Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
What is neurocritical care?
Neurocritical care is a branch of critical care medicine that deals with the intensive care management of patients with life-threatening disorders due to either neurologic and neurosurgical illnesses or other systemic diseases affecting the central nervous system (CNS), the peripheral nervous system, or both. Neurocritical care provides the interface between the brain and other organ systems in the setting of critical illness. One of the main goals of treatment is the prevention of secondary CNS insults to prevent further damage.
What is a neurointensivist?
A neurointensivist is an intensivist who specializes in the care of the neurocritically ill patient. Care of the neurocritically ill patient also includes prognostication of neurologic outcome and brain death determination. Neurointensivists may come from a number of medical and surgical backgrounds including neurology, neurosurgery, internal medicine, anesthesiology, emergency medicine, and pediatrics.
What are the most common diseases treated in a neurocritical care unit?
The most common clinical disorders in the neurocritical care unit are ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, brain tumors, brain trauma, status epilepticus (SE), neuromuscular emergencies (e.g., myasthenia gravis crisis, Guillain–Barré syndrome), spinal cord injury, infection of brain and spinal cord, and the cardiopulmonary complications of brain injury.
Airway management is the first step in the evaluation and resuscitation of the critically ill patient ( Table 19-1 ).
How do we evaluate airway?
The initial evaluation includes an assessment of airway patency, protective reflexes, respiratory drive, and oxygenation. A depressed level of consciousness (defined as a Glasgow Coma Scale [GCS] score <8) is the greatest risk factor for airway obstruction and aspiration.
When should a patient be intubated?
Common general indications for endotracheal intubation include the following: either cardiac or respiratory arrest; failure to protect the airway; inadequate oxygenation or ventilation; and impending or existing airway obstruction.
What are the goals of ventilator management?
The goals are to reverse apnea, respiratory distress, severe hypoxemia, and hypercapnia. These goals can be accomplished either invasively (i.e., tracheal intubation) or noninvasively (i.e., noninvasive positive pressure ventilation [NIVPPV] used for chronic obstructive pulmonary disease exacerbation with hypercapnia, pulmonary edema, myasthenia gravis crisis, and at home for amyotrophic lateral sclerosis).
What are the modes of ventilation?
There are four basic modes of assisted ventilation: assist control, synchronized intermittent mandatory ventilation, pressure support (PSV), and continuous positive airway pressure (CPAP).
What are the targets of ventilation modes?
There are two targets of ventilation modes:
Volume targeted in which the ventilator delivers a set tidal volume (Vt); and
Pressure targeted in which the ventilator delivers a fixed inspiratory pressure.
How can ventilator settings be adjusted to improve oxygenation?
Increase either fraction of inspired oxygen (FiO 2 ) or positive end-expiratory pressure (PEEP).
How can ventilator settings be adjusted to remove carbon dioxide in hypercapnia?
The most efficient way is to increase minute ventilation, which represents the total volume of gas passing into and out of the lungs per minute and is calculated by multiplying respiratory rate (RR) × Vt. Thus, you can increase RR, Vt, or both.
What is the lung protective strategy to prevent ventilator-induced lung injury?
The goal of the lung protective strategy is to improve alveoli recruitment while limiting derecruitment and overdistention. Currently, there is wide consensus that Vt restriction to 6 mL/kg ideal body weight and/or plateau airway pressures (PPlat) limited below 30 cm H 2 O may prevent lung injury. Vt could be decreased to a minimal value of 4 mL/kg of predicted body weight in both groups in case of PPlat higher than 32 cm H 2 O, or it could be increased to a maximal value of 8 mL/kg of predicted body weight in case of severe acidosis defined as arterial pH lower than 7.15. Patients with intracranial processes pose a unique challenge since carbon dioxide elevations can lead to increased intracranial pressure (ICP). Therefore, these patients need to be monitored closely and their ICP measured.
What are the criteria to wean from ventilators?
