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Neurological Critical Care
Introduction
Neurological critical care has evolved rapidly over the past 25 years. A rational amalgamation of the science of critical care with developments in neurosciences has paved way for a modern neurological intensive care unit (ICU). Comprehensive general medical care combined with specialized neurological care through management of intracranial pressure (ICP) and blood flow dynamics, advanced neuromonitoring [e.g., electroencephalography (EEG), brain tissue oxygen (PbtO 2 ), and microdialysis], and newer therapeutic modalities, is intended to decrease the mortality and improve the functional outcomes of the patients. Given the complexity of cerebral function in health and disease, it is intuitive that specialized expertise is required at all levels of staffing including physicians, nurses, and technologists to manage a neurocritical care unit.
History of Neurocritical Care
The critical care units developed in the 1950’s to cater to the requirements of the victims of poliomyelitis in the Europe may be considered as the forerunners of modern neurocritical care units. A rapid increase in the volume of neurosurgical work and the complexity of neurosurgical and neuroanesthesia procedures called for increase in dedicated neurocritical care units. Advent of specialized therapies with definite outcome benefit (e.g., plasmapheresis for immunomodulation and thrombolysis for stroke) has necessitated creation of critical care facilities for neuromedical patients. The specialized needs of patients with neurotrauma demanded dedicated beds for neurotrauma, especially in the light of anticipated outcome benefit with modern-day cerebral physiology monitors.
Critical care, in general, was rather late to develop in India. Critical care services for neurological and neurosurgical patients started in major academic centers like National Institute of Mental Health and Neurosciences (NIMHANS), All India Institute of Medical Sciences (AIIMS), and Postgraduate Institute of Medical Education and Research (PGIMER) in the 1970’s and the 1980’s.
Design of a Neurocritical Care Unit
Design of critical care facilities has an impact on organizational performance, clinical outcomes, and cost of care delivery. Organizations involved in design and construction projects are advised to engage experienced consultants who will collaborate with the users and make key design decisions on the basis of best current evidence. The design of the unit should take into account the requirements of the patients, staff, and the families. The construction should provide adequate space for patient care activities, offices, academic activities, and the staff and family necessities. The administration should commit itself to providing the requisite equipment, consumables, and other supplies. A realistic planning should be made of manpower depending on the nature of patients. There is little literature on the guidelines for a neurocritical care unit. However, the guidelines for a general ICU published in Critical Care Medicine journal could form the baseline document over which any other specific needs of a neurological ICU can be built up.
Clinical Conditions Requiring Admission to Neurocritical Care Unit
Critical care is an expensive resource, hence should be used very judiciously. It is all the more precious in case of neurocritical care, as the available beds are limited and the demands are high. Although absolute objectivity is not possible, prioritization of the services in favor of those patients who are salvageable avoids futile prolongation of the ICU care. With advances in technology and concepts of pathophysiology, many conditions that were considered nonsalvageable earlier have a good prognosis now.
The most common diagnostic entities in a neurological ICU are traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), stroke, postoperative care after major neurological surgery, neuromuscular paralysis due to polyneuropathy, and neuromuscular junction disorders. A comprehensive list of the clinical conditions admitted to NIMHANS neurological ICUs over a 1-year period is shown in Table 34.1 . In the current day practice, a neurological ICU should not be equated with a routine postoperative care unit for neurological patients. Over the years, there has been a progressive change in the patterns of admission to neurological ICUs. The demographic and epidemiological trends in neurological ICU are showing an overall increase in yearly admissions particularly in certain disease categories such as cardiac arrest, intracerebral hemorrhage (ICH), spine diseases, seizures, and TBI implying a trend for more aggressive management of these conditions. Also, there seems to be an increase in ICU length of stay (LOS) reflecting the implementation of aggressive therapeutic measures and the expanding role of critical care in health care delivery. The financial considerations of such aggressive therapy are a matter of serious concern and debate.
Table 34.1
Admissions to Neurological Intensive Care Units at NIMHANS in the Calendar Year 2014
| Diagnosis | No. of Admissions |
|---|---|
| Traumatic brain injury | 347 |
| Aneurysms | 165 |
| Brain tumors | 244 |
| Spinal lesions | 47 |
| Guillain-Barré syndrome | 56 |
| Myasthenia gravis | 16 |
| Status epilepticus | 18 |
| Meningitis/encephalitis | 24 |
| Cerebral venous thrombosis | 36 |
| Hydrocephalus | 29 |
| Others | 82 |
| Total | 1064 |
These data are exclusive of patients admitted to stoke ward and routine postoperative patients.
