Nervous System Disorders in Critical Care¶
Chapter 318 | Part 8: Critical Care Medicine · Part 8 – Critical Care Medicine · Chapter 318
Key Clinical Points¶
- Encephalopathy is a general term for diffuse, global, or multifocal brain dysfunction.
- Brain edema consists of vasogenic (BBB failure) and cytotoxic (cellular swelling) components.
- Cerebral autoregulation maintains constant blood flow; CPP = MAP - ICP.
- Target goals: ICP <20 mmHg and CPP ≥60 mmHg.
- Hypoxic-ischemic injury prognosis is better with intact brainstem function (pupillary, oculocephalic, oculovestibular, corneal reflexes).
- Secondary insults (hypotension, hypoxia, fever, hyperglycemia) must be aggressively managed to prevent worsening of primary injury.
- Targeted temperature management (TTM) for post-arrest patients: 32–37.5°C.
- Sepsis-associated encephalopathy presents as diffuse dysfunction without prominent focal findings.
- Prognostic indicators include EEG burst-suppression, absent N20 SSEP, and NSE >60 μg/L.
- Hyperventilation (PaCO2 30–35 mmHg) is for short-term use only to avoid rebound ICP.
DEFINITION & CLASSIFICATION¶
• Neurologic Critical Care: Focuses on preservation of tissue and prevention of secondary injury (ischemia, hemorrhage, edema, herniation, elevated ICP). • Encephalopathy:
Definition (Harrison's 22e): Encephalopathy is a general term describing brain dysfunction that is diffuse, global, or multifocal. • Severe Acute Encephalopathies: Group of disorders with varying etiologies sharing common themes of primary and secondary injury. • Systemic Links: May result from local neuro-axis issues or systemic failures (hepatic failure, multi-system organ failure, cardiac arrest).
EPIDEMIOLOGY¶
• Sudden Cardiac Death (SCD): ◦ Only ~20% occur in patients with poor left ventricular function. ◦ Most occur in individuals with preserved ventricular function (LVEF >35%). ◦ Prevention focuses on risk factor modification and standard medical therapy.
ETIOLOGY & PATHOPHYSIOLOGY¶
Brain Edema¶
• Vasogenic Edema: Influx of fluid/solutes due to incompetent blood-brain barrier (BBB). ◦ Triggered by ischemia, trauma, infection, or metabolic derangements. • Cytotoxic Edema: Results from cellular swelling and membrane breakdown leading to cell death. • Clinical Impact: Leads to increased ICP, tissue shifts, and potential herniation.
Ischemic Cascade & Cellular Injury¶
• Mechanism: Inadequate oxygen/glucose → release of glutamate → influx of Ca^{2+} and Na^{+} → activation of proteases/lipases → lipid peroxidation → cell death. • Penumbra: Area of ischemic tissue not yet irreversibly infarcted; potentially salvageable if ischemia is reversed. • Secondary Insults: Factors that exacerbate primary injury (e.g., hypotension, hypoxia, fever, seizures, hyperglycemia).
Apoptosis¶
• Definition: Programmed cell death occurring in stroke, global ischemia, trauma, or hemorrhage. ◦ Distinct from necrosis: No cerebral edema; often not visible on imaging.
Cerebral Perfusion & Autoregulation¶
• Cerebral Perfusion Pressure (CPP): Defined as MAP minus ICP. Provides driving force for capillary circulation. • Autoregulation: Mechanism where CBF is maintained via changes in cerebrovascular resistance despite wide ranges of systemic blood pressure. ◦ Low BP → vasodilation of arterioles to preserve flow. ◦ High BP → arteriolar vasoconstriction to prevent hyperperfusion. • Chemical Influence: CBF increases with hypercapnia and acidosis; decreases with hypocapnia and alkalosis. • Hyperventilation Effect: Reduces ICP by decreasing both CBF and intracranial blood volume (via lower PaCO_2). • Failure of Autoregulation: Occurs in traumatic brain injury or severe focal ischemia.
CSF & ICP Dynamics¶
• Components: Cranial contents = brain + CSF + blood. • Volume Constraints: Skull allows little tolerance for extra volume; expansion leads to increased ICP. • Vicious Cycle of Ischemia: Ischemia → vasodilation (autoregulation) → increased cerebral blood volume → increased ICP → lower CPP → further ischemia.