It is important to wean patients from mechanical ventilation as soon as possible to minimize the risk of ventilator-associated pneumonia. In general, the following criteria need to be met to ensure successful ventilator weaning and extubation:
The cause of respiratory failure has been reversed or is improving;
Patient is breathing spontaneously;
Patient is awake and alert or is easily arousable and cooperative;
Sedation has been discontinued;
Patient has achieved hemodynamic stability;
Patient has adequate cough and minimal secretions;
Adequate oxygenation is present, defined as a partial pressure of O 2 in arterial blood (PaO 2 )/FiO 2 ratio >150 to 200; requiring PEEP ≤5 to 8 cm H 2 O; FiO 2 ≤0.4 to 0.5; and pH (e.g., ≥7.25); and
Rapid shallow breathing index (RSBI) <105. RSBI is calculated as RR/Vt (L). A value of >105 breaths/min/L predicts weaning failure (negative predictive value 95%).
A successful spontaneous breathing trial (SBT) with PSV of ≤5 or T piece for 30 to 120 minutes is currently thought to be the best predictor of successful weaning. SBT must be performed once a day.
General | Ischemic Stroke | ICH | SAH | TBI | |
---|---|---|---|---|---|
Blood pressure goal | BP >100/80 MAP >70 | BP <220/120 with no thrombolytics BP <180/105 after thrombolytics for 24 hours |
BP <160/100 | BP <160/100 for unsecured aneurysm BP >160-220/100 for secured aneurysm |
SBP >90 |
Target | Oxygen delivery | Save penumbra | Avoid hematoma expansion | Avoid rebleeding | Avoid ischemia |
Volume status | Euvolemia | Euvolemia | Euvolemia | Euvolemia | Euvolemia |
DVT prophylaxis ∗ | On admission unless contraindicated | Within 24 hours if no thrombolytics >24 hours with thrombolytics | Low dose 1-4 days after onset | 24 hours after aneurysm repair | Timing unknown |
Seizure prophylaxis | Not needed | Not needed unless documented seizure | Not needed unless documented seizure | 3-7 days (avoid phenytoin) | 7 days |
Fever | Normothermia | Normothermia | Normothermia | Normothermia | Normothermia |
Glucose | <180 (NICE SUGAR trial) | Not known, recommend normoglycemia | 140-180 mg/dL based on (NICE SUGAR trial) | Not known, 80-200 mg/dL | Avoid hypoglycemia |
∗ Sequential compression device (SCD) on all patients and heparin 5000 U SQ bid if <60 kg or tid if >60 kg or enoxaparin 40 SQ mg daily adjusted for renal function.
What agents are used for peptic ulcer prophylaxis?
Famotidine is the first line of treatment. Pantoprazole should be used if the patient is already on a proton pump inhibitor at home or has gastrointestinal bleeding.
What bowel regimen should be used?
Docusate, senna, polyethylene glycol, bisacodyl, and lactulose on an as needed basis are acceptable medications used either individually or in combination.
How are nutrition and electrolytes managed?
Nutritional support is indicated for any critically ill patient who cannot take oral feeds and in whom oral intake is not expected to cover the full energy needs. There are two routes for nutrition administration in these patients, enteral and parenteral. Enteral nutrition is always the first choice and should be started 24 hours after intensive care unit (ICU) admission if no procedures are planned. Parenteral nutrition should be restricted to those situations in which there are contraindications to enteral nutrition.
Electrolytes: Electrolyte imbalances need to be worked up and corrected aggressively. Refeeding syndrome must be recognized in severe protein–calorie malnutrition, bearing in mind that hypophosphatemia is the hallmark of biochemical abnormality. Correction of hypophosphatemia should precede feeding.
What are the workup and management of fever in the ICU?
Fever is defined as a core temperature above 38.3° C. Fever has been associated with worse neurologic outcome in brain injury patients. Ventilator-associated pneumonia, catheter-related sepsis, and sinusitis are the three major causes of ICU fever of recent onset. Antipyretic agents (acetaminophen alone or in combination with ibuprofen for central fever) are the first line of therapy. Surface cooling devices are more effective and should be used if drug therapy fails. Antishivering medications may be used as needed ( Fig. 19-1 ).
What systemic hemodynamic monitoring is indicated in patients with acute brain injury?
See Table 19-2 .
Noninvasive | Invasive |
---|---|
ECG | Invasive blood pressure monitoring |
Arterial blood pressure | Central venous pressure monitoring |
Pulse oximetry | Mixed venous oxygen (SvO 2 ) and serum lactate |
Transthoracic echocardiogram (baseline when signs of cardiac dysfunction) | Arterial pressure waveform-derived (PiCCO, LiDCO) for cardiac output monitoring |
What are the different hemodynamic parameters in the etiology of shock?
