10. Diseases of the CNS may disrupt the control of water, glucose, and sodium. The unconscious patient can no longer adjust the intake of food and fluids by hunger and thirst. Both salt-losing and salt-retaining syndromes have been described with brain disease (see Chap. 26). Water intoxication and severe hyponatremia may of themselves prove damaging. If coma is prolonged, the insertion of a nasogastric tube will ease the problems of feeding the patient and maintaining fluid and electrolyte balance. It is quite acceptable to leave the tube in place for long periods. Otherwise, approximately 35 mL/kg of isotonic fluid should be administered per 24 h (5 percent dextrose in 0.45 percent saline with potassium supplementation unless there is brain edema, in which case the use of hypertonic normal saline is indicated).
11. Aspiration pneumonia is avoided by prevention of vomiting (gastric tube and endotracheal intubation), proper positioning of the patient, and restriction of oral fluids. Should aspiration pneumonia occur, it requires treatment with appropriate antibiotics and aggressive pulmonary physical therapy. Oral decontamination with chlorhexidine is advised to reduce the incidence of ventilator-associated pneumonia.
12. Leg vein thrombosis, a common occurrence in comatose and hemiplegic patients, often does not manifest itself by obvious clinical signs. An attempt may be made to prevent it by the subcutaneous administration of heparin, 5,000 U q12h, or of low-molecular-weight heparin, and by the use of intermittent pneumatic compression boots. There are few absolute contraindications to the prophylactic use of low-dose anticoagulants such as heparin and enoxaparin.
13. If the patient is capable of moving, suitable restraints should be used to prevent him from falling out of bed and to avert self-injury from convulsions.
14. Regular conjunctival lubrication and oral cleansing should be instituted.
Prognosis of Coma (See Also “Prognosis of Hypoxic-Ischemic Brain Injury” in Chap. 39.)
As a general rule, recovery from coma of metabolic and toxic causes is far better than from anoxic coma, with head injury occupying an intermediate prognostic position. Most patients who are initially comatose as a result of a stroke will die; subarachnoid hemorrhage in which coma is a result of hydrocephalus is an exception and those cases in which brain shift is relieved by craniectomy are also exceptions. In regard to all forms of coma, but particularly after cardiac arrest, if there are no pupillary, corneal, or oculovestibular responses within 1 day of the onset of coma, the chances of regaining independent function are practically nil (Levy et al). Other signs that predict a poor outcome according to an analysis of various studies by Booth and colleagues are absence of corneal reflexes, eye-opening responses, atonia of the limbs at 1 and 3 days after the onset of coma, and absence of the cortical component of the somatosensory-evoked responses on both sides. A consecutive series of comatose patients followed by Kowalski and colleagues found that predictors of awakening from coma included younger age, a nontraumatic etiology as alluded to above, an higher Glasgow Coma Score and lesser amounts of pineal shift (see Chap. 39 for further details).
The frequency of vegetative state after head injury and the negligible chances of improvement if the condition persists for several months have already been discussed, and a discussion of the outcome of anoxic–ischemic coma can be found in Chap. 39. The novel perspectives that have been introduced by demonstrating residual and willful cognitive activity in survivors of traumatic brain injury have been discussed in an earlier section.