Decompressive Craniectomy

Patients were treated in accordance with our standardized ICP- and CPP-oriented treatment protocol to avoid secondary insults [4 (link)]. The treatment protocol remained unchanged throughout the study period. Treatment goals were ICP ≤ 20 mm Hg, CPP ≥ 60 mm Hg, systolic blood pressure > 100 mm Hg, central venous pressure (CVP) 0–5 mm Hg before the aneurysm was occluded and 5–10 mm Hg afterward, pO₂ > 12 kPa, arterial glucose 5–10 mmol/L (mM), electrolytes within normal ranges, normovolemia and body temperature < 38 °C.
Patients who were unconscious (GCS M < 6) were intubated and mechanically normoventilated. Those patients were sedated with propofol and received morphine as analgesia. Wake-up tests were repeatedly performed. The patients were treated with early aneurysm occlusion, including endovascular embolization or surgical clipping, and all patients received nimodipine (first as infusion of 2 mg/h and later as tablets 60 mg × 6 for 3 weeks in total). The dosage of infusion was reduced temporarily in case of hypotension to avoid negative hemodynamic effects. In unconscious (GCS M < 6) patients, an external ventricular drain (EVD) was inserted to monitor and to drain cerebrospinal fluid (CSF) in case of high ICP. The EVD was initially kept closed to measure ICP and assess the need for CSF drainage. If ICP was above 20 mm Hg the EVD was opened at 15 mm Hg. In severe cases when basal ICP treatment was insufficient, thiopental coma treatment and/or decompressive craniectomy (DC) were last-tier treatments. Arterial blood pressure was maintained with fluids. Inotropes (dobutamine or in second hand norepinephrine) were only used if CPP was below 60 mm Hg and the patient did not respond to intravenous fluid treatment.
DCI was defined as new neurological deficits and/or decreased level of consciousness when other causes, e.g., hydrocephalus and hematomas, were excluded. If a manifest cerebral infarction was excluded, triple-H therapy (hypertension, hypervolemia, and hemodilution) including 500 ml dextran-40 solution (100 mg/ml, Meda AB) and 200 ml albumin (200 mg/ml) were administered for 5 days. Cerebral intra-arterial nimodipine was given in case of refractory vasospasm and angioplasty was performed in case of refractory large-vessel vasospasm. The main target for triple-H therapy was elevation of blood pressure but only to moderately elevated levels in relation to baseline, i.e., in general CPP to around 70–80 mm Hg and systolic blood pressure to around 140–160 mm Hg. Secondary targets were erythrocyte volume fraction (EVF) 32% and CVP 8–14 mm Hg, although these goals were in general met automatically by the fluid therapy given. The targeted levels were increased stepwise if clinical improvement was not seen.

We conducted a retrospective cohort study in KK Women's and Children's Hospital, Singapore. Our hospital is a large tertiary center that sees about 28,000 trauma patients at the emergency department (ED) annually. The majority of these comprise minor trauma. We traced all records coded under the International Classification of Diseases (ICD) diagnosis of head injury with a GCS of ≤13. All patients < 16 years of age who presented to the ED over the period from 2003 to 2013, with GCS ≤ 13, were included. Patients were excluded if they were ≥ 16 years, received prior treatment at another hospital and were transferred > 24 hours after the head injury, were drowsy from other causes (apart from the head injury), or did not have any glucose levels documented in the ED or PICU. Children with moderate to severe TBI in our institution are routinely maintained with head up nursing (once the cervical spine is cleared), normocarbia, strict temperature control and we utilize hyperosmolar therapy when indicated. Morphine and midazolam are routinely used for analgesia and sedation, whereas paralysis is reserved for cases with high intracranial pressure (ICP). During the 10-year period, mannitol was replaced with 3% hypertonic saline as the choice hyperosmolar agent. Secondly, where cooling was previously attempted in the past, we now aim for normothermia for the past 2-3 years following current evidence [17 (link), 18 (link)]. Throughout the 10-year period, second tier management included the use of thiopentone and, in some cases, decompressive craniectomy.
Our local institutional review board approved this study without the need for informed consent.