See Table 19-3 .
Etiology of Shock | Cardiac Output (CO) | Ejection Fraction (EF) | Mixed Venous Oxygen (SvO 2 ) |
---|---|---|---|
Hypovolemic | Normal/ | ||
Cardiogenic | |||
Sepsis | Normal/ | Normal/ | |
Obstructive |
What are the ways to monitor the brain during acute brain injury?
Clinically: The serial neurologic examination is still the best option.
Physiologically: ICP and cerebral blood flow (CBF).
ICP: Both intraparenchymal monitors and ventricular catheters measure ICP and indirectly measure cerebral perfusion pressure (CPP). ICP and CPP monitoring are recommended in patients who are at risk of elevated ICP based on clinical and/or imaging features. Refractory ICP elevation is a strong predictor of mortality.
CBF: Bedside techniques for monitoring CBF include both invasive methods such as thermal diffusion and laser Doppler flowmetry and noninvasive methods such as transcranial Doppler (TCD) ultrasonography and near infrared spectroscopy (NIRS). Trends in blood flow velocity changes measured with TCD can help predict delayed ischemic neurologic deficits due to vasospasm after aneurysmal subarachnoid hemorrhage (SAH).
Electrophysiologically: Electroencephalography (EEG) has been recommended in all patients with any acute brain insult and unexplained and persistent altered consciousness. In addition, urgent EEG should be considered in patients with convulsive SE who do not return to functional baseline within 60 minutes after seizure medication and in those with refractory status epilepticus (RSE). Furthermore, EEG also has been recommended during therapeutic hypothermia and within 24 hours of rewarming to exclude subclinical seizures in all comatose patients after cardiac arrest.
Metabolically: Oxygenation and substrate metabolism.
Brain hypoxia is associated with worse outcome. It is measured by either invasive methods such as bedside techniques, brain parenchymal oxygen tension (PbtO 2 ), and jugular bulb oxygen saturation (SjvO 2 ) or noninvasive bedside methods such as NIRS. It is currently recommended to monitor brain oxygen in patients with or at risk of cerebral ischemia and/or hypoxia using either brain tissue (PbtO 2 ) and/or jugular venous bulb oximetry (SjvO 2 ).
Brain extracellular concentrations of energy metabolism markers , including lactate, pyruvate, and glucose, are accurately measured by microdialysis. Monitoring cerebral microdialysis in patients with or who are at risk of cerebral ischemia, hypoxia, energy failure, and glucose deprivation should be considered only in combination with clinical indicators and other monitoring modalities for therapeutic interventions and prognostication.
What is the Monro–Kellie doctrine?
The Monro–Kellie doctrine states that the volume of intracranial components (brain, blood, and cerebrospinal fluid [CSF]) remains nearly constant due to the enclosure within the nonexpandable skull, after closure of the fontanelles. Additional volume will lead to the displacement of another of the contents and results in increased ICP.
What is elevated ICP?
The normal ICP ranges from 5 to 15 mm Hg (7.5 to 20 cm H 2 O) in an adult and 3 to 7 mm Hg (4 to 9.5 cm H 2 O) in children. The threshold that defines intracranial hypertension is uncertain but generally is considered to be >20 cm H 2 O for >10 minutes.
What is the Cushing’s triad?
The Cushing’s response, the classic triad of severe hypertension, bradycardia, and irregular respiration, occurs during terminal brain herniation.
What are the different herniation syndromes?
See Table 19-4 .
Types | Anatomy | Exam Findings |
---|---|---|
Uncal (lateral transtentorial) | Inferior displacement of medial temporal lobe (uncus) past free edge of tentorium cerebelli | Ipsilateral oculomotor nerve palsy, posterior cerebral artery infarction Kernohan’s notch phenomenon |
Subfalcine | Cingulate gyrus forced under falx cerebri | Behavioral changes Contralateral leg weakness Anterior cerebral artery infarction |
Central (transtentorial) | Progressive downward displacement of diencephalon and brain stem | Rostral to caudal progression of brain stem dysfunction |
Tonsillar | Downward displacement of cerebellar tonsils through foramen magnum | Medullary dysfunction Cardiorespiratory arrest |
What is the threshold for intervention to reduce ICP?
When ICP is >20 cm H 2 O for >10 minutes or when there are clinical signs of herniation.
