One important component of the initial evaluation is to determine the underlying etiology of the ICH based on imaging, history, exam, labs, and other diagnostic tools. The primary neuroimaging modalities used in ICH include CT, CTA, MRI, and cerebral angiography.

A head CT without contrast is the preferred imaging modality for the initial diagnosis of ICH. It is readily available, quick, and provides information about the size of the hemorrhage, location, edema, mass effect, midline shift, and any extension into the ventricles, also known as IVH [2]. Acute blood appears hyperdense on CT. A noncontrast head CT can also be used to calculate the hematoma volume. A common formula used for this calculation is ABC/2, where A is the greatest diameter of the hemorrhage on the CT slice with the largest area of hemorrhage, B is the largest diameter 90° to A on the same slice, and C is the approximate number of slices with hemorrhage multiplied by the thickness of the slice in centimeters [3]. A multiplied by B multiplied by C, divided by 2 gives the approximate volume of the hemorrhage in cubic centimeters. Referring to Fig. 5.3, A is measured at approximately 3.6 cm, B is approximately 2.0 cm, and C is determined to be 4 slices, which is then multiplied by the thickness of the slice (at our institution, 0.5 cm). Using the ABC/2 formula these values are multiplied and then divided by 2, which estimates an ICH volume of approximately 7 cc.

A CT angiography of the head and neck with IV contrast is commonly used to assess for underlying vascular lesions. It is important to remember, however, that sometimes, underlying lesions can be obscured by the hemorrhage; therefore, this is often repeated in a delayed fashion. One useful finding for predicting hematoma expansion with CTA is the spot sign. This finding is defined as a focus of contrast enhancement within the hemorrhage on a postcontrast image and represents an area of active contrast extravasation [4, 5].

MRI with and without contrast is another commonly used imaging modality in ICH. Susceptibility-weighted imaging (SWI) and Gradient-recalled echo (GRE) are two sequences that can be helpful in identifying small areas of hemorrhage (microbleeds) that are not detected on CT and are useful in diagnosing CAA. Additionally, contrast studies can be helpful to identify underlying neoplastic lesions, as these lesions enhance with gadolinium.

Cerebral angiography, or digital subtraction angiography (DSA), is yet another tool available to identify the underlying cause of an ICH. This is more invasive than previously discussed modalities, but may be considered in specific patients where CTA or MRA are inconclusive and a vascular abnormality is high on the differential.

Hypertension is the most common cause of ICH. Chronically elevated blood pressure is the main contributor to lipohyalinosis, a disease that affects the small deep-brain vessels, making them prone to rupture. Sudden fluctuations in blood pressure in otherwise healthy individuals can also, in rare instances, cause ICH. Hypertensive hemorrhages are located in deep-brain structures: basal ganglia, thalamus, cerebellum, and midbrain. Obtaining a thorough history can be helpful, with attention to any history of hypertension, events leading to symptom onset (such as a strenuous physical activity or emotional event), or drug use. In patients with unknown past medical history, it may be helpful to look for evidence of left ventricular hypertrophy on EKG or echo. A toxicology screen on all ICH patients to rule out illicit drug use is also useful.

Cerebral amyloid angiopathy (CAA) is another common cause of ICH. CAA is characterized by the accumulation of amyloid deposits in the walls of small and medium-size brain vessels, also making them prone to rupture [6]. The incidence of CAA is strongly age dependent and is most often seen in patients greater than age 60. Some helpful findings on imaging to distinguish CAA from other causes of ICH include lobar (cortical) location and multiple hemorrhagic lesions including small hemorrhages (microbleeds). Despite these helpful clues, definitive diagnosis can only be made by pathology.

Coagulopathy is an important cause of secondary ICH. Coagulopathy can be divided into acquired and congenital. Acquired coagulopathies include those related to medications (warfarin) and those secondary to renal or liver disease. With anticoagulation-induced ICH, it is extremely important to determine the date and time the medication was last taken and obtain a full coagulation panel, as the highest risk of hemorrhage expansion is within the first six hours of hemorrhage. The reversal strategy should be tailored to the type of anticoagulation used. Renal disease causes increased risk of ICH through uremia-related platelet dysfunction, while liver disease increases the risk of ICH due to impaired synthesis of clotting factors. Congenital forms of coagulopathy include hemophilia A and B as well as other rare conditions.

Intracranial tumors are a less common cause of ICH, with rates ranging anywhere from 1 to 10% of all ICH cases [7]. Neoplastic lesions can be classified into two major groups: primary brain tumors and metastatic disease. Of the primary brain tumors, malignant gliomas, such as glioblastoma multiforme and oligodendroglioma, are particularly predisposed to hemorrhage. Among metastatic disease, breast and lung cancer are commonly associated with ICH due to their high prevalence in the general population, while melanoma, renal cell, thyroid cancer, and choriocarcinoma are also associated with ICH due to their proclivity to bleed.

Vascular lesions are yet another cause of ICH. Vascular lesions include aneurysms, cavernous malformations, and arteriovenous malformations. Rupture of these lesions can lead to multicompartmental hemorrhage including not only subarachnoid hemorrhage but also ICH. Subarachnoid hemorrhage is discussed further in detail in Chap. 4.

Prognostication in patients with ICH remains difficult. The ICH score is a clinical grading scale designed to capture baseline disease severity and approximate a prognosis. The ICH score is determined based on five features: Glasgow Coma Scale, IVH volume, presence of IVH, infratentorial origin, and patient’s age [8]. Higher scores are associated with more severe baseline disease. Refer to Table 5.1 for scoring calculation.

The presence of IVH is another important factor not only in prognostication but also in guiding management. IVH occurs in approximately 45% of all patients with ICH [9, 10]. It is typically associated with worse outcomes, as patients are at increased risk of developing noncommunicating (obstructive) hydrocephalus.

Scoring systems, like the ICH score, should be used carefully to avoid self-fulfilling prophecies (patients labeled as having poor prognosis are more likely to have their care withdrawn, which in turn guarantees a poor prognosis). In other words, this scale constitutes one of the numerous factors to be considered when prognosticating and making code-status decisions. Studies have shown that early do-not-resuscitate (DNR) orders (within the first 24 h of hemorrhage) are associated with an increased risk of in-hospital mortality after acute ICH, even after adjusting for patient and hospital characteristics, suggesting that DNR use may be a proxy for overall aggressiveness of care [11, 12].

Early assessment of the patient’s respiratory status is essential. Patients may require urgent or emergent intubation for airway protection. Obtain an ABG, paying particular attention to CO₂. In the ICU setting, consider capnography and correlate this with the ABG.