CLINICAL FEATURES¶
General Assessment¶
• Primary Distinction: Determine if dysfunction is Diffuse (metabolic) or Focal (structural). ◦ Diffuse: Metabolic encephalopathies, drug overdose, hypoxia-ischemia. ◦ Focal: Stroke, tumor, abscess, hemorrhage, trauma. • Red Flags for Structural Lesion: Pupillary asymmetry, hemiparesis, gaze palsy, visual field deficit. • ICP Warning Signs: Drowsiness and diminished level of consciousness.
Hypoxic-Ischemic Brain Injury¶
• Time Sensitivity: If circulation restored within 3–5 min → potential full recovery; >3-5 min → likely permanent damage. • Tolerance: Brain is more tolerant to pure hypoxia (e.g., high altitude) than to hypoxia-ischemia (cardiac arrest). • Prognostic Indicators: ◦ Better Prognosis: Intact brainstem function (pupillary light response, oculocephalic, oculovestibular, and corneal reflexes). ◦ Poorer Prognosis: → Absent pupillary reflex or absent motor response to pain 5–7 days post-injury. → Bilateral absence of N20 component of SSEP after several days. → EEG burst-suppression pattern or nonreactive EEG. → Serum NSE >60 μg/L during first 1–3 days post-resuscitation.
Specific Syndromes¶
• Wernicke's Disease: Confusion, impaired eye movements, gait ataxia. • Hepatic Encephalopathy: Suggested by asterixis; occurs in liver failure. • Sepsis-Associated Encephalopathy: Diffuse dysfunction without focal findings; includes confusion, agitation, and hyperreflexia/frontal release signs. • Postcardiac Bypass Injury: Includes acute encephalopathy, stroke, and chronic cognitive impairment (often due to embolic disease).
DIFFERENTIAL DIAGNOSIS¶
• Metabolic/Diffuse: Organ failure (hepatic, renal), drug overdose, electrolyte disturbances (hyponatremia, hypoglycemia), hypoxia, meningitis, Wernicke's. • Structural/Focal: Ischemic stroke, tumor, abscess, hemorrhage, trauma. • Specific Indicators: → Asterixis → Hepatic encephalopathy. → Carbon monoxide poisoning → suggested by cherry red skin (inconsistent) and confirmed by carboxyhemoglobin levels.
DIAGNOSTIC APPROACH¶
- Initial Imaging: Computed Tomography (CT) scan. → Rapidly identifies hemorrhage, hydrocephalus, and tissue shifts.
- Advanced Imaging: Magnetic Resonance Imaging (MRI). → Used for specific details like acute ischemic stroke (DWI) or identifying posterior reversible encephalopathy syndrome (PRES).
- Neurovascular Imaging: CT/MR angiography or venography. → Identifies arterial occlusion or cerebral venous thrombosis.
- Electrophysiology: Electroencephalography (EEG). → Used to identify non-convulsive status epilepticus, burst-suppression patterns, or assess brain activity.
- Laboratory Markers: Serum NSE. → Measured in first 1–3 days post-cardiac arrest; >60 μg/L indicates significant damage.
MANAGEMENT & TREATMENT¶
• Hypoxic-Ischemic Brain Injury: Targeted temperature management (TTM) to 32–37.5°C for post-arrest patients without response to verbal commands.
Elevated ICP Management¶
• General Goals: Maintain ICP <20 mmHg and CPP geq60 mmHg. • Stepwise Protocol (for ICP >20-25 mmHg for >5 min): 1. Position: Elevate head of bed; maintain midline head position. 2. Drainage: Drain CSF via ventriculostomy (if in place). 3. Osmotherapy: → Mannitol 25–100 g q4h as needed (maintain serum osmolality <320 mOsmL). → OR Hypertonic saline (30 mL, 23.4% NaCl bolus). 4. Glucocorticoids: Dexamethasone 4 mg q6h (only for vasogenic edema from tumor or abscess; avoid in head trauma/stroke). 5. Sedation: Morphine, propofol, or midazolam; add neuromuscular paralysis if necessary. 6. Hyperventilation: Target PaCO_2 30–35 mmHg (short-term use only). 7. Pressor Therapy: Phenylephrine, dopamine, or norepinephrine to maintain MAP for CPP geq60 mmHg. 8. Second-tier options (refractory): → Decompressive craniectomy. → High-dose barbiturate therapy ("pentobarb coma"). → Hypothermia to 33°C.
PROGNOSIS & COMPLICATIONS¶
• Hypoxic-Ischemic Outcomes: Persistent coma, unresponsive wakeful state (bilateral thalamic scarring), dementia, visual agnosia, parkinsonism, choreoathetosis, cerebellar ataxia, myoclonus, seizures, and amnestic state. • Surgical Risks: Postcardiac bypass may lead to stroke or embolic-related complications.
