Abstract
A rapid increase in the volume and complexity of neurosurgical and neuroanesthesia procedures has necessitated the development of dedicated and specialized neurocritical care units. More invasive intracranial and hemodynamic monitoring as well as good general care with dedicated neurocritical care intensivists has resulted in improved outcomes in the neuro–intensive care unit (ICU). Cardiovascular care of these patients involves optimization of cerebral perfusion pressure based on objective monitoring of cerebral physiology, control of severe hypertension, and management of autonomic dysfunction. Prevention of hypoxia and selective use of hyperventilation to ensure adequate tissue oxygenation is important. Euvolemia, euglycemia, correction of electrolyte imbalance, and adequate nutrition are the goals in managing a patient with neurological disease. A wide variety of monitors for monitoring intracranial pressure and cerebral blood flow are available for use in the neuro-ICU. Multimodal monitoring appears to be the future of neuro-ICU.
Keywords
Cerebral blood flow, Cerebral perfusion pressure, Haemodynamics, Infections, Intracranial pressure, Neurocritical care, Neuromonitoring, Nutrition, Pathophysiology, Respiratory care
Outline
Introduction 595
History of Neurocritical Care 596
Design of a Neurocritical Care Unit 596
Clinical Conditions Requiring Admission to Neurocritical Care Unit 596
Justification for Neurological Critical Care Units 596
Pathophysiological Issues in Neurological Critical Care 597
Management of Patients in a Neurological Intensive Care Unit 598
Management of General Systemic Physiology 598
Cardiovascular Care 599
Optimization of CPP 599
Hemodynamic Manipulations in Vaso-Occlusive Conditions 599
Autonomic Dysfunction Initiated by the Neurological Injury 600
Autonomic Disturbances in Neuromuscular Diseases 601
Respiratory Care 601
Metabolic Milieu 602
Fluid and Electrolyte Balance 602
Infections 602
Nutrition 603
Thromboprophylaxis 603
Specific Therapeutic Issues in Individual Clinical Conditions 603
Advanced Neuromonitoring 603
Intracranial Pressure/Cerebral Perfusion Pressure 604
Cerebral Blood Flow Monitors 604
Transcranial Doppler Ultrasonography 604
Jugular Venous Oxygen Saturation 605
Near-Infrared Spectroscopy (NIRS) 605
Brain Tissue Oxygen Tension 605
Cerebral Microdialysis 605
Outcomes of Neurological Intensive Care Unit 606
End-of-Life Issues in Neurological Critical Care 606
Brain Death 607
Medical Futility 607
Withdrawal/Withholding of Care 607
Do-Not-Resuscitate Orders 607
Clinical Pearls 608
References 608
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.
| 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 |
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 ).
| 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.) |
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.
Autonomic Dysfunction Initiated by the Neurological Injury
Central nervous system (CNS) injuries of varied causes lead to autonomic dysfunction with consequences for the hemodynamic function.
Electrocardiographic (ECG) changes may manifest in 50% of patients with SAH. They may be in the form of dysrhythmias and morphological changes suggestive of cardiac ischemia. The range of changes described include T wave inversion, ST segment elevation or depression, QT prolongation, U waves, atrial flutter and fibrillation, ventricular fibrillation, supraventricular tachycardia, as well as premature atrial and ventricular contractions. Some patients manifest with ECG abnormalities suggestive of an acute myocardial infarction (MI). In most cases, these cardiac abnormalities resolve over a few days up to a few months following surgical clipping of the aneurysm.
Regional wall motion abnormalities are also common in SAH. The acute, reversible cardiac injury that occurs in 20–30% of patients with SAH ranges from hypokinesis with a normal cardiac index to low-output cardiac failure. Some patients exhibit both catastrophic cardiac failure and NPE. Takotsubo cardiomyopathy is a form of reversible cardiomyopathy diagnosed by transient left ventricular wall motion abnormalities involving the apical and/or midventricular myocardial segments with wall motion abnormalities extending beyond a single epicardial coronary artery distribution. Differentiating MI from reversible neurogenic left ventricular dysfunction associated with aneurysmal SAH is critical. Several studies have documented an increase in serum troponin concentration (cTn-I), which was a significant determinant of outcome in a multivariate study of SAH. Pulmonary edema occurs in 28.8% of patients after SAH.