What is CPP?
CPP is the driving arterial pressure gradient across the cerebral vasculature and is defined as the difference between the mean arterial pressure (MAP) and ICP.
The CPP goal is patient specific, and hence it is debatable. Based on studies, the recommended goal is 50 to 70 mm Hg, and values <50 mm Hg are associated with ischemia and poor outcome.
What is cerebral autoregulation?
Cerebrovascular resistance (CVR), which is determined by the diameter of small arteries and arterioles, modulates CBF.
A constant CBF over a wide range of systemic blood pressures, MAP 60 mm Hg–160 mm Hg, maintains CPP due to CVR. Outside this range of autoregulation, CBF varies directly with CPP. Below the lower limit of CPP, CBF decreases as vasodilation becomes insufficient to promote CBF, resulting in ischemia. Above the upper limit of CPP, increased intraluminal pressure results in a forceful dilation of arterioles (“luxury” perfusion), leading to disruption of the blood–brain barrier and brain edema. The upper and lower limits of cerebrovascular autoregulation vary from one person to another, so the targeted CPP must be individualized.
What is the etiology of elevated ICP and cerebral edema?
See Table 19-5 .
Mechanism | Etiology |
---|---|
Increased intracellular brain water (cytotoxic edema) | Ischemic stroke, lead intoxication, anoxic brain injury, fulminant hepatic failure, Reye’s syndrome |
Increased extracellular brain water (vasogenic edema) | Hypertensive encephalopathy, eclampsia, posterior reversible encephalopathy syndrome, brain tumors, abscess, encephalitis, high-altitude cerebral edema |
Transependymal edema (hydrocephalus) | Subarachnoid hemorrhage, idiopathic intracranial hypertension, meningitis |
Osmotic edema | Hyponatremia, reverse urea syndrome, osmotherapy rebound effect, diabetic ketoacidosis, and hyperglycemic nonketotic coma (correction phase) |
Ionic edema | Ischemic stroke |
Venous obstruction | Sinus venous thrombosis, jugular vein thrombosis |
Increased brain volume | Brain tumor, abscess, empyema, intracerebral hemorrhage |
Increased blood volume | Hypercarbia, anoxia, severe anemia, hyperperfusion syndrome (i.e., postcarotid endarterectomy), vein of Galen malformation, arteriovenous malformation, arteriovenous fistula |
Mass effect | Subdural hematoma, epidural hematoma, empyema, tension pneumocephalus |
How is intracranial hypertension managed?
Medical management: The initial steps in the medical management of elevated ICP are the universal mandates of assessing airway patency, breathing, and circulation. These goals should be followed sequentially and include the following:
Maintenance of adequate oxygenation helps with both brain and systemic perfusion. Additionally, normothermia, normoglycemia, euvolemia, and normonatremia help optimize outcomes.
Elevation of the patient’s head to 30° and positioning in midline facilitates cerebral venous drainage to decrease cerebral blood volume (CBV).
Controlled hyperventilation for a short period as a bridge to definitive therapy. Hyperventilation vasoconstricts cerebral arterioles and reduces CBV. Prolonged hyperventilation causes ischemia. The goal should be a minute ventilation to keep PaCO 2 ∼ 30 to 35 mm Hg.
Sedation and analgesia help decrease cerebral metabolism. Agitation and pain increase cerebral metabolic rate of oxygen (CMRO 2 ) and CBF. Propofol and barbiturates reduce CMRO 2 and CBF. Patients should receive adequate sedation with propofol and adequate analgesia with fentanyl.
Neuromuscular blockade may lower ICP by both muscle relaxation and preventing Valsalva-induced spikes in ICP related to coughing and straining. Disadvantages are loss of the neurologic exam and an increase in the risk of critical illness neuromyopathy.
Osmotherapy with mannitol and/or hypertonic saline exerts osmotic and vasoconstrictive effects to reduce CBV. Doses of 0.5 to 1.5 g/kg intravenous (IV) bolus of 20% mannitol, followed by 0.25 to 1 g/kg every 6 hours via peripheral line are recommended. Electrolytes, renal function, and serum osmolarity must be monitored every 6 hours. Check osmolar gap = measured − calculated. Hold mannitol if the gap >20 serum osmoles. Hypertonic saline also is available for management of elevated ICP before or concomitantly with mannitol administration. Doses and concentrations include 23% saline 30 cc × 1 over 10 minutes via central line to avoid hypotension followed by 30 cc every 6 hours; 3% infusion 40 to 50 cc/h can also be used via central line. The serum sodium goal is 145 to 155 mEq/L.
