Neurointensivismo Flashcards
Quando devemos monitorizar a pressão intracraniana?
Monitoring of ICP can be an important tool in selected patients. In general, patients who should be considered for ICP monitoring are those with primary neurologic disorders, such as stroke or traumatic brain injury, who are at significant risk for secondary brain injury due to elevated ICP and decreased CPP.
Included are patients with the following: severe traumatic brain injury (Glasgow Coma Scale [GCS] score ≤ 8 [Table 36-2]); large tissue shifts from supratentorial ischemic or hemorrhagic stroke; or hydrocephalus from subarachnoid hemorrhage (SAH), intraventricular hemorrhage, or posterior fossa stroke. An additional disorder in which ICP monitoring can add important information is fulminant hepatic failure, in which elevated ICP may be treated with barbiturates or, eventually, liver transplantation.
In general, ventriculostomy is prefer
able to ICP monitoring devices that are placed in the brain parenchyma, because ventriculostomy allows CSF drainage as a method of treating elevated ICP. However, parenchymal ICP monitoring is most appropriate for patients with diffuse edema and small ventricles (which may make ventriculostomy placement more difficult) or any degree of coagulopathy (in which ventriculostomy carries a higher risk of hemorrhagic complications
Qual a abordagem, stepwise, do manejo de hipertensão intracraniana?
General goals: maintain ICP <20 mmHg and CPP v60 mmHg
(1) Insert ICP monitor—ventriculostomy versus parenchymal device
Coma and unilateral pupillary changes are late signs and Coma and unilateral pupillary changes are late signs and require immediate intervention.
For ICP >20–25 mmHg for >5 min:
- Drain CSF via ventriculostomy (if in place)
- Elevate head of the bed; midline head position
- Osmotherapy—mannitol 25–100 g q4h as needed (maintain serum osmolality <320 mosmol) or hypertonic saline (30 mL, 23.4% NaCl bolus) - avoid hypotonic solutions.
- Glucocorticoids—dexamethasone 4 mg q6h for vasogenic edema from tumor, abscess (avoid glucocorticoids in head trauma, ischemic and hemorrhagic stroke)
- Sedation (e.g., morphine, propofol, or midazolam); add neuromuscular paralysis if necessary (patient will require endotracheal intubation and mechanical ventilation at this point, if not before)
- Hyperventilation—to PaCO2 30–35 mmHg
- Pressor therapy—phenylephrine, dopamine, or norepinephrine to maintain adequate MAP to ensure CPP v60 mmHg (maintain euvolemia to minimize deleterious systemic effects of pressors)
- Consider second-tier therapies for refractory elevated ICP
a. High-dose barbiturate therapy (“pentobarb coma”)
b. Aggressive hyperventilation to PaCO2 <30 mmHg
c. Hypothermia
d. Hemicraniectomy
Como fazer o manejo de lesão secundaria do doente neurocritico ?
Avoiding (1) hypotension and (2) hypoxia is critical, as significant hypotensive events (systolic blood pressure <90 mmHg) as short as 10 min in duration have been shown to adversely influence outcome after traumatic brain injury. Likewise, fever (3) and hyperglycemia (4) both worsen experimental ischemia and have been associated with worsened clinical outcome after stroke and head trauma.
Quais as medidas terapêuticas para encefalopatia pós-anoxica?
(1) Treatment should be directed at restoration of normal cardiorespiratory function. This includes securing a clear airway, ensuring adequate oxygenation and ventilation, and restoring cerebral perfusion, whether by cardiopulmonary resuscitation, fluid, pressors, or cardiac pacing.
(2) Hypothermia may target the neuronal cell injury cascade and has substantial neuroprotective properties in experimental models of brain injury. In two trials, mild hypothermia (33°C) improved functional outcome in patients who remained comatose after resuscitation from a cardiac arrest. Treatment was initiated within minutes of cardiac resuscitation and continued for 12 h in one study and 24 h in the other. Potential complications of hypothermia include coagulopathy and an increased risk of infection.
(3) Posthypoxic myoclonus may respond to oral administration of clonazepam at doses of 1.5–10 mg daily or valproate at doses of 300–1200 mg daily in divided doses. Myoclonic status epilepticus within 24 h after a primary circulatory arrest generally portends a very poor prognosis, even if seizures are controlled.
(4) Severe carbon monoxide intoxication may be treated with hyperbaric oxygen
(5) PROGNOSTICATION ALGORITHM OF OUTCOME:
A. No brainstem reflexes at any time (pupil, cornea, oculocephalic, cough) = Brain death testing
B. Day 1 Myoclonus, status epilepticus
C. Day 3 Absent pupil or corneal reflexes; extensor or absent motor response
Como é o tratamento da encefalopatia de Wernicke?
Wernicke’s disease is a medical emergency and requires immediate administration of thiamine, in a dose of 100 mg either IV or IM. The dose should be given daily until the patient resumes a normal diet and should be begun prior to treatment with IV glucose solutions. Glucose infusions may precipitate Wernicke’s disease in a previously unaffected patient or cause a rapid worsening of an early form of the disease. For this reason, thiamine should be administered to all alcoholic patients requiring parenteral glucose.
Compare as escalas de WFNS e Hunt Hess na HSA.
