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Aneurysmal Subarachnoid hemorrhage: Clinical manifestation and diagnosis

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Aneurysmal Subarachnoid hemorrhage: Clinical manifestation and diagnosis

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In the United States, the proportion of stroke due to ischemia, intracerebral hemorrhage, and subarachnoid hemorrhage (SAH) is approximately 87, 10, and 3 percent, respectively. Most nontraumatic SAHs are caused by ruptured saccular aneurysms. This is often a devastating clinical event with substantial mortality, and high morbidity among survivors.

The epidemiology, etiology, clinical manifestations, and diagnosis of aneurysmal SAH are reviewed here. Other aspects are discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis" and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Unruptured intracranial aneurysms" and "Overview of infected (mycotic) arterial aneurysm" and "Nonaneurysmal subarachnoid hemorrhage" and "Perimesencephalic nonaneurysmal subarachnoid hemorrhage".)

CLINICAL PRESENTATION

● Headache characteristics - The classic presentation of patients with aneurysmal SAH is a sudden-onset, severe headache typically described as the "worst headache of my life" [ 1]. Every patient with this kind of headache, often referred to as a "thunderclap headache" (see "Overview of thunderclap headache"), should be evaluated for SAH. Headache is often an isolated finding. In neurologically intact patients with a severe-onset headache peaking within one hour, three large sequential studies with a total of 5283 patients found that 329 patients (6 percent) had SAH [ 2-5].

Importantly, the headache onset in SAH is not always noted as instantaneous, either because the patient does not perceive it that way or because the physician does not elicit that information. In a study that included 132 patients with SAH, the time to peak intensity was one hour in six (5 percent), and the physician interobserver agreement for sudden onset was only moderate (kappa = 0.49) [ 2].

Location is not useful since the headache can be localized or generalized.

This generalized information is a limited summary of diagnosis, treatment, and/or medication information. It is not meant to be comprehensive and should be used as a tool to help the user understand and/or assess potential diagnostic and treatment options. It does NOT include all information about conditions, treatments, medications, side effects, or risks that may apply to a specific patient. It is not intended to be medical advice or a substitute for the medical advice, diagnosis, or treatment of a health care provider based on the health care provider's examination and assessment of a patient's specific and unique circumstances. Patients must speak with a health care provider for complete information about their health, medical questions, and treatment options, including any risks or benefits regarding use of medications. This information does not endorse any treatments or medications as safe, effective, or approved for treating a specific patient. UpToDate, Inc. and its affiliates disclaim any warranty or liability relating to this information or the use thereof. The use of this information is governed by the Terms of Use, available at https://www.wolterskluwer.com/en/know/clinical-effectiveness-terms ©2022 UpToDate, Inc. and its affiliates and/or licensors. All rights reserved.

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Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis - UpToDate

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In the United States, the proportion of stroke due to ischemia, intracerebral hemorrhage, and subarachnoid hemorrhage (SAH) is approximately 87, 10, and 3 percent, respectively. Most nontraumatic SAHs are caused by ruptured saccular aneurysms. This is often a devastating clinical event with substantial mortality, and high morbidity among survivors.

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Aneurysmal subarachnoid hemorrhage: Treatment and prognosis

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Aneurysmal subarachnoid hemorrhage: Treatment and prognosis

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Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis

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Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis

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Aneurysmal subarachnoid hemorrhage: Epidemiology, risk factors, and pathogenesis - UpToDate

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Twenty percent of strokes are hemorrhagic, with subarachnoid hemorrhage (SAH) and intracerebral hemorrhage, each accounting for 10 percent. Most spontaneous SAH

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Subarachnoid hemorrhage (SAH) is often a devastating event. The appropriate therapy for SAH depends in part upon the severity of hemorrhage. Level of consciousness on admission, patient age, and the amount of blood on initial head computed tomography (CT) scan are the most important prognostic factors for SAH at presentation [ 1].

A number of grading systems are used in practice to standardize the clinical classification of patients with SAH based upon the initial neurologic examination and the appearance of blood on the initial head CT. This topic will provide an overview of the more commonly used clinical and radiologic grading scales for SAH. Treatment and other aspects of SAH are discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".)