Justification for Neurological Critical Care Units
Critical care requirements in neurologically ill patients are inherently different and more complex from those of general critical care units. While many of the issues related to systemic physiology are similar to those in general ICU’s, understanding and management of specific neurological derangements are more complex and need specialized knowledge and skills. The margin of safety is low as the brain is very highly vulnerable to ischemic/hypoxic complications. Delays in identification of even subtle problems have a major impact on the outcome while the monitoring technology is complex and expensive. Ambiguity about the utility of the monitored information and uncertainty about the efficacy of certain treatment strategies further complicates the matters.
The benefits of specialized neurological critical care units have been evaluated in several studies. Patel et al. documented that specialist neurocritical care with protocol-driven therapy is associated with a significant improvement in outcome for patients with severe head injury, including those who require complex therapeutic interventions. In another study, introduction of a neurocritical care team, including a full-time neurointensivist, who coordinated care, significantly reduced in-hospital mortality and LOS without changes in readmission rates or long-term mortality. Critical care unit stay and length of hospital stay were shortened and disposition of patients improved in those with strokes admitted to a neurological ICU. Certain clinical entities seem to benefit more than the others; improvements in clinical outcomes associated with neurointensivist-driven care are more definitive in SAH than in ICH. The improved outcomes in the neuro-ICUs are probably related to more invasive intracranial and hemodynamic monitoring, lower threshold for tracheostomy, good nutritional support, and less intravenous (IV) sedation when compared to general ICUs. Finally, patients with ICH brought directly to neurological emergency department had significantly better outcomes than patients admitted to the other services and subsequently transferred to neurological ICU. The difference is probably accounted for by delays in optimizing management prior to arrival at the dedicated neurological ICU.
Pathophysiological Issues in Neurological Critical Care
The pathology in a patient in the neurological ICU may involve the brain and spinal cord or the peripheral nervous system. Irrespective of the primary cause, ischemia and inadequate oxygen delivery form the basis of the neurological dysfunction in the majority of patients with encephalopathy (e.g., trauma, SAH, stroke) ( Fig 34.1 ). Several factors determine the delicate balance between cerebral oxygen demand (CMRO 2 ) and oxygen supply [cerebral metabolism, arterial blood pressure (BP), cardiac output, PaO 2 , PaCO 2 , pH, hemoglobin, ICP, drugs, and vasospasm]. Management of these patients revolves around optimization of these factors. Correction of the CMRO 2 /cerebral blood flow (CBF) imbalance calls for optimization of hemodynamic, respiratory, and other systemic physiology, in addition to management of ICP and CBF dynamics.
Neuromuscular diseases requiring critical care are generally caused by reversible demyelination (e.g., acute or chronic inflammatory demyelinating polyneuropathy) or reversible pathology of the neuromuscular junction (e.g., myasthenia gravis). At times, the pathological processes involved may be degenerative in nature but have a high probability of therapeutic success (e.g., multiple sclerosis). Patients with more complex underlying pathologies and documented poor prognosis are generally not candidates for neurological ICU admission, except when the ICU admission is intended to treat a reversible intercurrent problem (e.g., chest infection, cardiac failure) of short duration.
Management of Patients in a Neurological Intensive Care Unit
ICU management of patients involves optimization of general systemic physiology and disease-specific therapy ( Table 34.2 ).
Table 34.2
Management of Patients in a Neurological ICU
| General Systemic Physiology |
| Cardiovascular care |
| Optimization of CPP |
| Hemodynamic manipulations in vaso-occlusive conditions |
| Management of autonomic dysfunction |
| Respiratory care |
| Oxygen therapy |
| Tracheal intubation |
| Mechanical ventilation |
| Metabolic care |
| Glucose management |
| Fluid and electrolyte balance |
| Infection control |
| Systemic infections |
| CNS Infections |
| Nutritional management |
| Disease-specific neurological therapy (e.g., osmotherapy, corticosteroids, etc.) |
CNS , central nervous system; CPP , cerebral perfusion pressure; ICU , intensive care unit.
Management of General Systemic Physiology
Systemic insults account for a major proportion of the secondary neurological deterioration both in traumatic injury and non-TBI. While definitive treatment relevant to the primary pathology is in progress (e.g., evacuation of a mass lesion in TBI, thrombolysis in cerebrovascular accidents), efforts should be made to optimize the systemic physiology. Some practical issues in the management of these factors are discussed.
Cardiovascular Care
Hemodynamic disturbances in critically ill neurological patients have a diverse physiological background. All the causes of hypotension in any patient in the general ICU (e.g., hypovolemia, sepsis) could be operational in a patient in the neurological ICU too and will not be discussed here. Some important hemodynamic manipulations relevant to certain pathological states in neurological patients are: (1) optimization of cerebral perfusion pressure (CPP) in patients whose cerebral perfusion is compromised, (2) systemic hemodynamic manipulations to maximize CBF in vaso-occlusive conditions (stroke, SAH), and (3) management of cardiovascular consequences of autonomic dysfunction initiated by the neurological injury [TBI, SAH, cervical spine injury, neurogenic pulmonary edema (NPE), Guillain-Barré syndrome (GBS), etc.].
