Subarachnoid Hemorrhage Case File

Subarachnoid Hemorrhage Case File

Eugene C. Toy, MD, Ericka Simpson, MD, Pedro Mancias, MD, Erin E. Furr-Stimming, MD

CASE 12

A 50-year-old woman is brought to the emergency department (ED) after experiencing a sudden onset of severe headache associated with vomiting, neck stiffness, and left-sided weakness. She was noted to complain of the worst headache of her life shortly before she became progressively confused. Two weeks ago, she returned from jogging and noted a moderate headache with nausea and photophobia. She has a history of hypertension and tobacco use. On examination, her temperature is 37.6°C (99.8°F); heart rate is 120 beats/min; respiration rate is 32 breaths/min; and blood pressure is 180/90 mm Hg. She is stuporous and moaning incoherently. Her right pupil is dilated with papilledema and ipsilateral ptosis, and she vomits when a light is shone in her eyes. She has a left lower face droop and does not withdraw her left arm and leg to pain as briskly compared to the right. Her neck is rigid. Her chest examination reveals tachycardia and bibasilar crackles. During the examination, her head suddenly turns to the left, and she exhibits generalized tonic-clonic activity that lasts approximately 2 minutes before spontaneously abating. STAT laboratory tests show a sodium level of 125 mEq/L. The electrocardiograph (ECG) shows broad, deeply inverted T waves and a prolonged QT interval.

▶ What is the most likely diagnosis?

▶ What is the next diagnostic step?

▶ What is the next step in therapy?

ANSWERS TO CASE 12:

Subarachnoid Hemorrhage                                        

Summary: A 50-year-old woman with a history of hypertension and tobacco use presents with sudden onset of the worse headache of her life associated with confusion, vomiting, neck stiffness, and left-sided weakness. She was noted to complain of a headache 2 weeks ago. She is now hypertensive. Her neurologic examination is significant for stupor, right cranial nerve III paralysis, left-sided weakness, neck stiffness, and a new-onset seizure. Her workup is significant for hyponatremia and ECG changes.

• Most likely diagnosis: Subarachnoid hemorrhage
• Next diagnostic step: Noncontrast computed tomography (CT) of the head
• Next step in therapy: Cerebral angiography

ANALYSIS

Objectives

1. Identify the epidemiology and risk factors for subarachnoid hemorrhage.
2. Understand the prognosis and complications of subarachnoid hemorrhage.
3. Know a diagnostic and therapeutic approach to subarachnoid hemorrhage.

Considerations

This 50-year-old woman has multiple risk factors for subarachnoid hemorrhage caused by an underlying aneurysm: (a) her age (mean age for subarachnoid hemorrhage is 50); (b) gender (slightly higher risk for females); (c) hypertension; and (d) tobacco use. The complaint of “the worst headache of my life” to describe its sudden severe onset is classic, and it may or may not be associated with altered mentation and focal neurologic deficits. There is usually a history of a recent moderate headache as a result of a sentinel bleed, as in her case after running. Approximately 60% of subarachnoid hemorrhages occur during physical or emotional strain, head trauma, defecation, or coitus. The clinical severity of a subarachnoid hemorrhage is graded based on the degree of stupor, nuchal rigidity, focal neurologic deficits, and elevation of intracranial pressure (ICP). This patient exhibits neurogenic pulmonary edema, one of the many systemic complications of subarachnoid hemorrhage. Her neurologic signs localize to a ruptured right posterior communicating artery aneurysm, with the bleed causing compression of the nearby ipsilateral cranial nerve III with mydriasis, ptosis, and impaired extraocular movements. Her contralateral hemiparesis and complex partial seizure with secondary generalization can result from either parenchymal extension of the hemorrhage, edema, or middle cerebral artery (MCA) vasospasm, all three of which are complications of subarachnoid hemorrhage. Hyponatremia is frequently seen on chemistries, correlating with an elevation of atrial natriuretic factor, cerebral salt wasting, and/or the syndrome of inappropriate antidiuretic hormone (SIADH). ECG changes, especially QT prolongation, T-wave inversion, and arrhythmias, are also systemic complications common to subarachnoid hemorrhage.

APPROACH TO:

Subarachnoid Hemorrhage                                        

DEFINITIONS

SUBARACHNOID SPACE: The spongy potential space between the arachnoid mater and the pia mater. The headache and nuchal rigidity are caused by chemical inflammation of the pia and arachnoid from blood degradation products in this space.

SENTINEL BLEED: Intermittent aneurysmal subarachnoid hemorrhage causing lesser headaches that precede the “worst headache” that occurs with rupture of the aneurysm.

