Management of intracranial pressure (ICP) crisis varies between institutions depending on the availability of ICP monitoring [1,2,3,4]. The fourth edition of the Brain Trauma Foundation (BTF) Guidelines for the Management of Severe Traumatic Brain Injury (TBI) and The Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC) management algorithm for patients with ICP monitors have been applied for the treatment of ICP crises in severe brain injuries, not limited to TBI [2,3,4]. However, not every patient with clinically suspected intracranial hypertension has immediate access to the ICP monitor, and many of these patients are managed without ICP monitors [1, 5, 6].

A large randomized controlled trial (RCT) reported no significant difference in the functional outcome between severe TBI patients managed with and without ICP monitoring. In that study, the Imaging and Clinical Examination (ICE) Protocol was used in the unmonitored group [7]. The ICE protocol has recently been revised to the Consensus-based management protocol (Consensus REVised ICE, CREVICE) for the treatment of severe TBI without ICP monitoring [8].

In recent years, there has been increased knowledge of management and neuromonitoring for acute brain injury patients. This review combines the SIBICC and CREVICE protocol and updates the latest information on critical care management and neuromonitoring in ICP crisis patients.

Initial Management for ICP Crisis Patients

All patients with severe brain injury resulting in any form of cerebral edema, space-occupying lesions, or hydrocephalus are at risk for ICP crisis. These patients require immediate treatment of the specific cause of intracranial hypertension and frequent neurological examinations to evaluate the level of consciousness, pupillary size and reactivity, and new focal neurologic deficits. They should be initially managed according to the baseline measures (Tier zero) of the SIBICC recommendations in the intensive care unit (ICU; Table 1) [4, 9].

Table 1 Critical care management for patients with intracranial pressure crisis [4, 8,9,10,11,12,13,14,15,16,17,18]

Systemic abnormalities resulting in secondary brain injury include shock/hypotension, oxygen and carbon dioxide abnormalities, hyponatremia, anemia, dysglycemia, sepsis, fever, agitation, and paroxysmal sympathetic hyperactivity [10, 19]. The occurrence of seizures and status epilepticus is an important intracranial cause of secondary brain injury other than elevated ICP.

Respiratory Support

Patients who are unable to maintain airway patency or have Glasgow Coma Scale (GCS) ≤ 8, or those with respiratory failure should be intubated and mechanically ventilated to achieve adequate oxygen saturation (SpO2 ≥ 94%) by avoiding hyperoxemia and maintain arterial partial pressure of carbon dioxide (PaCO2) at 35–38 mmHg to prevent cerebral vasoconstriction or vasodilatation [4, 11, 12].

Although the high-quality evidence for optimal mechanical ventilation strategies in patients with ICP elevation is limited, prior studies suggested that lung-protective ventilation strategies with a low tidal volume of 6–8 ml/kg predicted body weight and positive end-expiratory pressure of 5–8 cmH2O may be safely employed in acute brain injury patients [12,13,14,15].

Hemodynamic Stabilization

Intravenous isotonic crystalloids should be given to maintain euvolemia and ensure adequate systemic and cerebral perfusions unless there is evidence of hypervolemia; 0.9% sodium chloride is a preferred crystalloid [16]. Critically ill TBI patients with TBI receiving balanced crystalloids had a higher 90-day mortality and were less likely to be discharged home compared with those receiving 0.9% sodium chloride solutions in subgroup analyses of two RCTs [17, 18].

The initial blood pressure target for severe TBI patients varies between guidelines. The BTF guidelines recommend targeting systolic blood pressure ≥ 100 mmHg for patients aged 50–69 years or ≥ 110 mmHg for patients aged < 50 or > 70 years, and CPP of 60–70 mmHg corresponding to the SIBICC recommendation [2, 4], while the CREVICE protocol suggests an initial mean arterial pressure (MAP) target of ≥ 90 mmHg for patients without ICP monitoring [8]. The blood pressure target for acute brain injury other than TBI refers to standard guidelines for individual diseases [20,21,22]. The initial MAP target of > 80 mmHg is recommended in the NeuroVanguard approach for taking care of brain-injured patients [10].

Data on the patient’s mean arterial blood pressure (MAP), the amount of fluid accumulation, urine output, blood lactate, central venous oxygen saturation, capillary refill time, level of consciousness, and cardiac output and neuromonitoring, when available, should be integrated to determine resuscitation endpoint and guide fluid therapy [16, 23, 24].

Supportive Measures to Prevent ICP Elevation

Other supportive measures to prevent ICP elevation include elevating the head of the bed to 30–45 degrees and keeping the head in the midline position to enhance cerebral venous return, pain and agitation control with fentanyl and propofol titrating to target light sedation assessed by the Richmond Agitation-Sedation Scale (RASS) score of 0 to −2 [25,26,27], early seizure prophylaxis for one week in TBI patients with phenytoin or levetiracetam, and fever control by targeting body temperature of < 37.5 °C [4].

Other Critical Care Measures

Blood glucose should be controlled within ranges of 110–180 mg/dl since tight glycemic control (blood glucose < 110 mg/dl) increases the risk of cerebral metabolic crisis [19, 28]. Hemoglobin (Hb) level should be initially targeted at > 7 g/dl since there is no difference in the unfavorable outcomes between TBI patients receiving liberal (transfusion when Hb ≤ 10 g/dl) or restrictive (transfusion when Hb ≤ 7 g/dl) red blood cell transfusion strategy in a recent RCT (68.4% vs 73.5%; relative risk [RR], 0.93; 95%CI, 0.83–1.04) [29].