GRADE HUNT-HESS SCALE / WORLD FEDERATION OF NEUROSURGICAL SOCIETIES (WFNS) SCALE
1 Mild headache, normal mental status, no cranial nerve or motor findings /GCSa score 15, no motor deficits
2 Severe headache, normal mental status, may have cranial nerve deficit/ GCS score 13–14, no motor deficits
3 Somnolent, confused, may have cranial nerve or mild motor deficit / GCS score 13–14, with motor deficits
4 Stupor, moderate to severe motor deficit, may have intermittent reflex posturing/ GCS score 7–12, with or without motor deficits
5 Coma, reflex posturing or flaccid / GCS score 3–6, with or without motor deficits
Quais os pilares do tratamento da HSA?
(1) The International Subarachnoid Aneurysm Trial (ISAT), was terminated early when 24% of patients treated with endovascular therapy were dead or dependent at 1 year compared to 31% treated with surgery, a significant 23% relative reduction. After 5 years, risk of death was lower in the coiling group, although the proportion of survivors who were independent was the same in both groups. Risk of rebleeding was low, but more common in the coiling group. Also, because some aneurysms have a morphology that is not amenable to endovascular treatment, surgery remains an important treatment option. Antifibrinolytic agents are not routinely prescribed but may be considered in patients in whom aneurysm treatment cannot proceed immediately. They are associated with a reduced incidence of aneurysmal rerupture but may also increase the risk of delayed cerebral infarction and deep-vein thrombosis (DVT).
(2) The medical management of SAH focuses on protecting the airway, managing blood pressure before and after aneurysm treatment, preventing rebleeding prior to treatment, managing vasospasm, treating hydrocephalus, treating hyponatremia, and preventing pulmonary embolus.
O que posso fazer para prevenir ressangramento, além do tratamento precoce e do controle pressórico?
(1) Seizures are uncommon at the onset of aneurysmal rupture. The quivering, jerking, and extensor posturing that often accompany loss of consciousness with SAH are probably related to the sharp rise in ICP rather than seizure. However, anticonvulsants are sometimes given as prophylactic therapy since a seizure could theoretically promote rebleeding.
(2) Glucocorticoids may help reduce the head and neck ache caused by the irritative effect of the subarachnoid blood. There is no good evidence that they reduce cerebral edema, are neuroprotective, or reduce vascular injury, and their routine use therefore is not recommended.
Como manejar o vasoespasmo da HSA?
Vasospasm remains the leading cause of morbidity and mortality following aneurysmal SAH. (1) Treatment with the calcium channel antagonist nimodipine (60 mg PO every 4 h) improves outcome, perhaps by preventing ischemic injury rather than reducing the risk of vasospasm. Nimodipine can cause significant hypotension in some patients, which may worsen cerebral ischemia in patients with vasospasm. (2) Symptomatic cerebral vasospasm can also be treated by increasing the cerebral perfusion pressure by raising mean arterial pressure through plasma volume expansion and the judicious use of IV vasopressor agents, usually phenylephrine or norepinephrine. Raised perfusion pressure has been associated with clinical improvement in many patients, but high arterial pressure may promote rebleeding in unprotected aneurysms. (3) Treatment with induced hypertension and hypervolemia generally requires monitoring of arterial and central venous pressures; it is best to infuse pressors through a central venous line as well. (4) If symptomatic vasospasm persists despite optimal medical therapy, intraarterial vasodilators and percutaneous transluminal angioplasty are considered. Vasodilatation by direct angioplasty appears to be permanent, allowing triple-H therapy to be tapered sooner. The pharmacologic vasodilators (verapamil and nicardipine) do not last more than about 24 h, and therefore multiple treatments may be required until the subarachnoid blood is reabsorbed
Como manejar a hipertensão intracraniana associada a HSA?
(1) Intracranial hypertension following aneurysmal rupture occurs secondary to subarachnoid blood, parenchymal hematoma, acute hydrocephalus, or loss of vascular autoregulation. Patients who are stuporous should undergo emergent ventriculostomy to measure ICP and to treat high ICP in order to prevent cerebral ischemia. Medical therapies designed to combat raised ICP (e.g., mild hyperventilation, mannitol, and sedation) can also be used as needed.
(2) Acute hydrocephalus can cause stupor or coma. It may clear spontaneously or require temporary ventricular drainage. When chronic hydrocephalus develops, ventricular shunting is the treatment of choice.
Como fazer o manejo do sódio na HSA?
Close monitoring (daily or twice daily) of electrolytes is important because hyponatremia can occur precipitously during the first 2 weeks following SAH. Free-water restriction is contraindicated in patients with SAH at risk for vasospasm because hypovolemia and hypotension may occur and precipitate cerebral ischemia. Many patients continue to experience a decline in serum sodium despite receiving parenteral fluids containing normal saline. Frequently, supplemental oral salt coupled with normal saline will mitigate hyponatremia, but often patients also require hypertonic saline. Care must be taken not to correct serum sodium too quickly in patients with marked hyponatremia of several days’ duration, as central pontine myelinolysis may occur
Como fazer profilaxia de TEV na HSA?
All patients should have pneumatic compression stockings applied to prevent pulmonary embolismUnfractionated heparin administered subcutaneously for DVT prophylaxis can be initiated immediately following endovascular treatment and within days following craniotomy and surgical clipping and is a useful adjunct to pneumatic compression stockings. Treatment of pulmonary embolus depends on whether the aneurysm has been treated and whether or not the patient has had a craniotomy.