Steroids should be used for vasogenic edema due to either brain tumors or encephalitis. Dexamethasone 10 mg IV × 1, then 4 mg q6h. Steroids must be avoided in traumatic brain injury (TBI) patients due to higher mortality.
Targeted temperature management has been advocated after the above measures have been utilized. The main goal is to prevent fever as fever has been associated with poor outcome. Active cooling to 32 to 34° C is used for refractory elevated ICP. It reduces CMRO 2 and CBV. However, induced hypothermia in TBI with elevated ICP should be used in conjunction with available management protocols.
Surgical management: CSF diversion via an intraventricular catheter reduces CSF volume and decreases ICP. It is indicated in obstructive hydrocephalus, diffuse cerebral edema, or mass effect due to space-occupying lesions.
Craniectomy reduces mass effect and CBV. The main indication for craniectomy is either a large hemispheric ischemic stroke or posterior fossa lesion with significant mass effect. Hemicraniectomy should be performed as early as possible, preferably before significant changes in the neurologic examination are observed. There is currently no evidence of benefit of craniectomy in TBI patients.
What is systemic inflammatory response syndrome (SIRS)?
SIRS refers to the clinical manifestations of systemic inflammation. The presence of SIRS requires that two or more of the following criteria are met:
Fever (>38° C) or hypothermia (<36° C)
Tachycardia (>90 b/min)
Either tachypnea (>20/min) or a fall in arterial PaCO 2 (<32 mm Hg)
Either leukocytosis (>12.0 × 10 9 /L) or leukopenia (<4.0 × 10 9 /L) or >10% immature (band) forms
What is sepsis, and what is severe sepsis?
Sepsis is defined as the presence (either probable or documented) of infection together with SIRS. Severe sepsis is sepsis-induced organ dysfunction or tissue hypoperfusion.
What is septic shock?
Severe sepsis plus hypotension not reversed with fluid resuscitation.
How should septic patients be evaluated?
The initial workup should focus on the identification of the infectious source including careful history and physical examination, two sets of blood cultures, urine culture, sputum culture, stool culture, and CSF studies.
How should septic patients be treated?
Early goal-directed therapy is a protocol for the first 6 hours of treatment of septic patients with shock refractory to fluids and vasopressors and requires administration of fluids, vasopressors, broad-spectrum antibiotics, and hydrocortisone.
A depressed level of consciousness (GCS <8) is the greatest risk factor for airway obstruction and aspiration.
In assessing the airway, always recognize the potential for cervical spine injuries.
Hypocapnia constricts coronary and cerebral arteries and hampers oxygen unloading.
Always treat fever aggressively.
Avoid hypovolemia.
What percentage of strokes is due to intracerebral hemorrhage?
10% to 15%.
What is the overall 30-day mortality of ICH?
34%.
What are the typical locations for nontraumatic ICH?
Basal ganglia, thalamus, pons, cerebellum, and lobar.
What is the etiology of nontraumatic ICH?
See Table 19-6 .
Hypertension: most common cause ∼70% |
Amyloid angiopathy: most common cause in the elderly |
Arteriovenous malformations: most common cause in children |
Intracranial aneurysm |
Vascular malformations: cavernous angioma, venous angioma |
Dural venous sinus thrombosis |
Coagulopathy |
Intracranial neoplasm |
Cocaine, methamphetamine, or alcohol |
Vasculitis |
Hemorrhagic ischemic stroke |
What neuroimaging modalities should be used in ICH evaluation and management?
Noncontrast computed tomography (CT) head scan is the imaging modality of choice to assess for ICH location, volume, ventricular extension, hydrocephalus, and mass effect. Hematoma volume can be calculated using the ABC/2 formula. A = longest diameter, B = largest diameter perpendicular to A, and C is the number of CT slices with hematoma × thickness of 10-mm slices in cm (if 5 mm divide C by 2). In most cases a noncontrast CT of the head is the only imaging modality that is required particularly in those patients with ICH located in the basal ganglia and thalamus.
