4.2 Core Workflows and Decision Points

Status Epilepticus: The Timed Algorithm

Most seizures self-terminate in under 2 minutes. Generalized convulsive status epilepticus (SE) is defined as a single seizure lasting 5 minutes or longer, or two or more seizures without a return to baseline consciousness between them. SE is a true emergency because prolonged neuronal firing causes excitotoxic injury, hyperthermia, rhabdomyolysis, and aspiration; the longer it runs, the more refractory it becomes to drugs.

Management follows a strictly timed staircase. Stabilization phase (0-5 minutes): protect the airway, give high-flow oxygen, position laterally, obtain IV access, and check a point-of-care glucose — hypoglycemia is a rapidly reversible cause. First-line/initial therapy phase (5-20 minutes): a benzodiazepine is the abortive agent. If IV access exists, give IV lorazepam 0.1 mg/kg (max 4 mg per dose, may repeat once); without IV access, give IM midazolam 10 mg or rectal diazepam. The most common error tested is giving an inadequate dose or delaying the benzodiazepine.

Second-Line and Refractory Seizures

If seizures persist after adequate benzodiazepine dosing, enter the second-line/urgent control phase (20-40 minutes) with a single IV anti-seizure medication: levetiracetam (Keppra) 60 mg/kg, fosphenytoin 20 mg PE/kg, or valproate 40 mg/kg. These have comparable efficacy. If seizures continue, the patient has refractory status epilepticus and the third-line phase (40-60 minutes) uses continuous IV anesthetic infusions — propofol, midazolam, or pentobarbital — which requires intubation and continuous EEG.

Throughout, treat reversible causes: hypoglycemia, hyponatremia, eclampsia (which needs magnesium sulfate, not standard drugs), toxin ingestion, and fever in children (febrile seizure).

Increased Intracranial Pressure and Herniation

The skull is a fixed box; per the Monro-Kellie doctrine, brain, blood, and cerebrospinal fluid must stay in balance, so a growing mass, edema, or bleed eventually raises intracranial pressure (ICP). Normal ICP is 7-15 mmHg; sustained pressure above 20-22 mmHg demands treatment. What actually matters to the neuron is cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) − ICP, targeted at 60-70 mmHg. As ICP climbs, CPP falls and the brain ischemizes.

Early signs of rising ICP are a declining level of consciousness (the most sensitive indicator), headache, vomiting, and pupillary changes. The late, ominous sign is Cushing's triad: widening pulse pressure (hypertension with bradycardia) plus irregular respirations — this signals impending herniation. A blown (fixed, dilated) pupil reflects uncal herniation compressing cranial nerve III.

Core interventions: elevate the head of bed to 30 degrees with the head midline to promote venous drainage, avoid hypotension and hypoxia, control fever and pain, and give hyperosmolar therapy — mannitol 0.25-1 g/kg or 3% hypertonic saline. Brief controlled hyperventilation (target PaCO2 30-35 mmHg) is a temporizing bridge to surgery, not a sustained therapy.

Tying the Workflows Together

Both of these workflows share a logic the CEN rewards: stabilize the airway and reversible physiology first, act within a defined time window, and escalate in a fixed order. In status epilepticus the enemy is the clock — every minute of seizure recruits more neurons and makes the next drug less likely to work, so hesitating at the benzodiazepine step is the cardinal failure. In rising ICP the enemy is the rigid skull — small volume changes cause large pressure changes once compensation is exhausted, so a subtle drop in the level of consciousness is your cue to act before the catastrophic Cushing reflex appears.

A few cross-cutting traps deserve naming. Do not routinely hyperventilate ICP patients to a low PaCO2 for long; aggressive hypocapnia causes vasoconstriction and worsens ischemia, so it is a short bridge only. Do not give hypotonic fluids to a neuro patient — they pull water into brain cells and raise ICP; isotonic saline is the maintenance fluid. And do not sedate a seizing or agitated head-injured patient so heavily that you lose the neurologic exam without a plan to monitor pupils and ICP.

The pattern to internalize is threat-first, time-boxed, stepwise escalation — the same discipline that drives the stroke pathway in the previous section.

Causes, Monitoring, and Decompression

Know the common drivers of raised ICP so a scenario's backstory points you to the right concern: traumatic brain injury (epidural, subdural, or contusion), hemorrhagic stroke, large ischemic strokes with malignant edema, brain tumors, hydrocephalus, and severe central nervous system infection. The buildup may be slow (tumor) or explosive (epidural hematoma with the classic lucid interval before rapid deterioration), and the tempo changes your urgency.

For monitoring, an external ventricular drain (EVD) or intraparenchymal bolt measures ICP directly and, in the case of an EVD, lets cerebrospinal fluid be drained to relieve pressure. When you manage an EVD, the transducer is leveled at the tragus or external auditory canal (the level of the foramen of Monro), and you watch for over-drainage and infection. Pharmacologically, beyond mannitol and hypertonic saline, adequate sedation and analgesia blunt ICP spikes from coughing or suctioning, seizures are aggressively prevented because they raise metabolic demand, and normothermia is maintained.

The definitive rescue for refractory intracranial hypertension is surgical: decompressive craniectomy removes part of the skull to give the swelling brain room. Recognizing when medical measures have failed and surgery is needed is the higher-order judgment the CEN samples in this area.