SPECIAL POPULATIONS¶
• Pregnancy/Preeclampsia: Associated with Posterior Reversible Encephalopathy Syndrome (PRES).
KEY PEARLS & HIGH-YIELD POINTS¶
• Rule of Thumb: Always distinguish between metabolic (diffuse) and structural (focal) causes immediately. • ICP Target: ICP <20 mmHg; CPP geq60 mmHg. • Hyperventilation: Use only as a short-term bridge to avoid rebound ICP elevation. • Sepsis Encephalopathy: Characterized by diffuse dysfunction without focal signs.
Reference Tables¶
TABLE 318-1 Neurologic Disorders in Critical Illness¶
Harrison's 22e, p.2343
| LOCALIZATION ALONG NEUROAXIS |
SYNDROME |
|---|---|
| Central Nervous System | |
| Brain: Cerebral hemispheres |
Global encephalopathy |
| Delirium | |
| Sepsis | |
| Organ failure—hepatic, renal | |
| Medication related—sedatives, hypnotics, analgesics, H blockers, antihypertensives 2 |
|
| Drug overdose | |
| Electrolyte disturbance—hyponatremia, hypoglycemia |
|
| Hypotension/hypoperfusion | |
| Hypoxia | |
| Meningitis | |
| Subarachnoid hemorrhage | |
| Wernicke’s disease | |
| Seizure—postictal or nonconvulsive status epilepticus |
|
| Hypertensive encephalopathy | |
| Hypothyroidism—myxedema | |
| Focal deficits | |
| Ischemic stroke | |
| Tumor | |
| Abscess, subdural empyema | |
| Intraparenchymal hemorrhage | |
| Subdural/epidural hematoma | |
| Spinal cord | Mass effect and compression |
| Disk herniation | |
| Epidural hematoma | |
| Epidural abscess Ischemia—hypotension/embolic |
|
| Trauma | |
| Myelitis | |
| Peripheral Nervous System | |
| Neuromuscular junction | Prolonged effect of neuromuscular blockade |
| Medication effects—aminoglycosides | |
| Myasthenia gravis, Lambert-Eaton syndrome, botulism |
TABLE 318-2 Stepwise Approach to Treatment of Elevated Intracranial Pressure (ICP) a Insert ICP monitor—ventriculostomy…¶
Harrison's 22e, p.2345
- Insert ICP monitor—ventriculostomy versus parenchymal device
General goals: maintain ICP <20 mmHg and CPP ≥60 mmHg. For ICP
>20–25 mmHg for >5 min:
1. Elevate head of the bed; midline head position
2. Drain CSF via ventriculostomy (if in place)
3. Osmotherapy—mannitol 25–100 g q4h as needed (maintain serum osmolality
<320 mosmol) or hypertonic saline (30 mL, 23.4% NaCl bolus)
4. Glucocorticoids—dexamethasone 4 mg q6h for vasogenic edema from tumor,
abscess (avoid glucocorticoids in head trauma, ischemic and hemorrhagic
stroke)
5. 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)
6. Hyperventilation—to Paco 30–35 mmHg (short-term use or skip this step)
2
7. Pressor therapy—phenylephrine, dopamine, or norepinephrine to maintain
adequate MAP to ensure CPP ≥60 mmHg (maintain euvolemia to minimize
deleterious systemic effects of pressors). May adjust target CPP in individual
patients based on autoregulation status.
8. Consider second-tier therapies for refractory elevated ICP
a. Decompressive craniectomy
b. High-dose barbiturate therapy (“pentobarb coma”)
c. Hypothermia to 33°C
TABLE 318-3 Common Etiologies of Posterior Reversible Encephalopathy Syndrome Disorders in which increased capillary…¶
Harrison's 22e, p.2350
- Disorders in which increased capillary pressure dominates the pathophysiology
- Hypertensive encephalopathy, including secondary causes such as
renovascular hypertension, pheochromocytoma, cocaine use, etc. - Postcarotid endarterectomy syndrome
- Preeclampsia/eclampsia
- Disorders in which endothelial dysfunction dominates the pathophysiology
- Calcineurin inhibitor toxicity (e.g., cyclosporine, tacrolimus)
- Chemotherapeutic agent toxicity (e.g., cytarabine, azathioprine, 5-fluorouracil,
cisplatin, methotrexate, tumor necrosis factor α antagonists) - HELLP syndrome (hemolysis, elevated liver enzyme levels, low platelet count)
- Hemolytic-uremic syndrome (HUS)