Magnetic resonance imaging (MRI) of the brain may be needed to assess for ischemic stroke, underlying tumor, vascular lesion, and prior microbleeds or macrobleeds on gradient echo (GRE) sequence. Abnormalities in the latter would indicate the presence of cerebral amyloid angiopathy (CAA) (superficial lobar region) or hypertension-related changes (deep subcortical and infratentorial region).
CT angiography (CTA) spot sign is an indicator of active hemorrhage, which has been associated with increased risk of hematoma expansion, mortality, and poor outcome ( Fig. 19-2 ). However, further studies are under way to determine the significance of the spot sign in daily clinical practice.
Vascular imaging: Noninvasive imaging such as CTA and MR angiogram (MRA) and/or an invasive modality such as digital subtraction angiography (DSA) should be considered in those patients where a vascular abnormality is suspected.
How rapidly does hematoma volume expand in acute ICH?
Twenty-six percent within 1 hour and another 12% within 20 hours after the initial CT scan.
What are the imaging predictors for hematoma expansion (>33% growth from baseline CT)?
Irregular shape, heterogeneous density, and the spot sign.
When should a head CT be repeated in an ICH patient?
Follow-up head CT scanning is usually performed 6 to 24 hours after presentation or earlier if there is a change in neurologic examination. Given the chance of hemorrhage expansion, repeat imaging is common, but it is expensive and may be dangerous. It is important to recognize that without a clinical change, the yield of repeat CT is low. It may be safely deferred in most circumstances. Some exceptions may include patients with increased ICP, a GCS score <12, or epidural hematoma, as the clinical examination may be less sensitive and the likelihood of intervention greater in these circumstances.
When does swelling peak in ICH?
Days 3 to 7.
What are the predictors of poor outcome in ICH?
GCS on admission
High degree of systolic blood pressure variability or episodic hypertension
Hematoma location (extension to ventricles)
Hematoma volume
Hyperglycemia and fever
What are the best predictors of 30-day mortality in ICH?
See Table 19-7 .
Component | Finding | ICH Score Point |
---|---|---|
GCS | 3-4 | 2 |
5-12 | 1 | |
13-15 | 0 | |
ICH volume (cc) | >30 | 1 |
<30 | 0 | |
Intraventricular hemorrhage | Yes | 1 |
No | 0 | |
Infratentorial origin | Yes | 1 |
No | 0 | |
Age (years) | >80 | 1 |
<80 | 0 | |
Total score | 0-6 |
What are the risk factors for recurrence of ICH?
Lobar location of the initial ICH, older age, ongoing anticoagulation, presence of the apolipoprotein E e2 or e4 alleles, and greater number of microbleeds on MRI are currently considered the main factors associated with ICH recurrence.
What are the diagnostic criteria for CAA?
Definite CAA:
Full postmortem examination demonstrating:
Lobar, cortical, or corticosubcortical hemorrhage
Severe CAA with vasculopathy
Absence of other diagnostic lesion
Probable CAA with supporting pathology:
Clinical data and pathologic tissue (evacuated hematoma or cortical biopsy) demonstrating:
Lobar, cortical, or corticosubcortical hemorrhage
Some degree of CAA in specimen
Absence of other diagnostic lesion
Probable CAA:
Clinical data and MRI or CT demonstrating:
Multiple hemorrhages restricted to lobar, cortical, or corticosubcortical regions (cerebellar hemorrhage allowed)
Age >55 years
Absence of other cause of hemorrhage
Possible CAA—clinical data and MRI or CT demonstrating:
Single lobar, cortical, or corticosubcortical hemorrhage
Age >55 years
Absence of other cause of hemorrhage
What are the predictors of symptomatic ICH recurrence in CAA?
The number of microbleeds and the presence of superficial siderosis on brain MRI predict recurrence risk of intracerebral hemorrhage in patients with CAA.
See Tables 19-8 and 19-9 .
Number of Micro- or Macro-Bleeds | 3-Year Cumulative Risk of Recurrent Symptomatic ICH (%) |
---|---|
1 | 14 |
2 | 17 |
3-5 | 38 |
>6 | 51 |
Cortical superficial siderosis | No | Focal | Disseminated |
4-year cumulative risk of recurrent symptomatic ICH | 25% | 28.9% | 74% |
What is the blood pressure goal in the acute phase of ICH?
