The most important differential diagnosis in this case is head injury following a fall.

Therefore, the paramedics arriving on scene must take spinal precautions. Other differential diagnoses are various causes of syncope (Overview).

According to Table 2.1 Mr. Parker has the suspected diagnosis of a Grade 4 SAH. The medic does not have the necessary clues to come to the exact diagnosis, especially since it is not obvious if the loss of consciousness occurred before or after the fall. Table 2.2 shows the Glasgow Coma Scale (GCS).

On physical exam, Mr. Parker opened his eyes in response to pain and had no verbal response, but showed flexion/withdrawal to pain – thereby obtaining a GCS of 7 points.

The CT (Fig. 2.1) shows subarachnoid blood in the area of the circle of Willis, the basal cisterns, the anterior cerebral fissure, and the fourth ventricle. It is seen as a hyperdense (white) structure.

The most important complication of SAH is recurrent hemorrhage. It usually occurs in the first few days following the event. The risk of recurrent hemorrhage from an untreated aneurysm is 35–40 % in the first 4 weeks, decreasing after the first month 1–2 % per day and finally stabilizing at 3 % per year [2]. Apart from the acute rebleed, patients are at risk of intracerebral and intraventricular hemorrhages.

Due to the altered cerebrospinal fluid reabsorption after SAH, occluding and malabsorption hydrocephalus often results. This leads to an increase in intracranial pressure, which acutely endangers the patient. The head CT shows the typical ventricular dilation, often together with CSF diapedesis, and additional signs of increased intracranial pressure such as flattening of the gyri. The therapy of choice is insertion of an external ventricular CSF drain (EVD).

Cardiac complications are not rare in SAH patients. ECG changes can be seen in ¾ of the patients; the varied symptoms include sinus brady-/tachycardia, QT prolongation, heart blocks, ST elevation and depression, T-wave changes, and pathological Q waves.

Cardiac markers can also be raised. ECHOs often show wall dysfunction and histopathological changes in the myocardium. These signs can mimic acute MI. Acute heart failure can lead to arterial hypotension, pulmonary edema, cardiac arrest, and sudden cardiac death. However, coronary angiography shows typically no evidence of coronary artery stenosis. Causes of the cardiac signs are excessive releases of epinephrine and norepinephrine, as well as imbalances in the parasympathetic nervous system.

Once the acute dangers of the SAH have passed, the patients are at risk for cerebral vasospasms. Vasospasm can cause cerebral ischemia, which further worsens the prognosis. Vasospasm usually occurs between the fourth and fourteenth day (maximum on the seventh day) and last approximately 3 weeks after the SAH. Permanent neurological deficits due to the recurrent hemorrhage/ischemia include paralysis, cognitive disorders, epilepsy, neuroendocrine dysfunction, and dysfunction of the sleep wake cycle.

>> The radiological tests showed an advanced SAH with beginning CSF accumulation and an elbow fracture with dislocation. Mr. Parker’s pupils remained reactive. The anesthesia team inserted hemodynamic monitoring including an arterial line and a central venous catheter (CVC). Mr. Parker was then taken to the OR for the insertion of an EVD. The EVD delivered bloody CSF. ICP monitoring showed normal values. Digital subtraction angiography revealed a left anterior cerebral artery aneurysm. The neurosurgeon decided on immediate intervention, and the aneurysm was clipped the same day.

After surgery, Mr. Parker was transferred to the ICU intubated, ventilated, and sedated. Mrs. Parker had been waiting there for several hours already. She seemed lost in shock and had her two children with her.

As outlined in Sect. 2.1.5, treatment of the bleeding source prevents rebleeding. The prognosis of SAH is not definitively known. A SAH is potentially life-threatening, and in an uncomplicated SAH, possible neurological deficits can appear as early as 14 days after the original bleed.

The first goal is preventing rebleeding. It is therefore important to identify the source of the hemorrhage – usually an aneurysm. Early intervention, within 24–36 h, is recommended to reduce the risk of rebleeding. Cerebral aneurysms can be treated in either of the following two ways:

Lowering the blood pressure reduces the likelihood of rebleeding, especially in untreated aneurysms. But hypotension also increases the danger of cerebral ischemia, if the patient develops vasospasm. As a compromise to both risks, blood pressure in patients with untreated aneurysms should be maintained below 180 mmHg systolic and 100 mmHg diastolic.

If the aneurysm has been treated, the main goal is preventing cerebral ischemia due to vasospasm. Calcium channel blockers appear to have a beneficial effect and are begun early after the diagnosis of SAH. The standard dose is 60 mg nimodipine every 4 h PO or via gastric tube. IV administration is not recommended due to hypotension. Nimodipine therapy should be continued for 21 days.

The second mainstay of vasospasm therapy is the so-called triple-H therapy: hypervolemia, hypertension, and hemodilution. Triple-H therapy improves cerebral perfusion; however, it is unclear if cerebral infarction can be avoided. Side effects of the triple-H therapy are not uncommon and include cerebral edema, repeat bleeding, hyponatremia, and heart failure accompanied by pulmonary edema. Hence, aggressive triple-H therapy is not appropriate for all patients. Some neurointensivists prefer to avoid volume overload and instead restrict the therapy to arterial hypertension and hemodilution (double-H therapy). Scientific evidence supporting triple-H or double-H therapy is relatively weak.

Target values of the volume and blood pressure therapies are CVP of 8–12 cm H₂O, hematocrit of 30–35 %, and blood pressure of 20 % above the individual’s normal value. Hypovolemia must be avoided. However, there is no evidence that hypervolemia is better or worse than normovolemia.

New therapeutic, largely experimental treatments to prevent cerebral vasospasm include intraventricular administration of thrombolytic agents; vasodilators; platelet aggregation inhibitors; anticoagulants; neuroprotection agents, such as tirilazad; and the administration of statins, magnesium, nitric oxide (NO) donors, endothelin antagonists, potassium channel activators, and erythropoietin. The quality of the scientific evidence for these treatments varies; in general, more research is necessary.

If cerebral vasospasm is detected, triple- or double-H therapy is begun. Further options to treat vasospasm include endovascular balloon angioplasty and intra-arterial administration of vasodilators [2].

>> Standard SAH therapy was initiated in the ICU. The trauma surgeons indicated the need for surgical repair of the elbow fracture. However, considering the acute cerebral trauma, they agreed to wait a few days. Mrs. Parker mentioned that her husband had been complaining of a bad headache lately. “He thought his blood pressure was too high and he wanted to go to his doctor. If only he hadn’t postponed the appointment.”