VASOSPASM: Most alarming complication of aneurysmal subarachnoid hemorrhage in which irritation causes constriction of major cerebral arteries, vasospasm, lethargy, and delayed cerebral infarction. Vasospasm occurs mostly with aneurysms rather than other causes of subarachnoid hemorrhage, and it peaks between 4 and 14 days. Transcranial Doppler can be used to detect a change in flow velocity in an affected MCA.

ACUTE COMMUNICATING HYDROCEPHALUS: Complication that occurs because of obstruction of the subarachnoid granulations in the venous sinuses by the subarachnoid blood. CT shows enlarged lateral, third, and fourth ventricles, with clinical signs of headache, vomiting, blurry and double vision, somnolence, and syncope.

CLINICAL APPROACH

Etiologies

Subarachnoid hemorrhage is the underlying cause of approximately 10% of stroke presentations and results from a number of etiologies. Ruptured saccular or berry aneurysms account for up to 80% of nontraumatic subarachnoid hemorrhage and portend the worst prognosis. More than three-fourths of intracerebral aneurysms arise in the anterior circulation. The most frequent sites of aneurysms are in the anterior communicating artery (up to one-third of aneurysmal subarachnoid hemorrhages), followed by the bifurcation of the internal carotid artery with the posterior communicating artery and then by the bifurcation of the internal carotid artery with the MCA. One-fourth of patients will have more than one aneurysm, with risk for rupture increasing with the size of the aneurysm. Fibromuscular dysplasia is an associated etiology in one-fourth of aneurysm patients, whereas polycystic kidney disease is related to 3% of cases. Other risk factors for aneurysms include chronic severe hypertension with diastolic blood pressure greater than 110 mm Hg, liver disease, tobacco and alcohol use, vasculitides, collagen vascular disorders such as Marfan syndrome, infections (mycotic aneurysms), and oral contraception. Nonaneurysmal causes of subarachnoid hemorrhage include trauma, arteriovenous malformations, and cocaine or amphetamine abuse.

Diagnosis and Prognosis

CT of the head without contrast is the most sensitive neuroimaging study for detecting subarachnoid bleeding, appearing as hyperdensity within the cerebral convexities, cisterns, and parenchyma (Figure 12–1). Intraventricular hemorrhage portends a worse prognosis and increased risk for hydrocephalus. Sensitivity of CT is greatest 24 hours after the event, with 50% of cases still detectable after 1 week. Negative CT of the head occurs in 10% to 15% of cases and should be further evaluated with lumbar puncture looking for xanthochromia (yellowish discoloration of cerebrospinal fluid [CSF]) and increased red blood cells. CSF studies are most sensitive 12 hours after onset but can be negative in 10% to 15% of patients, in which case the prognosis is better. CT, magnetic resonance imaging (MRI), or conventional angiography can be used to screen for an underlying aneurysm (Figure 12–2).

Figure 12–1. Noncontrast CT scan subarachnoid blood in the left sylvian fissure (bright) and within the left lateral ventricle. (Reproduced, with permission, from Kasper DL, et al. Harrison’s Principles of Internal Medicine. 16th ed. New York, NY: McGraw-Hill; 2004:2389.)

Figure 12–2. Conventional angiogram of the right vertebral and basilar artery showing the large aneurysm. (Reproduced, with permission, from Kasper DL, et al. Harrison’s Principles of Internal Medicine. 16th ed. New York, NY: McGraw-Hill; 2004:2389.)

Up to 60% of patients die in the first 30 days after a subarachnoid hemorrhage, 10% instantly without warning. First month mortality is 40% for hospitalized patients, with worsening of mortality to 50% to 80% with rebleeding. Severity of cases and their prognoses can be graded using a variety of scales. One of the most common is the Hunt and Hess scale based on alertness and presence of focal signs:

• Grade I subarachnoid hemorrhage patients are alert with mild headache and nuchal rigidity and have a 5% chance of deteriorating with a 3% to 5% mortality risk.
• Grade II patients have moderate-to-severe headache and nuchal rigidity and a 6% to 10% mortality risk.
• Grade III is similar to Grade II but with drowsiness, confusion, and a mild focal deficit.
• Grade IV patients have stupor and moderate-to-severe hemiparesis.
• Grade V patients are comatose with signs of severe increased ICP, and they have the worst prognosis with 80% chance of deteriorating, 25% to 30% rebleeding rate, and 50% to 70% mortality risk. Delayed vasospasm is a potentially serious complication that occurs in up to 20% of cases.

