25 Daniel Hutton and John D. Cantando The neurosurgical intensive care unit (NICU) treats a variety of patients with a multitude of pathologies, ranging from aneurysms, both pre- and postop, to head and spinal cord injuries, to brain tumors. The goal of any systemic complication is the prompt diagnosis and return of adequate perfusion and oxygenation to neural tissue. Though focused on the management of neurologic injury, physicians and surgeons must maintain proper perspective of the primary tenets of intensive care medicine. This chapter reviews the chief systemic complications associated with the NICU patient and offers recommendations to prevent their occurrence. Aberrant electrolytes are the most common complication seen in the NICU, occurring in 59.3% of the Traumatic Coma Data Bank (TCDB) register.1 They are primarily in the category of early complications, seen from the time of admission through the first 5 days. It is therefore imperative to monitor fluid status, including total intake and output, daily body weight, and color and specific gravity of urine, so as to avoid unnecessary cerebral edema orvolume contraction. Consideration must be made for patients on chronicdiuretics, nasogastric or orogastric suction tubes, or with fever or diarrhea.Serum sodium and glucose are principally addressed due to their effects onserum osmolarity. Abnormalities in serum potassium are frequentlyencountered due to gastric suctioning, diarrhea, and medications. Alongwith correcting the underlying pathology, normal serum concentrationsshould be maintained (Tables 25–1 and 25–2). Hyperglycemia usually reflects a stress reaction and can worsen outcomeafter traumatic brain injury.2,3 To avoid this complication, serum glucoseshould be kept <110 mg/dL.
Systemic Complications
Electrolyte Disturbances
Hyperglycemia
| Syndrome of Inappropriate Antidiuretic Hormone (SIADH) |
Usually a euvolemic to slightly hypervolemic state, with urine osmolarity greaterthan serum osmolarity and elevated urine sodium Diagnosis: Serum sodium < 135 mEq/L Serum osmolarity < 280 mOsm/L Urine sodium > 40 mEq/L Treatment: Fluid restriction is paramount. Keep total fluid intake to <1000 mL/day. If volumerestriction may be detrimental to other coexisting pathology, demeclocycline maybe used. It is an antibiotic that partially blocks the renal collecting duct’s responseto ADH. For patients with elevated ICP or actively seizing due to hyponatremia, hypertonicnormal saline (3%) may be instituted. |
| Cerebral Salt Wasting Syndrome (CSW) |
Usually a hypovolemic state, with low serum sodium, elevated urine sodium, and elevated urine sodium Diagnosis: Urine sodium > 40 mEq/L in the setting of a hypovolemic state Treatment: Replacement of intravascular volume with isotonic normal saline (0.9%) is theinitial treatment of choice. If refractory, use hypertonic saline or salt tablet per mouth or feeding tube, depending on level of consciousness. |
ADH, antidiuretic hormone; ICP, intracranial pressure.
| Diabetes insipidus |
Inability to concentrate urine due to insufficient ADH in the circulatory system Pathophysiology based on damage to the pituitary stalk from increased ICP or shearing injury. May also be seen in patients with recent surgery in the sellar region (pituitary adenoma, craniopharyngioma, aneurysms of the circle of Willis, etc.). Extremely grave prognostic sign Diagnosis: Urine output >200–250 cc/hour for 2 hours Elevated serum sodium and other signs of volume contraction: increasing hematocrit, creatinine, urine specific gravity Treatment: Tenuous, due to the unwanted effect of excessive fluid exacerbating cerebral edema. Judicious doses of exogenous vasopressin are suggested to rapidly decrease the urine output and maintain vascular volume. |
ADH, antidiuretic hormone; ICP, intracranial pressure.
Pneumonia
Pneumonia is the second most common systemic complication in severe head injury.1 It usually occurs 5 to 10 days following injury. It also occurs more frequently due to impaired airway reflexes, leading to greater possibility of aspiration.
Risk factors include the following:
- Ventilatory assistance > 24 hours
- Use of barbiturates for treatment of increased intracranial pressure (ICP)4
- Presence of ICP monitor5
The diagnosis of pneumonia includes the following:
- High index of suspicion
- Obtaining routine surveillance sputum cultures
- Low threshold to start broad-spectrum antibiotics
To prevent this complication, avoid neutralizing gastric pH. The use of alkaline antacids and histamine type 2 blockers increases the risk of pneumonia.6 Sucralfate binds to negatively charged ions of damaged gastric mucosa and prevents ulcers without increasing the gastric pH.