INDIVIDUAL GRADING SCALES

An ideal SAH grading scale would provide the following capabilities [ 2-4]:

●Guide management decisions that are influenced by the severity of SAH

●Provide prognosis for clinicians, patients, and family members

This generalized information is a limited summary of diagnosis, treatment, and/or medication information. It is not meant to be comprehensive and should be used as a tool to help the user understand and/or assess potential diagnostic and treatment options. It does NOT include all information about conditions, treatments, medications, side effects, or risks that may apply to a specific patient. It is not intended to be medical advice or a substitute for the medical advice, diagnosis, or treatment of a health care provider based on the health care provider's examination and assessment of a patient's specific and unique circumstances. Patients must speak with a health care provider for complete information about their health, medical questions, and treatment options, including any risks or benefits regarding use of medications. This information does not endorse any treatments or medications as safe, effective, or approved for treating a specific patient. UpToDate, Inc. and its affiliates disclaim any warranty or liability relating to this information or the use thereof. The use of this information is governed by the Terms of Use, available at https://www.wolterskluwer.com/en/know/clinical-effectiveness-terms ©2022 UpToDate, Inc. and its affiliates and/or licensors. All rights reserved.

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Subarachnoid hemorrhage grading scales - UpToDate

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Subarachnoid hemorrhage (SAH) is often a devastating event. The appropriate therapy for SAH depends in part upon the severity of hemorrhage. Level of consciousness on admission, patient age, and the amount of blood on initial head computed tomography (CT) scan are the most important prognostic factors for SAH at presentation [ 1].

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Subarachnoid hemorrhage (SAH) is often a devastating event with a high mortality and morbidity. Most SAH are caused by ruptured intracranial saccular aneurysms. In most cases, the presence of the aneurysm is unsuspected until SAH occurs. After aneurysmal SAH, the patient is at substantial risk of rebleeding: 3 to 4 percent in the first 24 hours and 1 to 2 percent each day in the first month [ 1]. Rerupture is associated with a mortality that is estimated to be 70 percent. Aneurysm repair is the only effective treatment to prevent this occurrence [ 2].

Unruptured cerebral aneurysms may manifest clinically by their mass effect on adjacent neurologic structures, or they may be discovered incidentally when a patient has a neuroimaging study for another indication. Such aneurysms have a future risk of rupture and SAH that depends in part on their size and location.

The treatment of cerebral aneurysms is discussed in this topic. Other aspects of the clinical features, diagnosis, and management of cerebral aneurysms and aneurysmal SAH are discussed separately. (See "Unruptured intracranial aneurysms" and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".)

TECHNIQUES

Surgical and endovascular techniques are available for aneurysm treatment. In many cases, anatomic considerations, such as size, location, along with other morphological features determine which treatment is most appropriate for the patient.

Surgery - Surgical management of cerebral aneurysms, in which a clip is placed across the neck of the aneurysm, is an effective and safe procedure with the evolution of microsurgical techniques in the hands of an experienced surgeon ( image 1). This applies to patients with unruptured cerebral aneurysms and those with subarachnoid hemorrhage (SAH) [ 3].

This generalized information is a limited summary of diagnosis, treatment, and/or medication information. It is not meant to be comprehensive and should be used as a tool to help the user understand and/or assess potential diagnostic and treatment options. It does NOT include all information about conditions, treatments, medications, side effects, or risks that may apply to a specific patient. It is not intended to be medical advice or a substitute for the medical advice, diagnosis, or treatment of a health care provider based on the health care provider's examination and assessment of a patient's specific and unique circumstances. Patients must speak with a health care provider for complete information about their health, medical questions, and treatment options, including any risks or benefits regarding use of medications. This information does not endorse any treatments or medications as safe, effective, or approved for treating a specific patient. UpToDate, Inc. and its affiliates disclaim any warranty or liability relating to this information or the use thereof. The use of this information is governed by the Terms of Use, available at https://www.wolterskluwer.com/en/know/clinical-effectiveness-terms ©2022 UpToDate, Inc. and its affiliates and/or licensors. All rights reserved.