Optimization of CPP
TBI is a typical clinical condition that calls for optimization of CPP. Concepts on CPP management have gone through a radical change in the recent years. CPP-based strategy, founded on the premise that high CPP alleviates cerebral ischemia, is questioned by several studies. A value not less than 50 mmHg, but not above 70 mmHg, is recommended in the latest guidelines of the Brain Trauma Foundation (BTF). CPP values higher than 70 mmHg are discouraged as the aggressive measures to maintain high systemic arterial pressures (IV fluids, inotropes, etc.) required to achieve a high CPP may be fraught with cardiopulmonary complications that compromise systemic and cerebral oxygenation. The benefit of CPP values higher than 60 mmHg has been questioned in some studies. A more objective argument that is arising recently is that CPP should be optimized for each individual patient based on some direct measure of cerebral physiology [e.g., pressure reactivity index (PR X ), PbtO 2 , cerebral metabolite concentrations from microdialysis], than arbitrary mean arterial pressure (MAP) and CPP values.
Hemodynamic Manipulations in Vaso-Occlusive Conditions
Ischemic stroke and cerebral vasospasm caused by SAH exemplify vaso-occlusive states wherein hemodynamic management plays a major role.
Triple H has formed the mainstay of therapy of clinical vasospasm in most centers, although controversies exist as regards its efficacy and the relative importance of its three components, namely, hemodilution, hypervolemia, and induced hypertension.
- 1.
Hypervolemia is generally achieved by using normal saline, colloids, or albumin. A pulmonary artery catheter helps to monitor the degree of hypervolemia. A pulmonary capillary wedge pressure value between 10 and 20 mmHg that produces maximum increase in cardiac output is chosen. The major risk of aggressive hypervolemia is fluid overload leading to pulmonary edema. Radiographic evidence of pulmonary edema and decreasing cardiac output and oxygenation suggest unacceptable levels of hypervolemia.
- 2.
Hypertension is induced when hypervolemia fails to revert a neurological deficit in 1–2 h. An ideal hematocrit for hemodilution is 35%. Transfusion of blood is generally considered when the hematocrit decreases to less than 30%.
It is beyond the scope of this chapter to discuss, in detail, the hemodynamic management of stroke, but some principles are as follows. The international stroke trial for ischemic stroke showed a “U”-shaped relation between BP and mortality in patients with ischemic stroke. Excessively high or low values are associated with poor outcome; for every 10 mm Hg increase in systolic blood pressure (SBP) > 150 mmHg, mortality increased by 3.8%, and for every 10 mmHg decrease in SBP < 150 mmHg, mortality increased by 17.9%. Although elevated blood pressure improves penumbral perfusion, if rapid and sustained, it can lead to cerebral edema and hemorrhagic transformation. However, for patients who are not candidates for thrombolytic therapies and have critical vascular stenosis, BP augmentation is the only way to perfuse the penumbra. The American Heart Association/American Stroke Association (AHA/ASA) 2007 guidelines recommend treatment of hypertension when SBP >220 mmHg or diastolic blood pressure (DBP) > 120 mmHg with a maximum reduction of 15% in the first 24 h in patients who are not candidates for thrombolytic therapies and when SBP > 185 mmHg and DBP > 110 mmHg in candidates for thrombolytic therapy. Hypotension is relatively rare after stroke. However, when it occurs, the clinician should look for and correct hypovolemia and decreased cardiac output state. Inotropes and vasopressors have been successfully used to augment the BP after the aforementioned measures have failed.
In patients with ICH the AHA/ASA guidelines recommend aggressive control of SBP >200 or MAP >150 mmHg guided by frequent BP monitoring (every 5 min). In patients with elevated ICP, the recommended MAP is <130 mmHg for the first 24 h, and in patients without suspected elevated ICP, the MAP goal is <110 mmHg. After a decompressive craniotomy, the recommended MAP is 100 mmHg. Similarly, the recommended lower limits are >90 mmHg for MAP and >70 mmHg for CPP. Comparison of the hematoma volume at 24 h with aggressive BP reductions versus standard ASA-recommended BP control revealed a 22.6% difference (13.7% vs. 36%, respectively) in hematoma growth. The 2010 AHA/ASA guidelines suggest that lowering of SBP to 140 mmHg (within 1 h) is probably safe. Short-acting IV drugs like labetalol, esmolol, nicardipine, and enalapril are preferred over nitroglycerin or nitroprusside to decrease the BP.
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