Initiation of ICP-Lowering Therapy

The primary goal for the management of intracranial hypertension includes preventing brain herniation and cerebral ischemia. Patients with a decreased level of consciousness who have a cisternal compression, midline shift, or unevacuated mass lesion on brain imaging, or herniation syndromes are suspicions of intracranial hypertension; the ICP-lowering therapies should be initiated (Tier one of the SIBICC recommendation and the CREVICE protocol), and early neurosurgery consultation is recommended [4, 8, 30, 31].

The selection between hypertonic saline and mannitol depends on the patient's condition and center preference. A recent cohort study evaluating TBI patients receiving mannitol or hypertonic saline treatment in the ICU (CENTER-TBI) found no differences in the ICU mortality (odds ratio [OR], 1.0; 95%CI, 0.4–2.2) and Extended Glasgow Outcome Scale (GOSE) at 6 months (OR, 0.9; 95%CI, 0.5–1.6) between the two groups [32].

Mannitol is an osmotic diuretic that may cause hypotension from intravascular volume depletion, hypokalemia, and metabolic alkalosis. Other adverse effects of mannitol include hyperglycemia as it is a sugar alcohol and acute kidney injury in patients receiving mannitol treatment > 200 g/day [33, 34]. The recommended initial dose of 20% mannitol for emergency treatment of ICP crisis is 0.5–1 g/kg intravenous infusion over 5–15 min.

Hypertonic saline results in intravascular volume expansion and increased serum osmolarity; thus, it may cause cardiogenic pulmonary edema. Other adverse effects of hypertonic saline include hypernatremia, hyperchloremic metabolic acidosis, and osmotic demyelination syndrome. The given amount of hypertonic saline depends on the sodium concentration in the solution: 150 ml of 3%NaCl, 100 ml of 5%NaCl, 75 ml of 7.5%NaCl, or 30–60 ml of 23.4%NaCl can be administered intravenously over 10–30 min. Hypertonic solutions with a concentration of > 7.5% should be given through a central venous catheter [3, 9, 33, 35]. Dose adjustment for mannitol or hypertonic saline depends on the patient's symptoms, brain imaging, and ICP and neuromonitoring data.

Corticosteroids can be considered as an adjunctive treatment in patients with perilesional edema from brain tumors or abscesses [3, 36, 37]. Although there is limited data on the dosage and type of corticosteroids in this condition, dexamethasone is the most commonly used with a suggested dose of 10–20 mg bolus intravenously, followed by 4–24 mg/day, divided into 2–4 times daily [3, 36].

External ventricular drain (EVD) should be placed in patients with intraventricular hemorrhage or hydrocephalus [22, 35]. Surgical removal of the intracranial mass or hematoma or surgical decompression should be performed when indicated [20, 21, 38,39,40,41].

Clinical Neuroworsening

Clinical neuroworsening is defined as a decrease in the motor GCS of ≥ 1 point, a new decrease in pupillary reactivity, pupillary asymmetry of > 2 mm, bilateral pupillary dilatation, a new focal motor deficit or abnormal posturing, a herniation syndrome, or Cushing’s triad [3, 4, 8].

Patients with clinical neuroworsening should be re-evaluated for both extracranial and intracranial etiologies by reassessing physiological parameters, including ICP, MAP, cerebral perfusion pressure (CPP), SpO2, end-tidal CO2, and body temperature, and performing a blood test for serum glucose, complete blood count, blood chemistry, arterial blood gas, septic work up and emergency computed tomography (CT) of the brain [4, 8].

Adjustment of Intracranial Pressure-Lowering Therapies without ICP Monitoring

When no ICP monitor is available, either in resource-limit settings or while awaiting ICP insertion, escalating ICP-lowering treatments should be considered when patients develop new clinical neuroworsening or have no improvement in clinical examination or brain imaging after initial treatment. The recommended time for the follow-up brain imaging is 24 and 48 h after the onset of the brain injury and whenever the patients have clinical neuroworsening [8].

The CREVICE protocol recommends a three-tier stepwise approach for ICP treatment (Table 1), starting with the scheduled infusion of hypertonic saline or mannitol every 4 h [8]. Hyperosmolar therapy with hypertonic saline and mannitol can be administered in combination in severe cases. A serum sodium of ≥ 155 mEq/L, serum osmolarity of ≥ 320 mEq/L, or osmolar gap of ≥ 20 mEq/L are sometimes used as a limit for hypertonic saline and mannitol administration, although it is clear that additional dosing can continue to lower ICP even after these thresholds have been exceeded (tier one).

For patients with ongoing clinical neuroworsening, continuous infusion of 3% NaCl to increase serum sodium level, hyperventilation to target PaCO2 of 30–35 mmHg, or increasing dose of sedation can be considered (tier two). Although continuous hypertonic saline infusion did not improve functional outcome and mortality at 6 months in patients with moderate to severe TBI in a randomized controlled trial, only 35% of the study population had documented intracranial hypertension, and 72% had severe TBI (GCS ≤ 8) [42]. Treatment with continuous hypertonic saline infusion was associated with reduced risk of mortality, intracranial hypertension, and unfavorable outcomes in patients with acute brain injury in prior cohort and meta-analysis studies [43, 44].

In refractory cases, secondary decompressive craniectomy, barbiturate coma with high-dose thiopental, or pentobarbital titrating to target burst-suppression on continuous electroencephalography monitoring, or mild hypothermia with a core temperature of 35–36 °C can be used (tier three) [3, 8, 45,