Cardiac dysfunction is common in patients with TBI. Prathep et al. examined data from 139 patients with isolated TBI who underwent echocardiographic evaluation. Of this cohort, 22.3% had an abnormal echocardiogram: reduced left ventricular ejection fraction was documented in 12% (left ventricular ejection fraction, 43% ± 8%) and 17.5% of patients had a regional wall motion abnormality. Hospital day 1 was the most common day of echocardiographic examination. Abnormal echocardiogram was independently associated with all-cause in-hospital mortality (9.6 [2.3–40.2]; p = 0.002). TBI can lead to myocardial damage and ECG changes that have a significant association with the severity of injury. ST-T changes and QT prolongation are the independent prognostic factors for the unfavorable outcome of these patients.
Increased sympathetic activity as detected by heart rate variability (HRV) analysis has been correlated with raised ICP and higher mortality. Episodic autonomic dysfunction may occur after any type of brain injury, but is best defined in the paroxysmal sympathetic hyperactivity (PSH) following TBI. PSH occurs in 8–33% of patients with moderate-to-severe TBI. PSH has also been reported following hypoxia, stroke, and hydrocephalus. Patients with PSH have worse Glasgow outcome scores and worse functional independent measures than their counterparts. Magnetic resonance imaging studies discovered an increased number of deep lesions in patients with PSH. Imaging studies have revealed diffuse axonal injury rather than single causative lesion in patients with PSH. PSH seems to be a marker for severity of injury. Patients with PSH require mechanical ventilation for a longer period; they tend to have more infections and receive more tracheostomies than patients with TBI without PSH. In a retrospective review, patients with PSH spent 207 days in rehabilitation on an average compared with 44 days for their non-PSH counterparts.
Autonomic Disturbances in Neuromuscular Diseases
Cardiac abnormalities occur in patients with several forms of neuromuscular diseases including GBS, myasthenia gravis, and multiple sclerosis. Cardiac arrhythmias and postural hypotension are the most commonly reported abnormalities. Studies on HRV have documented significant autonomic imbalance in the acute phase of the disease in GBS with a progressive improvement with the clinical recovery of the primary pathology. Life-threatening myocardial failure in the form of neurogenic stunned myocardium has been reported in these conditions.
Patients with spinal cord injury (SCI) are a special group with a severe impairment of sympathetic tone and enhanced risk of cardiovascular disturbances. Apart from neurogenic shock immediately after a high-level SCI, other manifestations of cardiovascular dysfunctions include orthostatic hypotension, autonomic dysreflexia, and cardiac arrhythmias. Patients with SCI exhibit a lesion-dependent impairment in resting cardiovascular function; those with the highest injury tend to have the greatest degree of dysfunction. Life-threatening bradycardia in some of the patients may warrant insertion of a pacemaker.
Respiratory Care
Maintaining adequate tissue oxygenation is very important in the setting of neurological critical care. Respiratory care should be directed at preventing cerebral hypoxia and worsening of brain injury. The most common causes of hypoxia are airway obstruction, hypoventilation, irregular breathing patterns, aspiration pneumonia, pulmonary edema, and atelectasis. Patients with decreased consciousness or brain stem dysfunction have the highest risk of airway compromise. Recent evidence suggests that cough and swallowing mechanisms are impaired even in patients with cerebral hemispheric involvement. Medical complications occur in 59% of patients with stroke, with pneumonia occurring in about a third of them and contributing to prolonged ICU/hospital stay and higher mortality (26.9% vs. 8.2% with and without pneumonia). Elective intubation, good oral care, appropriate antibiotic therapy, frequent positional change, chest physiotherapy, and prompt diagnosis and treatment of chest infection along with early mobilization and swallowing rehabilitation go a long way in improving outcomes after any major neurological injury. Elective tracheal intubation apart from preventing aspiration pneumonia also helps in the management of patients with increased ICP or malignant brain edema. Therefore, tracheal intubation may be considered when any of the aforementioned respiratory abnormalities are not corrected by simple measures such as introduction of an oropharyngeal airway and administration of oxygen by mask. Tracheal intubation, however, is not without its risks in patients with intracranial pathology. Laryngoscopy and intubation may cause cardiovascular stress, intracranial hypertension, and pulmonary aspiration. An ideal technique of intubation requires suppression of these responses with sedative/hypnotic drugs and cricoid pressure to prevent pulmonary aspiration. Attention must be paid to the hypotension that may be caused by the sedative drugs. Pragmatic choice of the sedative drugs and their dosages, a good IV access for administration of fluids/vasopressors, and adequate preoxygenation before intubation helps to prevent dangerous levels of hypotension and hypoxia that threaten the viability of the already vulnerable brain.
