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Hemorrhage
Updated: Sep 22, 2015
Author: Rami C Zebian, MD; Chief Editor: Robert E O'Connor, MD, MPH more...
Overview
Emergent management of subarachnoid hemorrhage (SAH), including prehospital care, is
critical: An estimated 10-15% of patients die before reaching the hospital. Moreover,
mortality rate reaches as high as 40% within the first week, and about 50% die in the first 6
months. [1, 2, 3, 4, 5]
The common medical use of the term subarachnoid hemorrhage (SAH) refers to the
nontraumatic presence of blood within the subarachnoid space from some pathologic process,
usually from rupture of a berry aneurysm or arteriovenous malformation (AVM) (see the
following image).
Grade II: Severe headache and a nonfocal examination, with or without mydriasis
Prehospital Care
Advances in the management of subarachnoid hemorrhage (SAH) have resulted in a relative
reduction in mortality rate that exceeds 25%. However, more than one third of survivors have
major neurologic deficits. Mortality and morbidity rates increase with age and poorer overall
health of the patient.
Early identification of sentinel headaches is key to reduced mortality and morbidity rates. Use
sedation judiciously.
Secure intravenous access, and closely monitor the patient's neurologic status.
Address the patient's airway, breathing, and circulatory status (ABCs). In addition, reliable
neurologic examinations before and after initial treatment are critically important to
optimizing management and to deciding on the appropriate neurosurgical intervention.
Intubation
Endotracheal (ET) intubation of obtunded patients protects them from aspiration caused by
depressed airway protective reflexes. Also intubate to hyperventilate patients with signs of
herniation.
Thiopental and etomidate are the optimal induction agents in subarachnoid hemorrhage
(SAH) during an intubation. Thiopental is short-acting and has a barbiturate cytoprotective
effect. It should be used only in hypertensive patients because of its propensity to drop
systolic blood pressure (SBP), which is the leading cause of secondary brain injury. In
hypotensive and normotensive patients, use etomidate.
Use rapid sequence intubation if possible. In the process, to blunt intracranial pressure (ICP)
increase, ideally use sedation, defasciculation, short-acting neuromuscular blockade, and
other agents with ICP-blunting properties (such as intravenous lidocaine).
Precautions
Avoid excessive or inadequate hyperventilation. Target the partial pressure of carbon dioxide
(pCO2) at 30-35 mm Hg to reduce elevated ICP. Excessive hyperventilation may be harmful
to areas of vasospasm.
Avoid excessive sedation. It makes serial neurologic exams more difficult and has been
reported to increase ICP directly. However, avoid any increase in ICP due to excessive
agitation from pain and discomfort.
Use the following interventions early and judiciously to decrease elevated ICP when
herniation is suspected:
Use osmotic agents, such as mannitol, which reduces ICP 50% in 30 minutes, peaks
after 90 minutes, and lasts 4 hours
Loop diuretics, such as furosemide, also decrease ICP without increasing serum
osmolality
Provide supplemental oxygen for all patients with central nervous system (CNS) impairment.
Consultations
Monitoring
Monitor the patient's cardiac activity, oximetry, automated blood pressure (BP), and end-tidal
carbon dioxide, when applicable. End-tidal carbon dioxide monitoring of intubated patients
enables the clinician to avoid excessive or inadequate hyperventilation. Target the partial
pressure of carbon dioxide (pCO2) at about 30-35 mm Hg to reduce elevated intracranial
pressure (ICP).
Invasive arterial line monitoring is indicated when dealing with labile BP (common in high-
grade subarachnoid hemorrhage).
Antihypertensive agents were previously advocated for a systolic blood pressure (SBP)
greater than 160 mm Hg or a diastolic BP (DBP) greater than 90 mm Hg.
Keep systolic blood pressure 90-140 mm Hg before aneurysm treatment, then allow
hypertension to keep the SBP less than 200 mm Hg. [8] Use medications that can be titrated
rapidly.
Vasopressors may be indicated to keep the SBP over 120 mm Hg; this avoids central nervous
system (CNS) damage in the ischemic penumbra from the reactive vasospasm seen in
subarachnoid hemorrhage (SAH).
Consult critical care providers who will be involved in ongoing care of the patient, as
individual practices vary.
Elevate the head of the bed 30 to facilitate intracranial venous drainage. Emergent
ventricular drainage by the neurosurgeon may be necessary.
Maintain the patient's serum glucose level at 80-120 mg/dL; use sliding or continuous
infusion of insulin if necessary. [8]
Maintain euvolemia (central venous pressure [CVP], 5-8 mm Hg); if cerebral vasospasm is
present, maintain hypervolemia (CVP of 8-12 mm Hg, or pulmonary capillary wedge
pressure [PCWP] of 12-16 mm Hg). [8, 9]
Do not overhydrate patients because of the risks of hydrocephalus.
Patients with subarachnoid hemorrhage (SAH) may also have hyponatremia from cerebral
salt wasting.
Seizure prevention
Prophylactic use of anticonvulsants does not acutely prevent seizures after subarachnoid
hemorrhage (SAH), but use anticonvulsants in patients who have had a seizure or if local
practice dictates routine use.
Begin with anticonvulsants that do not change the level of consciousness (ie, phenytoin first;
use barbiturates or benzodiazepines only to stop active seizures).
Controversial measures
A randomized study of patients in an intensive care unit (ICU) demonstrated fewer ischemic
events after aneurysmal subarachnoid hemorrhage (SAH) when high-dose magnesium was
given for 10 days. The presumed mechanism was decreased cerebral vasospasm. [10] A meta-
analysis demonstrated similar findings. [11] However, other studies have shown no benefit from
magnesium. [12] Clearly, further study is indicated.
Stabilize patients promptly for transfer in an advanced cardiac life support (ACLS)
monitored unit. Address airway and the possible need for intubation or other emergent
interventions, such as mannitol and hyperventilation, prior to transfer.
http://emedicine.medscape.com/article/794076-overview#showall