This study was approved by the Johns Hopkins University School of Medicine Institutional Review Board. Data was obtained from prospectively collected de-identified databases of patients treated for stroke at The Johns Hopkins Hospital and Johns Hopkins Bayview Medical Center. A waver of consent was granted based on the following criteria based on 45 CFR 46.116: 1. The research involves no more than minimal risk to subjects; 2. The waiver will not adversely affect the rights and welfare of the subjects; 3. The research could not be practicably carried out without the waiver; and 4. The IRB will advise if it is appropriate for participants to be provided with additional pertinent information after participation. An IRB waiver of HIPAA privacy authorization was also granted to allow review of medical records to abstract data to de-identify for use in research.
We retrospectively analyzed the medical records of all patients who were treated with IV tPA within 4.5 hours of symptom onset in the ED, at Johns Hopkins Hospital or Bayview Medical Center, between January 2010 and March 2013. Patients with in-hospital strokes and patients who were subsequently transferred to or from other hospitals after tPA administration were excluded. Demographic data including age, sex, and race were collected for all patients. The presence of stroke risk factors including hypertension, hyperlipidemia, diabetes mellitus, smoking status, history of atrial fibrillation, and prior history of stroke, as well as the pre-hospital use of antiplatelet agents, anticoagulation, and statins were also recorded. National Institutes of Health Stroke Scale (NIHSS) is a standardized and easy to obtain tool used by providers and researchers in order to quantify stroke severity [7] (link), [8] (link). Possible values on the NIHSS range from 0 to 42, higher values indicating increased stroke severity. NIHSS and the following physiologic parameters at presentation were recorded: blood pressure, international normalized ratio (INR), and estimated glomerular filtration rate (eGFR) by Modification of Diet in Renal Disease (MDRD) equation. The most likely stroke localization (anterior vs. posterior circulation) was recorded based on the patient's presenting symptoms.
The primary outcome was the need for a critical care intervention at any time point from the end of tPA infusion until transfer from the ICU to the floor. A critical care intervention was considered any therapy or intervention that required ICU resources, as defined previously [9] (link), [10] (link). Specifically, ICU admission criteria included: uncontrolled hypertension requiring titration of IV antihypertensives, use of vasopressors either for symptomatic systemic hypotension or blood pressure augmentation, need for invasive hemodynamic monitoring, uncontrolled hyperglycemia requiring IV Insulin, respiratory compromise resulting in either initiation of bilevel positive airway pressure (BiPAP) or mechanical ventilation, arterial bleeding, management of cerebral edema and increased ICP, neurosurgical intervention such as decompressive craniectomy, or interventional angiography with or without intervention. Our definition of an ICU intervention also included patients with any event or complication that would require monitoring in an ICU setting even if no immediate ICU intervention was performed, such as progressive decrease in mental status with impaired airway protection, increasing oxygen requirement, or detection of potentially life-threatening arrhythmia. Patients who required ICU resources by the end of their tPA infusion or at any time over the next 24 hours were compared with those patients who did not have an ICU intervention during the same time period.

Scalp MMN examinations were performed at the patients’ besides, while they were free from visible body shaking. Data were recorded at four electrodes (F3, F4, Fz, and Cz) according to the 10–20 international system using a Rinjie medical event-related potentiometer (WJ-IA, Guangzhou, China). The impedance of all electrodes was kept below 5 KΩ, and the sampling rate was 1,024 Hz with an online 1–100 Hz bandpass filter. Data were referenced with the mean potential at electrodes A1 and A2.
Raw ERP data with amplitudes exceeding 100 μV were automatically rejected, thus eliminating eye movements and other artifacts. Subsequently, the standard and deviant responses were averaged by extracting the data of 100 ms before each stimulus onset and 500 ms after the stimulus; the former was primarily used for baseline correction. After that, a 3–30 Hz bandpass filter is applied and the MMN can be obtained by subtracting the waveform evoked by standard stimuli from the waveform evoked by deviant stimuli. Finally, ERP components such as N1 and MMN were presented and calculated by an automatic algorithm.
The criteria for identifying MMN components were: (1) Considering that N1 is one of the representative indicators of the auditory gating system and the information stream among the auditory cortex areas is directed from the core area to the band area and then to the sub-band area. Meanwhile, the core area and band area are the main generators of the standard N1 and deviation N1 components, respectively (Jones, 2002 (link)). We considered that MMN was not present only if the standard and deviation N1 were both evoked (Rosburg, 2019 (link)); (2) The largest negative waves of averaged difference waveforms in the latency interval between 100 and 300 ms were considered to represent the presence of MMN components (Grimm et al., 2011 (link); Wang et al., 2018 (link)); (3) Considering that some of the patients underwent unilateral or bilateral decompressive craniectomy and MMN had maximal amplitude at Fz (Wang et al., 2018 (link)), we mainly investigated the absolute amplitude of MMN at the Fz site in this study.