Blood Pressure
Hypotension
Patients in the NICU frequently have episodes of hypotension. In multitrauma patients, other etiologies must be entertained, necessitating examination of pulse pressure, oxygen saturation, arterial blood gases, and cardiopulmonary and abdominal compartments. In patients with severe traumatic brain injury (GCS ≤8), it has been shown that a single episode of systolic blood pressure (SBP) < 90 mm Hg, from injury to arrival at the hospital, doubles the mortality. In the NICU, eliminating hypotension would reduce unfavorable outcome (Glasgow Outcome Scores 1, 2, and 3) by 9.3%.1 Additionally, patients with spinal cord injuries are prone to sustained hypotension, which, if not corrected, can lead to infarction.
To limit the effects of hypotension, the following recommendations are made:
- Patients with severe traumatic brain injury should have cerebral perfusion pressure (CPP) >70 mm Hg in most cases.
- Patients should be kept euvolemic, with a normal central venous pressure (CVP).
- Episodes of hypotension/suboptimal CPP should be treated first with fluids, then with vasopressors as necessary.
Spinal Cord Injuries and Hypotension
Patients with spinal cord injuries develop hypotension from a lack of sympathetic input to the vasculature, causing pooling and decreased return to the right heart, as well as unopposed parasympathetic tone to the heart, resulting in bradycardia. The goal of therapy is to maintain SBP >90 mm Hg.
The following general considerations apply to the treatment of spinal cord injuries:
- Maintain spinal precautions
- Provide adequate oxygenation
- Prescribe atropine for bradycardia and hypotension
- Continue judicious fluid management
- Watch for development of pulmonary edema
- Start vasopressors (dopamine is the vasopressor of choice)
Methylprednisolone must be given within 8 hours of injury.6 The initial dosage is 30 mg/kg intravenous (IV) bolus over 15 minutes (rate [mL/hour] = patient’s weight [kg] × 1.92). After a 45-minute pause, the maintenance dose is 5.4 mg/kg/hour (rate [mL/hour] = weight [kg] × 0.0864). The duration of maintenance therapy depends on the timing of the initial bolus. If it is given <3 hours from injury, maintenance steroids should be continued for 23 hours. If the initial dose is given 3 to 8 hours after injury, continue for 47 hours.7
Other investigational medications are naloxone, tirilizad mesylate, and lazaroid.8
Hypertension
Elevated blood pressure is of particular consequence in the NICU. Patients with unsecured aneurysms, arteriovenous malformations (AVMs), or intraparenchymal hematomas should have strict parameters for hypertension. However, hypertension associated with bradycardia and respiratory depression (Cushing’s triad) is symbolic for dangerously elevated ICP pressure and demands immediate evaluation. These symptoms may be easily missed if the patient is on a ventilator or because of autonomic instability.
Intravenous Treatment of Hypertension
Nitrates, specifically, nitroglycerine and nitroprusside, may elevate ICP and should be used cautiously. They preferentially dilate peripheral vasculature, creating a cerebral steal phenomenon. Prolonged use of nitroprusside may lead to thiocyanate toxicity.
Labetalol blocks α1 and β1, and β2 receptors. It has no effect on ICP. Labetalol may be used in controlled congestive heart failure (CHF): no coronary steal effect. It is contraindicated in asthma. The maximum dose is 300 mg/day.
Enalaprilat is an angiontensin converting enzyme (ACE) inhibitor that acts within 15 minutes. Side effects include hyperkalemia.
Thromboembolism
Deep venous thrombosis (DVT) is a common complication in the NICU. Although no hypercoagulable state is usually present, other risk factors, including endothelial damage and venous stasis, are due to immobilization or predisposing trauma. DVT may be as prevalent as 58% if no prophylaxis is used.9 Other risk factors include spinal cord injury; pelvic, femur, or tibia fractures; surgery; blood transfusion; and older age.9
Prophylaxis
Sequential compression stockings and low-dose heparin have been found to decrease the incidence of thromboembolism from 8.98 to 2.9%. Heparin is relatively contraindicated in patients with traumatic brain injury; therefore, compression stockings are generally advocated. Vena cava filters are advocated for first-line prophylaxis. However, with repeated embolization, filters may provide a more reliable means to protect against hypoxia.
Coagulopathy
Serologic markers for disseminated intravascular coagulation (fibrinogen split products) and degree of traumatic brain injury have been positively correlated.10 The most common site for diffuse intravascular thrombosis is the central nervous system, often resulting in necrosis.11 Microvascular and radiographically evident petechial hemorrhages and contusions are thought to be the result of disseminated intravascular coagulation.