In patients in whom the possible futility of therapy is a major issue, the decisions should be made with greater prudence. Mechanical ventilation may be initiated with the understanding that it could be withdrawn if there is no neurologic improvement or further deterioration. Defining, in advance, a specific degree of neurologic improvement within a predetermined time frame may serve to establish futility in a given situation. Mechanical ventilation may also be used in preparation for other, potentially useful but unproved interventions.
Hyperventilation, as an ICP control measure, has attracted the clinicians’ attention for a long time. While its ability to cause cerebral vasoconstriction and decrease the ICP rapidly remains undisputed, its potential to cause cerebral ischemia has come under closer scrutiny over years. Hyperventilation should be restricted to a treatment strategy used only for intracranial hypertension that is not amenable for other simpler measures. Any ventilatory setting that achieves normocapnia (PaCO 2 = 35 mmHg) and mild to moderate hyperoxia (PaO 2 = 150–200 mm Hg) and does not impose excessive work of breathing on the patient’s respiratory muscles is acceptable. Most often, mechanical ventilation is started in a controlled mode (either volume or pressure control) and then changed to an assisted mode (pressure support mode) as neurological improvement occurs.
Concerns have been expressed about the effect of positive pressure ventilation and positive end expiratory pressure (PEEP) in particular, on ICP and cerebral perfusion. However, PEEP up to 10 cm H 2 O has been shown to decrease CPP only in patients with impaired and not intact autoregulation.
Sedation and/or neuromuscular blockade are necessary to facilitate mechanical ventilation in all patients with encephalopathy, except in those who have a profound neurological deterioration. Opioids (morphine, fentanyl) and benzodiazepines (midazolam) are commonly used for this purpose. Of late, dexmedetomidine is being increasingly used in neurologically critical patients, as it has a favorable respiratory profile and it facilitates frequent neurological assessment. Most often, sedatives are given as continuous infusions. Some centers prefer to use hypnotic drugs such as propofol as continuous infusions. Apart from providing hypnosis, it also decreases the ICP, but has a potential to cause systemic hypotension, which may adversely affect CPP and CBF. Muscle relaxants are to be used sparingly. Succinylcholine offers ideal conditions for smooth and rapid intubation in acute situations. However, it may cause hyperkalemia, cardiac arrhythmias and transient increase in ICP. Vecuronium, rocuronium, and atracurium are the competitive neuromuscular blocking agents that are commonly used as continuous infusions. All of these cause minimal hemodynamic changes.
Metabolic Milieu
A variety of metabolic disturbances may accompany brain injury. Two most common disturbances relate to glucose and sodium.
Hyperglycemia accompanying brain injury has gone through extensive clinical research. Still, it is not clear if hyperglycemia is a cause of poor outcome or it is just a marker of the severity of illness. However, for the time being, there is a consensus that aggressive control is detrimental to the patient and a modest control to 120–150 mg/dL is appropriate.
Both hyponatremia and hypernatremia are common in neurological patients. Traditional description of salt-wasting and syndrome of hormone secretion is probably an oversimplification of the problem. Same is the argument with diabetes insipidus as the cause of hypernatremia. An elaborate clinical and laboratory assessment is warranted in individual cases to provide a treatment appropriate to the pathophysiology of the patient.
Hypothalamic injury may lead to endocrinal derangement in TBI and SAH. Appropriate hormonal supplements are warranted to stabilize the cardiovascular and metabolic status (e.g., hypotension, hyperglycemia, electrolyte disturbances).
Fluid and Electrolyte Balance
The contradictory needs of cerebral dehydration with osmotic and nonosmotic agents and maintenance of adequate intravascular volume to ensure optimal cerebral perfusion demand careful monitoring of filling pressures, fluid intake–output charts, and serum electrolytes. The management becomes even more complex if the patient has other common complications in the ICU such cardiac failure, sepsis, and renal failure. The use of hypervolemic therapy to augment cerebral perfusion adds additional complexity to the fluid management. Repeated echocardiography might help to optimize preload and contractility.