The 2010 AHA Stroke Council Guidelines recommended to keep blood pressure <160/90 mm Hg or MAP <110 mm Hg. However, data from the INTERACT trial suggested that intensive systolic blood pressure lowering to <140 mm Hg is safe and was associated with better functional outcome on ordinal analysis of modified Rankin scale scores. In practice, many neurointensivists recommend keeping systolic blood pressure <140 mm Hg pending the results of ongoing ATACH 2 phase 3 clinical trials comparing intensive blood pressure lowering (<140 mm Hg) versus standard blood pressure (<180 mm Hg).
How is recurrent ICH prevented?
Blood pressure control is still the best treatment to prevent ICH recurrence. After the acute ICH period, a goal target of a normal blood pressure of <140/90 mm Hg (<130/80 mm Hg is diabetes or chronic kidney disease) is reasonable and would be in accordance with current guidelines.
When should an ICH patient receive a platelet transfusion?
Studies of the effect of prior antiplatelet agent use or platelet dysfunction on ICH hematoma growth and outcome have found conflicting results.
The usefulness of platelet transfusions in ICH patients with a history of antiplatelet use and normal platelet count is unclear and is considered investigational. For patients with a coagulation factor deficiency and thrombocytopenia (platelet count <100,000), replacement of the appropriate factor or platelets is indicated.
When and how should coagulopathy be reversed?
Warfarin is both a risk factor for hematoma enlargement even after 24 hours and for worse outcomes after ICH. There are no randomized clinical trials available comparing the efficacy of different reversal agents and their impact on clinical outcome. Consequently there is considerable variability in clinical practice.
Patients with ICH whose international normalized ratio (INR) is elevated due to oral anticoagulants should have their warfarin withheld, receive therapy to replace vitamin K–dependent factors, correct the INR, and receive intravenous vitamin K with a goal INR of <1.4.
Prothrombin complex concentrates (PCC) have not shown improved outcome compared with fresh frozen plasma (FFP) but may have fewer complications compared with FFP and are reasonable to consider as an alternative to FFP.
FVIIa does not replace all clotting factors, and although the INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is not routinely recommended as a sole agent for oral anticoagulant reversal in ICH.
There is currently no specific antidote available to antagonize the effects of novel oral anticoagulants.
When is it safe to resume anticoagulation after spontaneous ICH?
Anticoagulation after nonlobar ICH and antiplatelet therapy after all ICH might be considered 2 to 4 weeks after symptom onset, particularly when there are definite indications for these agents.
When is it safe to resume antiplatelet agents?
In practice many recommend restarting antiplatelet medications within ∼1 week after ICH.
What is the role of surgery in ICH?
For most ICH patients, the role of surgery remains uncertain. Patients with cerebellar hemorrhage who are either deteriorating neurologically or who have brain stem compression and/or hydrocephalus from ventricular obstruction should undergo surgical removal of the hemorrhage as soon as possible. Surgical evacuation also may be considered for those patients presenting with lobar clots >30 mL and within 1 cm of the brain surface.
What are the indications for external ventricular drain (EVD) placement and ICP monitoring?
Patients with a GCS score of <8, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus might be considered for ICP monitoring and treatment.
How should thrombolytic-related symptomatic ICH be managed?
The following recommendations have been proposed for patients experiencing thrombolytic-related ICH: keep systolic blood pressure <140 mm Hg; check platelet count, fibrinogen, thromboplastin time, and activated partial thromboplastin time; and infuse both platelets (6 to 8 U) and cryoprecipitate, which contains factor VIII to rapidly correct the systemic fibrinoytic state created by tissue plasminogen activator. If fibrinogen is <100 mg/dL administer cryoprecipitate 0.10 μ/kg IV. Repeat fibrinogen in 1 hour, and if it is <100 mg/dL, repeat cryoprecipitate dose IV and consult neurosurgery.
Hematoma expansion usually occurs in the hyperacute setting.
Intensive blood pressure lowering to systolic blood pressure values <140 mm Hg is safe and results in better functional outcome on ordinal analysis of modified Rankin scale scores.
Rapid reversal with IV vitamin K and PCC in warfarin-induced ICH is indicated.
Consider surgery for lobar hematomas >30 mL and within 1 cm of the surface and cerebellar hemorrhage >3 cm.
Avoid corticosteroid administration in ICH.
Think of CAA in spontaneous lobar ICH age >55.
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here