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PREVENTION AND TREATMENT OF COMPLICATIONS

Dalam dokumen Acute stoke care 2 ed (Halaman 134-139)

As with other strokes, general medical complications such as DVT, pneumonia, and other infections are common. SAH has particular complications that we will address here: hydrocephalus, seizure, cerebral vasospasm and delayed ischemic deficits.

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114 Subarachnoid hemorrhage (SAH)

Hydrocephalus

Significant hydrocephalus occurs in ~20% of patients with SAH. This may be already present at the time of presentation with SAH.

Diagnosis

Clinical signs include a decrease in level of consciousness, agitation, hypertension, and bradycardia. However, these signs are not specific.

CT of head without contrast: enlargement of ventricles.

Treatment

External drainage of CSF via intraventricular catheter (ventriculostomy or external ventricular drain).

Ventriculostomy must be monitored for amount of CSF drained and for infection.

If hydrocephalus is persistent, CSF drainage can be converted to internal drainage by placement of ventriculo-peritoneal, ventriculo-atrial, or lumbo-peritoneal shunt by a

neurosurgeon.

Seizure

Seizure may increase blood pressure and may increase rebleeding risk.

Prevention

Without good evidence for efficacy, we do not routinely administer antiepileptic agents unless a seizure has occurred– or, if we do, it is only for a short term.

Phenytoin 300 mg per day and adjusted to maintain level of 10–20μg/mL.

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Ruptured aneurysms: management 115

Diagnosis

Non-convulsive seizure may go unrecognized. Bedside EEG may help if SAH itself or sedative drugs affect assessment.

Treatment

Phenytoin is most commonly used and is available in intravenous and oral formulations. Among other

anticonvulsants, levetiracetam, valproic acid and phenobarbital are available in IV formulation.

Cerebral vasospasm and delayed ischemic deficits

Onset usually 3–5 days after SAH, maximal at 5–10 days.

~30% of SAH patients develop vasospasm, and 15–20% go on to have ischemic strokes.

Prevention

Calcium channel blockers: nimodipine (Nimotop) 60 mg PO every 4 hours × 3 weeks*, but adjust dose downwards if blood pressure falls so low that adequate CPP is endangered. This should be started early after diagnosis of SAH to prevent vasospasm.

Magnesium: phase II data suggest that magnesium sulfate started within 4 days after SAH and given continuously until 14 days after aneurysm treatment may reduce delayed ischemic deficits.127 The dose used was magnesium sulfate 64 mmol/L per day with aim of magnesium level of 1.0–2.0 mmol/L.

A recent study of statins did not show benefit, and other therapies are still under evaluation.

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116 Subarachnoid hemorrhage (SAH)

Diagnosis

TCD: Velocity trend with daily or sequential measurements is more useful than one-time snapshot of velocities. So get a baseline and follow daily. Lindegaard ratio is the velocity ratio of MCA to extracranial ICA. Increasingflow velocity may indicate either vasospasm or overall increased bloodflow. Increasing Lindegaard ratio may be more reliable sign of MCA vasospasm.

CTA: CT angiography requires iodine contrast injection but may be combined with CT perfusion to diagnose vasospasm and ischemia.

Angiography: more invasive, but can also be linked to treatment with angioplasty or intra-arterial papaverine.

Clinical symptoms and signs: focal deficits similar to ischemic stroke, though in addition may have bilateral frontal lobe dysfunction in the case of anterior communicating artery vasospasm, or decreased level of consciousness if

vertebrobasilar. You want to diagnose and treat vasospasm before these symptoms and signs develop.

Treatment

Hypertension–hypervolemia–hemodilution (HHH). Some or all parts of this triad are commonly used. Combination of pressors and volume expanders such as albumin, synthetic starches, colloid, blood.

Direct endovascular treatment can be performed with balloon angioplasty or drug infusion of papaverine or nicardipine.

n Prognosis

Mortality: in a population-based study, 3% died before reaching medical attention and one-third died in thefirst month.128A

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Prognosis 117

quarter of the deaths are directly attributable to initial bleed, another quarter to vasospasm, and another quarter to rebleeding.

Morbidity: one-third had neurologic deficit. SeeTable 9.1.

Rebleeding risk: with unclipped aneurysm, 6% rebleed within first 3 days, and 12% in thefirst 2 weeks.129Hypertension increases chance of rebleeding.

n Admission sequence

Since these patients are usually admitted to Neurosurgery, we are not providing sample admission orders, but do provide the usual sequence of events upon admitting a patient with SAH.

Establish diagnosis of SAH with CT or lumbar puncture as soon as possible.

Table 9.1.One-month outcome after SAH by clinical status at presentation, a population-based study.

Clinical status at presentation

Poor outcome (severe neurologic deficits, vegetative, or dead)

Relative risk of poor outcome (95% CI) Hunt & Hess

scale

Grade I Grade II Grade III Grade IV Grade V

22%

22%

50%

87%

100%

1

1.0 (0.4–2.2) 2.2 (1.1–10.9) 3.9 (2.3–7.8)

∞ Glasgow Coma

Scale

13–15 9–12 3–8

24%

84%

97%

1

3.6 (2.4–5.2) 4.1 (2.9–5.8) Source:Longstreth WT Jr, Nelson LM, Koepsell TD, van Belle G. Clinical course of spontaneous subarachnoid hemorrhage: a population-based study in King County, Washington.Neurology1993;43: 712–18.128 Reproduced with permission from Lippincott Williams & Wilkins.

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118 Subarachnoid hemorrhage (SAH)

Blood pressure control, prophylactic anticonvulsants.

Neurosurgery consult, admission to ICU.

■ If necessary, transfer emergently to an appropriate hospital that has adequate neurosurgical, neurointerventional (coiling), and neurocritical care capability.

■ Consider ventriculostomy if hydrocephalus is present.

Determine location of ruptured aneurysm with CT angiogram or digital subtraction angiography (do on thefirst day).

Definitive aneurysm treatment (coiling or clipping).

Nimodipine per nasogastric tube.

Watch for and treat vasospasm (first 2 weeks).

n Unruptured aneurysms

Unruptured aneurysms are sometimes found incidentally as part of brain imaging or due to neurologic symptoms other than rupture and SAH. Some patients with SAH are found to have other aneurysms that have not ruptured. Some unruptured aneurysms are found due to screening of those with family history of SAH.

DIAGNOSIS

The diagnostic strategy is the same as for ruptured aneurysms, with DSA being the gold standard for accurate diagnosis and

measurement of an aneurysm. CT angiography and MRA are fair screening tools.

Dalam dokumen Acute stoke care 2 ed (Halaman 134-139)