Infections
Meningitis or ventriculitis, brain abscess, subdural or epidural empyema, and encephalitis are the most common forms of intracranial infections seen in a neurological ICU. Apart from these primary infections, nosocomial infections may complicate the clinical course of the neurological patients admitted for noninfective conditions. A history of neurosurgery; cerebrospinal fluid (CSF) leakage or recent head trauma; presence of cranial or extracranial infectious foci such as otitis, sinusitis, or pneumonia; and a potentially immunocompromised state are the important risk factors for nosocomial intracranial infections. A recent meta-analysis of 23 retrospective studies reported a cumulative rate of positive CSF cultures of 8.8% per patient and 8.1% per external ventricular drainage. The incidence of bacterial meningitis after moderate or severe TBI has been estimated to range between 1% and 2% with CSF leakage as the major risk factor and fracture of the basal skull increasing the risk up to 25%. Multidrug-resistant pathogens contribute to the complexity of the management of nosocomial infections of the CNS. Continuous surveillance including systematic collection and analysis of the local epidemiological data, timely diagnosis, and prompt initiation of appropriate antimicrobial chemotherapy is important to improve the outcome.
Nutrition
Meeting the nutritional requirements of the critically ill neurological patients could be challenging. Fortunately, the majority of patients tolerate nasogastric/gastrostomy/jejunostomy feeds. Caloric requirement of the patient may be calculated by using indirect calorimetry or established equations such as Harris Benedict’s equation, or by using weight-based formulae (approximately 25–30 cal/kg body weight). Patients with TBI who are not paralyzed have a resting energy requirement of 140% of the estimated normal value; the requirement in paralyzed patients is equal to 100%. The requirement for protein is 0.8–1.2 g/kg/day in patients without any additional stressors and 1.0–1.5 g/kg/day in patients with stress. Protein requirement calculated as calorie/nitrogen ratio is 150:1 under normal conditions and 125–100:1 under conditions of stress. The lipid to carbohydrate ratio should be around 30:70 to 60:40. The requirements of electrolytes in an adult are as follows: potassium, 1–1.2 mEq/kg/day; magnesium, 8–20 mEq/day; calcium, 10–15 mEq/day; and phosphate, 20–30 mmol/day. Trace elements such as copper, molybdenum, selenium, zinc, manganese, chromium, iron, and iodine need to be added in patients on parenteral nutrition. Commercial multivitamin preparations that usually contain all vitamins have to be added.
A 2013 meta-analysis of nutrition in TBI demonstrated that, compared with delayed feeding, early feeding is associated with a significant reduction in the rate of mortality [relative risk (RR) = 0.35; 95% confidence interval (CI), 0.24–0.50], poor outcome (RR = 0.70; 95% CI, 0.54–0.91), and infectious complications (RR = 0.77; 95% CI, 0.59–0.99). Compared with enteral nutrition, parenteral nutrition showed a slight trend toward reduction in the rate of mortality (RR = 0.61; 95% CI, 0.34–1.09), poor outcome (RR = 0.73; 95% CI, 0.51–1.04), and infectious complications (RR = 0.89; 95% CI, 0.66–1.22), without statistical significances. The immune-enhancing dietary formulae are associated with a significant reduction in infection rate compared with the standard formulae (RR = 0.54; 95% CI, 0.35–0.82). Small-bowel feeding was associated with a decreasing rate of pneumonia compared with nasogastric feeding (RR = 0.41; 95% CI, 0.22–0.76).
Yet another study has shown that the Glasgow Coma Scale (GCS) did not significantly affect the mean percentage of caloric goal administered in patients with a minimum daily GCS <11. Clinical care factors, such as time to enteral nutrition orders and enteral access confirmation, were significant impediments to provision of enteral nutrition than the patient’s clinical condition.
Thromboprophylaxis
Prevention of deep venous and pulmonary thromboembolism requires prophylactic anticoagulation. This therapy, however, entails the risk of increase in the hemorrhagic cerebral lesions. In a study of 87 patients with trauma, the rate of clinically significant deep venous thrombosis (DVT) was 6.9%. A thromboprophylactic protocol in the neurosurgical ICU was useful in controlling the number of complications from DVT and pulmonary embolism while avoiding additional intracerebral hematoma.
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