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Treatment of cerebral aneurysms - UpToDate

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Subarachnoid hemorrhage (SAH) is often a devastating event with a high mortality and morbidity. Most SAH are caused by ruptured intracranial saccular aneurysms. In most cases, the presence of the aneurysm is unsuspected until SAH occurs.

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Vasospasm, Cushing triads. Drugs used for vasospasm.

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Vasospasm, Cushing triads. Drugs used for vasospasm.

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EVD Management (EVD insertion, Difference between EVD and ICP. EVD challenge. VP shunt)

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EVD Management (EVD insertion, Difference between EVD and ICP. EVD challenge. VP shunt)

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Pathophysiology of aneurysmal Subarachnoid haemorrhage (SAH)

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Pathophysiology of aneurysmal Subarachnoid haemorrhage (SAH)

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Definition of Aneurysmal SAH. Types and common location of aneurysm. Risk Factors and Signs and symptoms.

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Definition of Aneurysmal SAH. Types and common location of aneurysm. Risk Factors and Signs and symptoms.

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Medical and Nursing management of High ICP: Mannitol, 3% Saline, Atracurium and BIS&TOF. Ventilator and temperature management.

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Medical and Nursing management of High ICP: Mannitol, 3% Saline, Atracurium and BIS&TOF. Ventilator and temperature management.

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SAH grading scale and prognosis. Diagnostic (CTB, CTA) 

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SAH grading scale and prognosis. Diagnostic (CTB, CTA) 

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Surgical and Nursing management of SAH. (4VA, coiling, clipping, craniotomy, craniectomy) 

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Surgical and Nursing management of SAH. (4VA, coiling, clipping, craniotomy, craniectomy) 

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Diabetes insipidus (DI) is defined as the passage of large volumes (>3 L/24 hr) of dilute urine (< 300 mOsm/kg). It has the following 2 major forms:
Central (neurogenic, pituitary, or neurohypophyseal).
DI is characterized by decreased secretion of antidiuretic hormone.

Nephrogenic DI is characterized by decreased ability to concentrate urine because of resistance to ADH action in the kidney.

The most common form is central DI after trauma or surgery to the region of the pituitary and hypothalamus, which may exhibit 1 of the following 3 patterns:
Transient
Permanent
Triphasic

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Indication :

-Potentially survivable head injury

-No surgically treatable lesion accounting for intracranial hypertension

-Other conventional therapies of controlling ICP have failed

– Posture
– Hyperventilation
– osmotic and tubular diuretics
corticosteroids

-ICP > 20 to 25 mmHg for more than 20 min or >40 mmHg at any time

-unilateral cerebral hemispheric edema with significant shift (> 0.7 mm) of midline structures shown on CT

-gcs drop or low score

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Vasospasm is defined as focal or diffuse temporarily narrowed vessel caliber due to contraction of smooth muscle in the wall of arteries. It is detected by angiography or imaging studies (transcranial dopper [TCD], magnetic resonance [MR], and CT) or as seen during surgical clipping.
Vasospasm occurs in 67% of aSAH patients, is symptomatic in 30% to 40%, and results in ischemic infarction in 10% to 45% of patients.

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Management of Cerebral Vasospasm and DCI After aSAH: Recommendations

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Management of Cerebral Vasospasm and DCI After aSAH: Recommendations

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Oral nimodipine should be administered to all patients with aSAH (Class I; Level of Evidence A). (It should be noted that this agent has been shown to improve neurological outcomes but not cerebral vasospasm. The value of other calcium antagonists, whether administered orally or intravenously, remains uncertain.)

Maintenance of euvolemia and normal circulating blood volume is recommended to prevent DCI (Class I; Level of Evidence B).

Prophylactic hypervolemia or balloon angioplasty before the development of angiographic spasm is NOT RECOMMENDED (Class III; Level of Evidence B).

Transcranial Doppler is reasonable to monitor for the development of arterial vasospasm (Class IIa; Level of Evidence B). (New recommendation)

Perfusion imaging with CT or magnetic resonance can be useful to identify regions of potential brain ischemia (Class IIa; Level of Evidence B).

