral conjugate gaze paresis
    • Confusion
    • Hydrocephalus (intraventricular extension of haemorrhage)
  • Thalamus
    • Contralateral sensory loss, with or without contralateral hemiparesis
    • Vertical gaze paresis
    • Confusion, aphasia
    • Homonymous hemianopia
    • Possible hydrocephalus
  • Brain stem
    • Onset with coma, quadriparesis, gaze paresis and autonomic instability
    • Ocular bobbing, miosis
    • Cranial nerves deficit
  • Cerebellum: Close monitoring!
    • Ataxia, usually beginning in the trunk
    • Dizziness
    • Homolateral dysmetria
    • Dysphagia, dysartria
    • Ipsilateral facial weakness, sensory loss
    • Gaze paresis, skew deviation, miosis, or decreased level of consciousness
  • Lobar: Exclude cerebral AVM.
    • Contralateral hemiparesis or sensory loss
    • Contralateral conjugate gaze paresis
    • Homonymous hemianopia
    • Abulia, aphasia, neglect, or apraxia

Differential Diagnosis

Intracranial Mass

Head trauma

Evaluation

Workup


Diagnostic approach for ICH[5]

  • A baseline severity score should be performed as part of the initial evaluation of patients with ICH (Class I; Level of Evidence B)
  • Rapid neuroimaging with CT or MRI is recommended to distinguish ischemic stroke from ICH (Class I; Level of Evidence A)
  • CTA and contrast-enhanced CT may be considered to help identify patients at risk for hematoma expansion (Class IIb; Level of Evidence B), and CTA, CT venography, contrast-enhanced CT, contrastenhanced MRI, magnetic resonance angiography and magnetic resonance venography, and catheter angiography can be useful to evaluate for underlying structural lesions including vascular malformations and tumors when there is clinical or radiological suspicion (Class IIa; Level of Evidence B).


ECG role (elevated intracranial pressure)[6]

    • Diffuse T-wave inversions
    • Prolonged QT
    • Bradycardia (the Cushing reflex – indicates imminent brainstem herniation)
  • Other possible ECG changes that may be seen:
  • ST segment elevation / depression — this may mimic myocardial ischaemia or pericarditis.
  • Increased U wave amplitude.
  • Other rhythm disturbances: sinus tachycardia, junctional rhythms, premature ventricular contractions, atrial fibrillation.


STE in Traumatic Brain Injury. No cardiac injury / abnormality to explain the ST elevation
T Waves inversion in subarachnoid hemorrhage

Management

Elevating head of bed

  • 30 degree elevation will help decrease ICP[7]

Seizure Prophylaxis and Treatment

  • Prophylactic antiepileptics not recommended[8]
  • Continuous EEG monitoring probably indicated in ICH patients with depressed mental status that is out of proportion fo degree of brain injury[9]
  • Antiepileptics indicated for clinical seizures or seizures on EEG in patients with altered mental status[10]

Blood Pressure

  • Rapid SBP lowering <140 has been advocated with early research showing improved functional outcome[11], but more recent work has found no difference between SBP <140 and <180[12]
  • SBP >200 or MAP >150
    • Consider aggressive reduction w/ continuous IV infusion
  • SBP >180 or MAP >130 and evidence or suspicion of elevated ICP
    • Consider reducing BP using intermittent or continuous IV meds to keep CPP >60-80
  • SBP >180 or MAP >130 and NO evidence or suspicion of elevated ICP
    • Consider modest reduction of BP (e.g. MAP of 110 or target BP of 160/90)


  • Nicardipine in ICH: Start at 5mg/hr, increase 2.5mg q5min until the target blood pressure is achieved and then immediately titrate down to maintenance infusion of 3mg/hr.
  • Labetalol in ICH: 20mg bolus over 1-2 minutes, repeat q3-5 mins until target blood pressure is achieved and then start an infusion of 1-8mg/min.

Reverse coagulopathy

Antiplatelet Reversal

Includes aspirin, prasugrel, clopidogrel

  • Consider desmopressin (0.3mcg/kg)
  • Platelet transfusion
    • No known thrombocytopenia: increases mortality; do NOT give[14]
    • Known or diagnosed thrombocytopenia: consider if platelets <50,000
      • Some hematologists and neurosurgeons recommend for <100,000, despite lack of evidence for improved outcomes

Disposition

  • Admit

External Links

See Also

References

  1. Hemphill JC, et al. AHA/ASA Guideline: Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2015.
  2. Bederson J. et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage: A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Heart Association. Stroke. 2009;40:994-1025 PDF
  3. Hemphill JC, et al. AHA/ASA Guideline: Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2015.
  4. Choosing wisely ACEP
  5. AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage (2015)
  6. https://litfl.com/raised-intracranial-pressure-ecg-library/
  7. http://stroke.ahajournals.org/content/38/6/2001.full
  8. AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage 2015
  9. AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage 2015
  10. AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage 2015
  11. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013; 368:2355-2365.
  12. Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016; 1-11. [Epub ahead of print].
  13. Crash-3 Trial
  14. (PATCH trial)