Anemia
Optimal hematocrit is not well established. Patients with multisystem trauma or prolonged stays in the NICU are at greater risk of developing anemia of various etiologies. All primary sources of bleeding should be aggressively sought. Patients with blunt chest or abdominal injury should be evaluated for hemothorax and retroperitoneal bleeding, respectively. Other rare causes include medication reaction but are usually accompanied by hemolysis. A hematocrit greater than 33% is generally used to optimize cerebral blood flow.12
Fever
Fever is a potent vasodilator and can raise ICP and cerebral metabolic requirement for oxygen (CMRO2). Infectious causes should be aggressively sought and treated. Prophylactic antibiotics are generally unwarranted, with the exception of ventricular catheters. Antipyretics and cooling blankets should be used.
Hypoxia
In ventilated patients, common etiologies of hypoxia must be aggressively determined. To maintain adequate cerebral and systemic oxygenation, oxygen-carrying capacity, acid–base balance, and pulmonary pathologies should be determined. The initial evaluation should include hemoglobin/ hematocrit, arterial blood gases, chest x-ray, D-dimer, and venous duplex. If there is further suspicion of pulmonary embolism, spiral chest computed tomography (CT), ventilation/perfusion (V/Q) scan, or the gold standard pulmonary angiography should be expedited.
Sepsis
Sepsis is diagnosed by positive blood cultures along with meeting the crite ria for systemic inflammatory response syndrome (SIRS). SIRS can from a wide variety of etiologies, including infections, trauma, and stress The criteria for the diagnosis of SIRS are heart rate >90, temperature >38°or <36°C, tachnypnea >20 breaths/minute, and white blood (cell) (WBC) >12,000 cells/mm3 or <4000 cells/mm3.
Sepsis results in a derangement of fluid balance via an array of pathologies Insensible water loss results from elevated temperatures. Depleted intravas cular volume is multifactorial, but principally due to increased microvascular permeability13 and increased venous compliance, resulting in pooling.
Diagnosis hinges on a thorough examination of the patient and guided laboratory studies. Examination of the patient’s skin for decubitus ulcers infiltrated IVs or central lines is crucial. Removal of all indwelling central catheters, peripheral lines, and Foley catheters with culture is paramount for removing a possible nidus of infection. A chest x-ray should be per formed to evaluate for pneumonia or empyema.
Initial empiric treatment should be employed after cultures are taken Broad-spectrum treatment with two or more antibiotics may be started tailored once final cultures and sensitivities have returned. Aggressive hydration is also a cornerstone of treatment. When crystalloid fluids are adequate to maintain perfusion, dopamine is typically the initial vasopressor/inotrope of choice. Depending on the severity of sepsis, a Swan-catheter is often necessary to assess fluid volume, vascular resistance, cardiac output.
Gastrointestinal Bleed
Ulceration of gastric mucosa is commonly seen with traumatic brain injury Although the mechanism is not fully understood, most experts theorize that excess of gastrin with the resultant increase in gastric acidity weakens the gas tric mucosa. Kamada et al13 found that endoscopic evaluation of gastric mucosa demonstrates damage within the first 24 hours, with 17% of these erosions progressing to systemically significant hemorrhages. The severity of injury is directly related to the development of gastric bleeding.14 Other factors for gastric bleeding include respiratory failure, burns >25% body surface area, hypotension, sepsis, jaundice, peritonitis, coagulopathy, and hepatic fail ure. Prophylaxis includes antacids, which neutralize gastric acidity but time consuming; histamine type 2 blockers, which block acid production are potentially sedating and have a possible side effect of thrombocytopenia; and sucralfate, which strengthens gastric mucosa; does not alter gastrin, production, or pH; and produces less nosocomial pneumonia association.
Seizures
In those patients with severe head injury, seizures occur in ~15%.12 At times seizures may be difficult to monitor in the NICU because of sedatives and paralytics. There should be a heightened clinical suspicion to detect and subsequently initiate treatment. Therefore, if clinically warranted, continuous electroencephalography is the method of choice for detection. Though not associated with worse morbidity or mortality, seizures can potentially impair jugular venous oxygen saturation (SjvO2) if cerebral blood flow is already compromised.13 Prophylaxis against post-traumatic seizures is controversial and should be discontinued after 7 days.2,15
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