Induction of hypertension is recommended for patients with DCI unless blood pressure is elevated at baseline or cardiac status precludes it (Class I; Level of Evidence B).
Cerebral angioplasty and/or selective intra-arterial vasodilator therapy is reasonable in patients with symptomatic cerebral vasospasm, particularly those who are not rapidly responding to hypertensive therapy (Class IIa; Level of Evidence B).

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Physiological nervous system response to acute elevations of intracranial pressure.
Leads to Cushing’s triad of widened pulse pressure (increasing systolic, decreasing diastolic), bradycardia, and irregular respirations

In the first stage of the Cushing reflex, blood pressure and heart rate rise in response to sympathetic activation to overcome increases in ICP.

This sympathetic response allows for brain perfusion as long as the ICP is not too high to overcome. For the brain to remain adequately perfused, mean arterial pressure (MAP) must be maintained higher than ICP.

In the second stage of the Cushing reflex, hypertension continues to be present, but the patient becomes bradycardic rather than tachycardic.

Wide acceptance that bradycardia is a late-stage and likely terminal sign of worsening intracranial pathology.

Blood pressure will continue to rise until the MAP overcomes the ICP, and blood can adequately perfuse the brain, thereby resolving hypoxia and avoiding infarction.

In the later stages of the Cushing reflex, brainstem dysfunction secondary to increased ICP, tachycardia, or bradycardia is observable clinically as an irregularity in breathing; this is characterized initially by shallow breaths with occasional periods of apnea.

This activity occurs due to compression of the brainstem by increased ICP, and as a result, distortion of the respiratory centers.

Eventually, agonal breathing may develop as herniation of the brain begins, progressing to respiratory and cardiac arrest.

Overall, it seems that the Cushing reflex is the very last hemodynamic response to a systemic sympathetic activation that follows the acute rise in ICP.

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Vasospasm typically begins no earlier than day 3 after haemorrhage, reaching a peak at days 7 to 8.

Vasospasm can also occur even at the time of hospital admission.

Vasospasm is believed to be produced by spasmogenic substances (substance which induce spasm) generated during the lysis of subarachnoid blood.

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Intra-arterial administration of vasodilators are generally used for diffuse vasospasm involving smaller arterial branches.

Various article reported as effective for improving vasospasm in case series include intra-arterial nicardipine, milrinone, papaverine, nimodipine, verapamil, and intrathecal nitroprusside. Intra-arterial vasodilator therapy and angioplasty also may be used in combination.

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Often mentioned as the worst headache ever experienced by the patients

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Often mentioned as the worst headache ever experienced by the patients

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Case fatality for SAH is high with outcome that’s less than half. One-third of patients will survive with good recovery; one-third would survive with a disability; and one-third will die.
thus prevention is one of the very way to bring substantial improvement, early recognition of sign and symptom of SAH could bring a good outcome and recovery of SAH.

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The hunt and Hess scale

The Hunt and Hess scale describes the clinical severity of SAH resulting from the rupture of an intraceleberal aneurysms  and is widely used as a predictor of survival rate. Grades 1, 2 and 3 have better outcomes than 4 and 5.

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WFNS clinical scale
The World Federation of Neurological Surgeons as grades SAH according to motor score and total GCS. Their grading scale gives us an idea as to what to expect in terms of survival. Advantage is that it uses the GCS score to identify the grading.

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The Glasgow Coma Scale (GCS) is used to describe the extent of impaired consciousness in all types of acute medical and trauma patients, baseline to determine patients neurological changes. GCS had less detailed description yet it can provide a useful summary of the overall severity.

Despite the usefulness of GCS, there’s some disadvantages of GCS such as,

It’s hard to apply for those with hearing loss or speech impediment.

If a patient is intubated or unable to speak, they are evaluated only on the motor and eye-opening response and the suffix T is added to their score to indicate intubation.

If patient is sedated or paralysed, GCS should not be valid thus if possible, the clinician should obtain the score before sedating the patient to at least gain the baseline of the patients score as comparison thereafter.

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Temperature management using Blanketrol machine for patients with strict ICP control with IV sedation

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Temperature management using Blanketrol machine for patients with strict ICP control with IV sedation

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Recommendation ventilator setting  algorithm 

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Recommendation ventilator setting  algorithm 