Treatment

Grades I and II subarachnoid hemorrhage may be observed after diagnostic measures. Emergent conventional angiography is warranted if ruptured aneurysm is suspected and neurosurgical intervention is required. Repeat angiography can be necessary if the underlying etiology is obscured by vasospasm. Endovascular coiling is indicated to reduce rebleeding in low-grade cases of subarachnoid hemorrhage and has been shown to be superior to clipping. Clipping should be performed in the first 48 hours after onset or be delayed for 2 weeks to avoid the window of greatest risk for vasospasm, especially with complicated high-grade cases. The most notable complication of subarachnoid hemorrhage is delayed cerebral ischemia, which may be secondary to vasospasm or microthrombi. To avoid this often fatal complication, it is essential to support cerebral perfusion by administering fluids with the goal of euvolemia and allowing some degree of hypertension. Nimodipine, a calcium channel blocker, is often utilized to reduce vasospasm. It is also important to address other complications, including metabolic derangements (hyponatremia, SIADH, cerebral salt wasting), respiratory (neurogenic pulmonary edema) and cardiac (arrhythmias) complications, seizures, and hydrocephalus, which may require ventriculostomy.

COMPREHENSION QUESTIONS

Match the following etiologies (A-C) to the clinical situation of Questions 12.1 to 12.3:

A. Anterior communicating artery aneurysm

B. Posterior communicating artery aneurysm

C. Vasospasm

12.1 A 35-year-old woman was admitted last week for a subarachnoid hemorrhage caused by a left MCA aneurysm. Today during rounds, she appears much less alert.

12.2 A 45-year-old man with a history of alcohol consumption complains of a “thunderclap headache,” nausea, and blurry vision with right anisocoria and diplopia on examination.

12.3 A 20-year-old woman is found to have hypertension, kidney cysts, and intermittent headaches.

12.4 An emergency room physician consults you for the best first study to evaluate a possible subarachnoid hemorrhage in a 54-year-old woman who came in for severe headache.

A. Transcranial Doppler study

B. Electroencephalograph (EEG)

C. Positron emission tomography (PET) scan of the brain

D. CT scan of the head without contrast

E. MRI of the brain without contrast

12.5 An internist consults you for the best study to evaluate for the possible development of vasospasm 1 week after admission for a subarachnoid hemorrhage. Which of the following would be the most appropriate first study?

A. Transcranial Doppler study

B. EEG

C. PET scan of the brain

D. CT scan of head without contrast

E. MRI of the brain without contrast

ANSWERS

12.1 C. Delayed vasospasm (and acute hydrocephalus) can arise days after a ruptured aneurysm with subarachnoid hemorrhage. Emergent neuroimaging should be performed to assess the need for angiography or ventriculostomy.

12.2 B. Ipsilateral ptosis, pupil dilation, and ophthalmoplegia result from compression of the third nerve by a posterior communicating artery aneurysm and bleed.

12.3 A. The most common site for a cerebral aneurysm in polycystic kidney disease is in the anterior communicating artery, although multiple aneurysms may be observed.

12.4 D. CT of the head without contrast is a rapid and sensitive imaging modality to detect subarachnoid blood. If it is negative and a high suspicion remains, a lumbar puncture should be performed.

12.5 A. Transcranial Doppler is sensitive for detecting elevated MCA velocity, a finding caused by vasospasm, although conventional angiography is usually needed to confirm vasospasm. For acute changes in level of consciousness, CT of the head is preferred as a faster way to evaluate for hydrocephalus and need for ventriculostomy.

    CLINICAL PEARLS    

▶ Most cases of subarachnoid hemorrhage with no history of head trauma are caused by an underlying aneurysm. ▶ Subarachnoid hemorrhage severity and prognosis can be assessed by the degree of change in consciousness, headache, nausea and vomiting, nuchal rigidity, focal deficits, and seizures. ▶ Mass effect from edema and parenchymal spread, vasospasm from subarachnoid involvement, and hydrocephalus from intraventricular spread are all serious delayed neurologic complications of subarachnoid hemorrhage that may not be apparent on the initial evaluation. ▶ Ensuring euvolemic volume status and using nimodipine are important parts of medical management of subarachnoid hemorrhage. Endovascular coiling and clipping are surgical options with appropriate windows of intervention.

REFERENCES

Al-Shahi R, White PM, Davenport RJ, Lindsay KW. Subarachnoid haemorrhage. BMJ. 2006; 333(7561):235-240. 

Dority JS, Oldham JS. Subarachnoid hemorrhage: an update. Anesthesiology Clin. 2016;34(2):577-600. 

Feigin VL, Findlay M. Advances in subarachnoid hemorrhage. Stroke. 2006;37(2):305-308.

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